SlideShare a Scribd company logo
1 of 69
COMPARISON OF RISK FACTORS IN YOUNG
ADULTS WITH OLDER ADULT PATIENTS WITH
RECENT MYOCARDIAL INFARCTION AT DR
RUTH PFAU CIVIL HOSPITAL KARACHI
A RESEARCH THESIS
Submitted to the Board of Advanced Studies and Research
Dow University of Health Sciences Karachi
By
Dr Sajad Ahmed Badvi
MBBS, DIPLOMA IN CARDIOLOGY (DIPCARD), DOCTOR OF
MEDICINE IN CARDIOLOGY (MD) {DUHS}
Table of Contents
Abstract ....................................................................................................I
Background...............................................................................................I
Objective...................................................................................................I
Methods....................................................................................................I
Results ...................................................................................................I-II
Conclusion................................................................................................II
Chapter 1 ...................................................................................................
1. Introduction......................................................................................1
1.1 Background......................................................................................4
1.2 Objective of Study.............................................................................6
1.3 Hypothesis.......................................................................................6
1.4 Operational Definitions ......................................................................6
Chapter 2 ...................................................................................................
2. Review of Literature ...........................................................................9
2.1 Definition of M.I and Types of M.I ...................................................9-10
2.2 Pathophysiology of M.I ....................................................................12
2.3 Causes of M.I .................................................................................15
2.4 Diagnosis of M.I .............................................................................28
2.5 Management of M.I ........................................................................29
2.6 Epidemiology of M.I ........................................................................30
Chapter 3 ...................................................................................................
3. Materials and Methods.....................................................................34
3.1 Research Design and Settings............................................................34
3.2 Study Duration ...............................................................................34
3.3 Inclusion Criteria ............................................................................34
3.4 Exclusion Criteria ............................................................................34
3.5 Sampling Techniques ......................................................................34
3.6 Sample Size Estimation ....................................................................34
3.7 Data Collection...............................................................................35
3.8 Data Analysis..................................................................................35
Chapter 4 ...................................................................................................
4. Results...........................................................................................36
Chapter 5 ..................................................................................................
5. Discussion ......................................................................................46
5.1 Limitations.....................................................................................49
5.2 Recommendations ..........................................................................49
5.3 Conclusion.....................................................................................50
References .............................................................................................51
LIST OF TABLES:
Table 1: Comparison of age between groups Page:40
Bar Graph 1: Comparison of gender between groups Page:4o
Table 2: Comparison of smoking between groups Page:41
Table 3: Comparison of diabetes between groups Page:41
Table 4: Comparison of hypertension between groups Page:41
Table 5: Comparison of family history of IHD between groups Page:42
Table 6: Comparison of sedentary lifestyle between groups Page:42
Table 7: Comparison of obesity between groups Page:42
Table 8: Comparison of dyslipidemia between groups Page:43
Table 9: Comparison of substance abuse between groups Page:43
Table 10: Comparison of blood urea between groups Page:44
Table 11: Comparison of serum creatinine between groups Page:44
Table 12: Comparison of lipid profile between groups Page:45
FIGURE
 Figure: Blood supply of heart Page:27
LIST OF ABBREVIATIONS
ACS = Acute Coronary Syndrome
AHA = American Heart Association
ACEI = Angiotensin Converting Enzyme Inhibitors
AMI = Acute Myocardial Infarction
ATP = Adenosine Triphosphate
ADP = Adenosine Diphosphate
BMI = Body Mass Index
CABG = Coronary Artery Bypass Grafting
CAD = Coronary Artery Disease
CHD = Coronary Heart Disease
CBC = Complete Blood Count
CKD = Chronic Kidney Disease
DM = Diabetes Mellitus
ECG = Electrocardiography
ESC = European Society of Cardiology
FH = Family History
FBS = Fasting Blood Sugar
HBP = High Blood Pressure
HDL = High Density Lipoprotein
IHD = Ischemic Heart Disease
LBBB = Left Bundle Branch Block
LDL = Low Density Lipoprotein
PCI = Percutaneous Coronary Intervention
RBS = Random Blood Sugar
SD = Standard Deviation
WHO = World Health Organization
i
ABSTRACT
BACKGROUND: Myocardial infarction occurs when a rise or fall recorded in
troponin and one of the values must be 99th
percentile of upper reference limit along
with ischemia evidence. There is a common factor in young patients having a family
history of coronary artery disease. More young patients were smokers, and drug
abusers. However, a history of previous MI or angina was found less in younger age
patients. Similarly, major risk factors of coronary artery disease like diabetes and
obesity were also found less in young age group, compared to the older age group.
OBJECTIVE: To compare the risk factors in young adults with older adults’ patients
suffering from recent myocardial infarction admitted in the cardiology unit of civil
hospital Karachi.
METHODOLOGY: The patients admitted in the cardiology department having age
<35 years or equal to 35 years were placed in one group and patients age >35 years
were placed in another group. The questionnaire has questions regarding socio-
demographic aspects with ST-elevation and risk factors like gender, family history of
myocardial infarction, hypertension, diabetes, smoking, substance abuse, and lifestyle.
These factors with ECG and lab tests were compared to determine statistical
significance in two groups. The collected data were analyzed through SPSS v25.0. To
find the statistical significance between the two groups Chi-square test is used. The
significance was done labelled as p<0.05. All these results were presented in tables and
graphs.
My study showed that young adult group(69.8% were males v/s 3o.2% females) older
adult group(76.2% were males v/s 23.3% were females), smoking was common in
young patients (63.5% in young v/s 31.7% in older group) similarly family history of
IHD was common in young patients (57.1% in young v/s 12.7% in older group),
ii
similarly substance abuse intake without smoking were (26.9% in young v/s 39.6% in
the older group) and substance abuse used with smoking 57.1% were young v/s 19.0%
were older), diabetes mellitus was less common in young patients (12.7% in young v/s
82.5% in older group), similarly hypertension was less common in young
patients(15.9% in young v/s 98.5% in older group), sedentary lifestyle was more
common in older patients (11.1% in young v/s71.4% in older group), again obesity was
more common seen in older patients (15.9% in young v/s 55.6% in older group),
similarly dyslipidemia was also common in older group (31.7% in young v/s 82.5% in
older groups).
CONCLUSION: Smoking, Substance abuse and Family History of IHD were the more
common risk factors among young age group patients of M.I. While conventional risk
factors are common in older age group .Hence more effort is required to protect young
population. Hence, we recommend at the national level to stop smoking, have physical
activities, chose healthy and better life style to promote good health in society and
advise policy makers to spread awareness through electronic, print media and arrange
seminars in societies to avoid substance abuse materials.
KEYWORDS: Coronary Atherosclerosis, Risk factors, Young v/s Old adults,
Myocardial Infarction.
1
Chapter: 1
INTRODUCTION
Myocardial Infarction (MI) occurs when rise and fall are recorded in troponin(1)
and one of the values
above 99th
percentile of upper reference limit along with evidence of ischemia. The main symptoms of
MI are chest pain(2)
, shortness of breath, feeling of discomfort with heart burning, cold sweat, and
nausea.
The pain mostly travels from chest to arm, shoulder, jaws, neck, and back. M.I. is an old age disease
however it can also develop in young age grown-ups. However, it has different risk factors and
complications as compared to old age patients. M.I. occurs due to plaque rupture which reduces the
supply of blood to the heart. (3)
In a study (4)
conducted in the USA, it was determined that the prevalence of M.I. in the younger age
group (<45 years) was 6 to 10 percent. In a study(5)
of India, it was observed that in South Asians, the
occurrence of MI in the young population is high as compared to other regions. According to the study,
the incidence of coronary arterial disease was determined as 12 to 16 percent.
According to a study,(6) conducted in Pakistan, AMI in<40 years of age accounts for approximately
19%. It is more common in men who were smokers. However, in 10% of cases, the cause was not
related to atherosclerosis.
Another study(92)
Abdul Samad et al. performed in Pakistan shows that the rising profile of patients with
AMI is that the bulk is male, comparatively younger were <45 years, have smoked 52%, hypertension
55% and diabetes 36% and IHD 44% were major risk factors. higher management of risk factors and
the awareness of preventive ways are needed.
Study(18)
Faisal et al. Smoking 76.66%, hypertension 6.6%, diabetes 3.3% and dyslipidemia 43.3% are
common modifiable risk factors in our young adults<35 years. Three or additional risk factors in a
personal incline to CAD at comparatively in younger age.
2
Study, (7)
concluded that clinical findings and major risk factors of acute MI are quite different in young
age patients as in old age patients. In the US, the main cause of mortality in either sex was M.I.
Similarly, myocardial infarction was the major reason for hospitalization worldwide.
The most common risk factor which contributed to the narrowing of coronary arteries was high
cholesterol in older age. (8)
Another study determined that elevated homocysteine and alcohol are major
risk factors for developing AMI among young patients whereas in old age patient’s hypertension is the
main risk factor. (9)
Another Study concluded that the risk profile of CAD is different in old age group as compared to
young age patients and mortality is much higher in the old age group compared to young age group. (10)
Mortality in long term is fivefold less in young age people suffering from M.I, compared to old age
people. (11)
According to a study, it was determined that predictors of non-invasive therapy were the
same for all ages but different in AMI cases. (12)
However, in young age CAD patients, the potential
remains more for improvement in the cardiovascular risk profile. (13)
In a study,(14)
in young age patients of M.I, the risk factors, such as the family history of CAD, smoking,
and dyslipidemia were found to be much higher (28.6%, 64.5%, and 49.7% respectively) compared to
old age patients (19.8%, 59.4%, and 38.8% respectively). However, M.I. history and angina history
were found less in young age patients of M.I. (17.4% and 9.2%) as compared to old age patients (26.7%
and 26,1%).
It was determined in a study that dyslipidemia, hypertension, and diabetes were the predominant risk
factors in old age patients of MI. Similar to it, in different studies, (15)
smoking (58.7% -76.7%) was the
most common risk factor in young age patients as compared to old age group patients with MI (31.7%-
59.4%). (16)
In another study, (17)
SRIKANTH YANDRRAPALLI and CHRISTOPHER NABORS 2019 by Journal
of American College of Cardiology the relative risk factors in the young age population were
determined that smoking, hypertension, and dyslipidemia were more prevalent. One study,(18)
reported
3
that dyslipidemia was high in younger population (49.7% v/s 38.85), whereas other studies (19)
reported
it higher in old age patients (43.3% v/s 49.5% and 20.0% v/s 29.0%).
The risk factors such as DM and obesity were found less in the young age group. Other studies (20)
also
shown diabetes (3.3- 5% in young v/s 30-38.6% in older) and obesity (6.6% in young vs. 21.4% in
older) as fewer risk factors in the young age population.
According to a study, (21)
the risk factors of MI have significant gender differences in short and long-
term clinical outcomes of young patients. Therefore, preventive strategies should be taken to reduce the
risk factor in young adults.
The aim of my study was to find out risk factors that are causing M.I.in young population so through
preventive measures reduce chances of IHD and protecting the patients from huge expensive heart
disease treatment. Since last more than five years no research occurred on such topic.
Further aim of my study was to determine the effects of substance abuse drugs on heart how these
substances causes IHD .because nowadays the tendency of our young population to take drugs has
increased especially they use alcohol,Gutka/ Betelnut more frequently.
Most of the cases registered in my study were also found to be addictive of smoking, alcohol,
gutka/betelnut.
4
BACKGROUND
The main reason behind myocardial infarction (MI) is an imbalance of oxygen supply and
demand which is caused by the formation of plaque rupture in an epicardial coronary artery, as
a result, acute reduction of blood supply in the myocardium occurs.
The findings of an acute MI are presented below in the electrocardiographic (ECG).
ECG shows Acute Inferior Wall Myocardial Infarction
Taken from: https://emedicine.medscape.com/article/155919-overview
In acute coronary syndrome, MI is considered a part of the spectrum (ACS). The spectrum of
ACS(22)
consists of ST-segment elevation M.I, non-ST-segment elevation M.I and unstable
angina that is collectively known as an acute coronary syndrome. Patients with non-ST-
segment elevation M.I might have T-wave or ST-segment changes that occur on the surface
(ECG),
Persistent and continuing transmural myocardial injury shows ST-segment elevation MI seen
on the ECG(23)
. Many patients who develop Q-waves have already dead myocardial area or
myocardium at risk of death unless immediate reperfusion therapy has been given.
5
In the presence of cardiac enzymes, the patients are diagnosed to have NSTEMI with the
absence of raised cardiac enzymes indicates UNSTABLE ANGINA.(24)
Both these conditions
produce ST and T wave morphological changes on surface ECG.
Due to MI systolic and diastolic impairment can occur and this leads to long-term
complications. (25,26)
Primary treatment of acute MI includes coronary thrombolysis and
percutaneous revascularization. (27)
Benefit of the open infarct-related artery with percutaneous
route is more pronounced when the door to balloon time is kept within 90 minutes after first
medical contact in same way benefit with fibrinolytic is achieved when the door to injection
time within 30 minutes after first medical contact. Ventricular functions, collateral blood flow,
prevention of ventricular remodeling improves by the opening of an infarct-related artery. (28)
6
OBJECTIVE
To compare the risk factors in young adults with older adult patients suffering from recent
myocardial infarction admitted in the cardiology unit of civil hospital Karachi.
Null Hypothesis:
There is no difference in risk factors of young adults and older adults’ patients suffering from
recent myocardial infarction.
Alternate Hypothesis:
The risk factors of young adults are different from the risk factors of older adults’ patients
suffering from recent myocardial infarction
OPERATIONAL DEFINITIONS
Myocardial Infarction
Myocardial Infarction (MI) occurs when a rise or fall in cardiac troponin levels recorded with
one value must be above the 99th
percentile of upper reference level along with ischemia
evidence.
ST-Elevation MI:
It is defined as 1mm ST-segment elevation in two or more adjoining leads often with reciprocal
ST depression in contra lateral leads. Except in leads V2, V3 where criteria for men is 2.5mm
of ST elevation<40 years and 2mmST elevation >40 years and in female 1.5mm ST-segment
elevation on ECG is considered diagnostic.(4,13)
7
NST Elevation MI:
It is distinguished from unstable angina by the presence of elevated serum levels of cardiac
biomarkers, serial measurements in patients presenting with ACS should be performed. In
patients of NST elevation, MI and unstable angina both produce ST and T wave changes on
ECGs.
Hyperlipidemia:
It is a condition in which total cholesterol is >200 mg/dl, LDLC >100mg/dl, and HDL goes to
<40mg/dl or they are on statin therapy.(19,59)
Young adult age:
<35 years of age or equal to 35 years.(18)
Old adult age:
>35 years of age
Diabetes Mellitus:
All the patients having HbA1c more than 6.5% or fasting blood sugar more than 126 mg/dl and
random blood sugar more than 200 mg/dl or they are on anti-diabetic therapy will be counted
as diabetics.(29)
Hypertension:
In patients with blood pressure >130/80mmHg or patients taking antihypertensive therapy for
control of blood pressure.(30)
8
Smoker:
Patients taking minimum five cigarettes per day for at least one-year duration is called a
smoker.(48)
• Current < 1 month
• Recent 1month to 1 year
• Ex-smoker More than 1 year
• Non-smoker
Obesity:
If BMI is exceeded to 30 Kg/m2.
.(61)
Normal 18.5 to 24.9 Kg/m2
.
Overweight 25 to 27.8 Kg/m2
.
Obese > 30Kg/m2
Sedentary Lifestyle
The patient achieved a METS score <1.5 Oxygen cost ml/kg /min. watching the T.V, playing
video games, sitting in the office between 6.7 to 8 hours /day.(93)
9
Chapter: 2
REVIEW OF LITERATURE
DEFINITIONS
The fourth universal definition of myocardial infarction(31)
Heart attack's second name is myocardial infarction (MI) which is defined pathologically when
myocardial cells are dead due to ischemia. Clinically myocardial infarction is a condition
apparent in most cases from major symptoms such as chest pain. It is supported by
electrocardiographic changes, elevated cardiac biomarkers that indicate myocardial necrosis.
Detection of an increase or decrease in cardiac markers while using troponin may be associated
with the following findings. By autopsy or angiographic the identification of thrombus
intracoronary.
• Ischemia symptoms
• New wave (ST-T) or LBBB significant.
• In ECG formation of Q waves (pathologic)
• Evidence by imaging with regional wall motion abnormality.
10
Types of MI
According to the joint WHF/ESC/AHA task force, MI has the following 5 types.
• Type 1 includes atherosclerotic plaque rupture. Dissection, erosion fissuring in the
coronary artery leads to decrease myocardial blood flow that nearly is myocyte necrosis
resulting. The patient may have CAD. (32)
• Type 2 leads to ischemic imbalance, at this stage cell demand more oxygen, but has
less supply. (33)
• Type 3 leads to patient death when biomarkers values are unavailable. Sudden before
blood sample to biomarker has taken when unexpected cardiac death can happen.
d) Type 4a MI is associated with PCI (34)
e) Type 4b MI is associated with stent thrombosis
f) Type 5 MI is associated with CABG
11
ACUTE CORONARY SYNDROME
The expression "intense coronary disorder" (ACS) alludes to a range of conditions that occur
because of intense myocardial ischemia or potentially localized necrosis because of a sudden
decrease in blood supply to the myocardium. (35)
STEMI
The major segregating highlight of STEMI is the nearness of indications of myocardial
ischemia/damage alongside tenacious ECG ST-Segment height not necessarily elevation of
cardiovascular biomarkers. (36)
RECENT M.I
Ongoing
myocardial localized necrosis characterized that had happened two days to five weeks after
M.I. (37)
12
PATHOPHYSIOLOGY
Cellular effects of myocardial infarction (MI)
A normal heart needs a blood supply to work properly and delivers blood to the entire body.
Oxygen is also needed to work properly. Hearts need oxygen supply properly and also need
supplements for their functioning by coronary dissemination. Ischemia is a condition when
blood supply to the myocardium is inadequate.
If this event persists then it damages heart cells and becomes it's fiery and biochemically, in
the long run, heart muscles cells become irreversibly damaged.
The progression of this disorder first indicates necrosis of coagulation and then a healing phase
of myocardial scar formation called myocardial fibrosis. That is a serious health concern.
These all things slowly build changes to contractile capacity and shape of the myocardium,
especially in the left ventricle. That all reduced heart contractile capacity. Later over time
heart's left ventricle becomes widens and changes to a round shape in a process called
redesigning of the left ventricle. With time serious health problems occur with this condition
of the heart.
Ventricular redesigning is a regulated process so specific treatment strategy particularly ACE
inhibitors or ARB should be used in AMI management to reduce the occurrence and
seriousness of ventricular redesigning. (38)
Myocardial stunning and hibernation are both triggered by the loss of fundamental metabolites,
for example, adenosine, necessary for adenosine triphosphate (ATP)-dependent contraction,
which is needed for normal myocardial contractility (39)
13
Plaque
Atherosclerotic plaques which cause M. I. Plaques occur in multiple stages in a dynamic
process. The process can be seen immediately after birth, initially, intima thickening occur
which comprise of vascular smooth muscle with very few or no inflammatory cells,
subsequently, a fibrous cap atheroma with a lipid-rich necrotic core surrounded by fibrous
tissue develops and finally a thin cap atheroma develop, which is with a large necrotic core
mainly isolated from blood vessels known as vulnerable plaque that are penetrated by
inflammatory cells and are susceptible to rupture due to lack of smooth muscle cells (40,41)
The course of acute coronary thrombosis leading to ACS involves a pathogenic mechanism of
plaque rupture and less frequent plaque erosion. When complete obstruction of the coronary
artery occurs by thrombus it causes ST-Segment elevation M.I and when partial obstruction
occurs it causes either NSTEMI or unstable angina.
The Brasilia Heart Study Group shows that the antiatherogenic capacity of (HDL) to transport
blood vessels lipids can be altered by modification of high-thickening lipoprotein (HDL) in the
MI. Specialists observed simultaneous lipid substitution to HDL and the limit HDL to efflux
cell cholesterol. (42)
Settled case-control study examining plasma metabolic markers relationships with the risk of
MI, ischemic and intra-cerebral bleeding showed that lipoproteins and lipids were in a
favorable relationship with MI and ischemic stroke but were not with intracerebral hemorrhage.
(43)
14
Non-modifiable risk factors for atherosclerosis include the following:
•
Sex
•
Age
•
Family history of CHD
•
baldness Male-pattern
Modifiable Risk Factors (44)
•
Dyslipidemia
•
Diabetes mellitus
•
Obesity (abdominal obesity)
•
Smoking
•
Psychosocial stress
•
Type A personality
•
Elevated homocysteine levels
•
lack of exercise
•
Presence of peripheral vascular disease
15
COMMON RISK FACTORS OF MYOCARDIAL INFARCTION
There are various risk factors of AMI. Among them, some are modifiable (treatable)
and others are non-modifiable (cannot be changed). The major risk factors of AMI are
described below.
Age
Old age increases mortality in acute myocardial infarction. (45)
The mechanism by
which elevated age contributes to increased mortality is unknown. About 80% of heart
disease deaths occur in people aged 65 or older. (46)
Gender
Men have more lifetime heart attacks than females. (47)
Women's heart problems occur
primarily after menopause. And now, both men and women face heart disease as the
leading cause of death.
Smoking
Smoking is an important risk factor for myocardial infarction. Smoking causes early
atherosclerosis and sudden cardiac death. Smoking primarily affects unhealthy patients
with early STEMI. (48)
Cigarette smoking by atherogenesis raises the risk of AMI.
Smoking raises serum LDL cholesterol, triglyceride and decreases serum HDL-
cholesterol levels. The cigarette smoke does not do radical damage to LDL so that the
arterial wall can absorb oxidized LDL-cholesterol
Smoking induces traditional artery inflammation atherosclerosis, with higher serum
levels of C-reactive protein in smokers than in non-smokers. (49)
Smoking stimulates
the sympathetic nervous system (SNS), increases heart rate and systolic blood pressure
through the content of nicotine. This rise in levels and pressure causes myocardial
oxygen demand to rise. Increasing SNS activity also contributes to coronary arterial
16
vasoconstriction that decreases myocardial oxygen supply and increases myocardial
oxygen demand this effect contributes to causing ischemia. (50)
Diabetes Mellitus
Diabetes mellitus is an important risk factor for cardiovascular disease (CVD). The
cardiovascular mortality and morbidity in people with type 2 diabetes mellitus are
higher. (51)
Diabetes patients have a greater risk of atherosclerotic vascular disease in
both the heart and other vascularized regions. Atheromatous plaques in diabetic patients
are more vulnerable to rupture. (52)
Diabetes raises the risk of myocardial infarction as it raises the rate of atherosclerotic
progression and influences the lipid profile and plaque formation. Diabetes reduces the
synthesis of nitric oxide resulting in increased platelet aggregation and activation of
thrombosis. Platelet function is also irregular in Diabetes, which raises the risk of
thrombosis at the site of the plaque break, resulting in up-regulation of factor VII,
thrombin, tissue factor, PAI-1 clotting for diabetes individuals,(53)
myocardial infarction
is often fatal in contrast to Non-diabetic patients.
Hypertension
All systolic and diastolic hypertension increase the risk of myocardial infarction. This
is a significant risk factor in coronary blood vessels causing atherosclerosis
contributing to cause myocardial infarction. (54)
In old age, hypertension is much
greater in the heart and responsible for at least 70 percent of heart disease.
Hypertension accelerates atheroma symptoms, increases shear stress on plaques,
adversely affects coronary circulation, and degrades endothelial function and.
Hypertension management with strict compliance with proper medication and dietary
changes greatly decreases the risk of myocardial infarction. (55)
17
Family history
The family history of myocardial infarction (MI) is an independent risk factor of MI.
Many genetic variations are associated with an increased risk of MI. (56)
The
strongest genetic effect on the risk of myocardial infarction is that of a variant found on
chromosome 9p21. Only a few of the myocardial infarction genes are associated with
classic risk factors. The history of AMI due to acute myocardial infarction in a first
degree raises the risk for men by around two times and almost three times the risk for
women. If a father has a heart attack before age 55 years and a mother before 65 years,
good family history may become very important to prevent a premature myocardial
infarction in the next generation.
Sedentary Lifestyle
In a sedentary lifestyle, people with multiple cardiac risk factors are more likely to
develop AMI. Sedentary lifestyle persons have double the risk for CAD death as that
of active people. (57)
Up to 20%-30% reduced risk of coronary heart disease through
physical activity like Brisk walking, climbing, and cycling activities provide safety
from CVD. The AHA recommends that 30 minutes or more of moderate-intensity
activity on most days of the week improves glucose tolerance, insulin sensitivity,
increases fibrinolysis, HDL and improves oxygen uptake in the heart, and increases
coronary artery diameter. (58)
Dyslipidemia
Overall, Dyslipidemia, which is a significant risk factor in cardiovascular disease was
generally referred to as total cholesterol, LDL, triglycerides or rates above the 90th
percentile or HDL-C below the 10th
percentile in the general population. (59)
The level
of non-fasting triglyceride appears to be a strong and independent predictor of potential
AMI risk, especially when the levels of total cholesterol also increase. The explanation
18
for this is that reduced levels of HDL-C and increased levels of triglyceride cause
metabolic worries and potentially adverse consequences. (60)
Framingham's study established the relationship between dyslipidemia and coronary
artery disease. The main risk factors for coronary atherosclerosis are elevated total
cholesterol, LDL, and low HDL levels. Dyslipidemia correction can reduce the risk of
myocardial disease.
Obesity
Increased BMI is directly related to increased incidence of myocardial infarction. (61)
Elevated BMI increase total cholesterol and triglyceride also decrease the level of HDL-
C. Although BMI and waist to hip ratios have a linear relation between obesity and
CAD. The waist to hip ratio is a more accurate predictor of CAD. (62)
Among
Abdominal obesity increased the risk of AMI. Obesity causes hyperinsulinemia which
is associate with lipid derangement, increase plasminogen activator inhibitor and
enhanced proliferation of cells in atherosclerotic plaque enhance chances of CAD.
Obese are those with a BMI of > 30kg/m2
.
Alcohol Consumption
Alcohol consumption increased the risk of myocardial infarction among those people
who drink alcohol daily. Heavy alcohol drinking enhances cardio-vascular risk. (63)
Heavy drinking has been shown to increase low-density lipoproteins, which increase
cardiovascular morbidity and mortality. Binge drinking has been associated with an
increased risk of thrombosis.
Most researches showed that alcohol consumption could increase LDL-C, triglyceride,
heart rate, blood pressure and thus increase the risks of atherosclerosis, atrial fibrillation
resulting in damaging cardiac muscle cells and cardiovascular system and producing
fibrinolytic enzyme inhibitors. Moderate drinking is not associated with any serious
19
morbidity; however, hypertriglyceridemias, cardiomyopathies, hypertension, and M.I.
are associated more often in those who drinks alcohol three or more times a day.
COCAINE USE
Cocaine increases the incidence of CAD also cocaine raises heart rate, blood pressure,
and enhances oxygen demand in heart muscle, and reduced coronary blood flow causes
ischemia. Cocaine abuse causes coronary spasm or thrombus formation by a-adrenergic
stimulation. (64)
Chest pain caused by infarction after 3 hours of cocaine ingestion and
also depends on the route of intake ( chest pain caused by M.I. after 30 min. with
intravenous use, 90 min with smoking , more than 80% of persons who use cocaine are
also cigarette smokers, and pain caused 135 minutes after nasal inhalation). Even single
use of cocaine caused Prinzmetals Angina which is due to coronary arterial vasospasm
(65)
Gutka/ Betel Nut:
People who chewed ten edible seeds each day were 4 times the additional possible risk to
induce CAD as compared to people who do not take it. Previously, mastication betel nut
was the reason behind several risk factors for CAD. One study established that chewing
betel nut was related to central blubber (Lin et al., 2009). However, Betel nut chewing
increase blood pressure in patients with D.M. It is also seen a positive association between
edible seed mastication and metabolic syndrome. It will so be projected that chewing betel
nut could either be a freelance factor associated with CAD(66)
or be an element by
influencing renowned risk factors for hypertension or diabetes. Several mechanisms justify
that edible seed chewing, causes narrowing of coronary arteries, and causes CAD.
Arecoline, the compound found in true pepper nut, has been reported to cause induction
of cyclooxygenase expression. The compound hydroxychavicol was found to induce the
reactive oxygen species and thereby mediating cells. Further more, the extracts of betel
nut modify LDL towards artery epithelium cells. These facts facilitate that the rationale for
CAD in betel nut mastication people may be specifically attributed to atherosclerosis.
20
Betel nut chewing could be an important risk factor for the event of CAD. it was found that
betel nut chewing increased the probability of CAD by almost 6 times. Furthermore, it was
established that those chewing edible seed for ten years had an eight-fold increase in the
risk of developing CAD. This shows that future betel nut chewing considerably vital risk
issue in conjunction with cardiovascular disease and polygenic disorder for CAD.
All these substance abuse materials like smoking, alcohol, charas, cocaine, and
Gutka/betel nut causes atherosclerosis, coronary spasm, atherogenesis, thrombosis,
increases fibrinogen level, LDLC, triglycerides, decreased HDLC, and increased C-
reactive protein .substance abuse also increases heart rate and SBP which causes
myocardial oxygen supply-demand mismatch all of these effects to contribute to
causing M.I.
A study was done by Dhruv Mohtta(67)
et al showed that patients who developed
atherosclerotic cardiovascular disease are those who use more substance abuse
materials like tobacco 62.9%, alcohol 31.8%, cocaine 12.9%, and cannabis 12.5% in
his study shows that recreational substances users had increase chances of ASCVD.
MI occurs by Non-atherosclerosis reasons are as below
• auxiliary to vasculitis coronary impediment
• hypertrophy of Ventricular (e.g., hypertrophic cardiomyopathy, left ventricular
hypertrophy)
• Coronary cholesterol, vein emboli, air, or sepsis.
• Injury to coronary arteries
• Vasospasm (angina variation)
• Arteritis
21
• Use of drugs (e.g., cocaine, ephedrine, amphetamines)
• Coronary courses aneurysms
• oxygen necessity factors expansion, for example, overwhelming effort or
hyperthyroidism, fever
• Factors that decline oxygen conveyance, for example, hypoxemia of extreme pallor
• Inclusion of the coronary courses with retrograde aortic analysis,
• Respiratory diseases
Moreover, because harmful effects of carbon monoxide or extreme aspiration problems can
lead to hypoxia which causes M.I. While not rare, diseases like Marfan, Kawasaki, Takayasu
arteritis, progeria, and cystic medial necrosis may be occur in child coronary supply.
In youth and immaturity, acute M.I is caused by acute inflammation of the coronary arteries or
irregular coronary artery origin is more common in adults with coronal corridors due to deep-
rooted affidavit of the atheroma and the plaque, which causes coronary artery spasm and
thrombosis. Intrauterine M.I, sometimes associated with coronary artery stenosis, also occurs.
(68)
SIGNS AND SYMPTOMS
In the case of acute MI, there are the following symptoms.
• Crushing Substernal chest pain. Pain is typically more severe of longer duration usually
more than 20 minutes. (69)
• Chest pain radiates to the neck, shoulder, jaw, back, left, &right arm and epigastrium.
22
• Sometimes it is due to pressure feeling that is characterized by aching, as squeezing or
constricting nature.
• Most patients have the feeling of indigestion, gas, fullness-like symptoms.
Patients that have myocardial infarction have fatigue, chest discomfort, and malaise as
symptoms. These symptoms can show in days and even in weeks. Sometimes
symptoms may occur suddenly or sometimes it happens without warning
In MI the patient’s vital signals may demonstrate as:
• The heartbeat of the patients is increased in case of high sympathoadrenal discharge.
(70)
• Sometimes due to atrial fibrillation, pulse rhythm can be irregular.
• Due to peripheral arterial vasoconstriction patient's blood pressure is initially elevated,
which can cause pain.
• When MI is in the right ventricular, cardiogenic shock can happen. (71)
• Due to pulmonary congestion or anxiety respiratory rate enhance.
• Sometimes wheezing, coughing, and the production of frothy sputum can occur.
• Sometimes patients develop respiratory distress for which they need ventilatory
support.
23
PHYSICAL EXAMINATION
While examining a patient with myocardial infarction, various clinical findings are sought out
which are described below.
Vital signs
Heart rate
Usually, heart rate is increased in AMI, Because during M. I heart muscles receive a small
amount of blood from arteries that supply blood to muscle, which are blocked. In M.I. the pulse
may be regular or irregular. Irregular pulse is seen in ventricular ectopy, atrial fibrillation,
sometimes ventricular tachycardia, flutter and accelerated idioventricular rhythm or other
supraventricular arrhythmias are seen.
Blood pressure
The blood pressure of M.I. patients is elevated initially, due to pain, anxiety, and agitation.
Also due to large infract area or impaired global cardiac contractility. As well as systolic blood
pressure may be decreased in M.I due to tachycardia which impairs stroke volume.
Respiratory rate
Due to pain, anxiety, or congestion the respiratory rate is increased. Patients with pulmonary
Oedema may have a respiratory rate of more than 40 breaths/min.
Temperature
Fever is a non-specific response to tissue necrosis. In between 24-48 hours fever usually
develops and the curve is generally parallel with the time that elevates creatine kinase level in
blood. Mostly body temperature does not exceed 102°F.
24
Neck veins
In the case of acute inferior-wall MI with RV infarct, the patients have right ventricular
immersion, the failure of the right ventricle makes the vein visible. (72)
Hepatomegaly, edema,
hypotension is caused by impaired right ventricular function.
Heart Sounds
An S3and S4 gallop sounds are audible in patients with large MI.(73)
Ruptured, mitral postero
medial, papillary muscle produce a state that is known as mitral regurgitation, produces a pan
systolic murmur. Pericardial friction rub that is produced through sliding contact of
inflammation-roughed surfaces of pericardium due to post-MI pericarditis.
Chest Auscultation
Wheezes and rales are auscultated, these conditions can occur from secondary to respiratory
venous hypertension. Extensive acute left ventricular MI is associated with this condition. (74)
Abdomen
MI Patient develops abdominal pain along with nausea, vomiting, and abdominal distension,
hepatomegaly, and positive Hepatojugular reflux are elicited in RV INFARCTION.
25
HISTORY
In the case of the initial diagnosis of MI, only some clues are obtaining from physical
examination while patients’ history is crucial in-patient presentations. The patient that has acute
MI, they usually have chest pain that led to prodromal symptoms of fatigue, malaise, chest
discomfort is symptoms of typical ST-elevation M.I. happen without warning.
In the case of acute MI typical chest pain can happen and it remains more than 20 minutes. It
also radiates to the shoulder, neck, and jaw and down to the left arm, this pain is retrosternal.
In the case of M.I. substernal pressure sensation can occur, which is also perceiving as aching,
burning, squeezing. Some patients have symptoms as epigastric condition, feeling of
indigestion, and fullness or gas. (75)
Sometimes many patients, do not recognize chest pain, and suddenly high pain threshold
happens to them. These patients have a disorder that impairs pain perception so this may result
in a defective anginal warning system. Moreover, some patients can have high threshold pain
due to mental status that is caused by medication.
MI mostly occurs in the daytime in the morning hours, as the morning increases the
sympathetic tone, this may increase the heart rate, high blood pressure, myocardial
contractility, coronary vascular tone, all these factors can explain better the whole circadian
variation. Morning is important because at that time blood viscosity is also high, and
coagulation can occur.
Rapid evaluation in case of initial state a brief history and focused physical examination is
included.
Other symptoms of myocardial infarction include the following:
Myocardial infarction symptoms are as follows:
26
• Anxiety
• Profuse sweating
• Cough
• Nausea, with or without vomiting.
• Shortness of breath
• Wheezes
• Rapid or irregular heart rate
• indigestion, Fullness
In United State, most deaths are due to heart disease. Heart diseases increase as age increase,
so it is an important, risk, albeit non-modifiable factor for cardiovascular disease in the general
population.(76)
It is also common in those patients that have chronic kidney disease.
In 1995 in the USA chronic heart disease in men and women was prevalent at the age of 65.
And the incidence in women was 90 per 1000 and in men, it was 83 per 1000. And the
cumulative prevalence was 217 per 1000 for men and 129 per 1000 women. It was proved that
the elderly had a high rate of chronic heart disease(77)
.
Patients that have chronic kidney disease have more chances to carry heart disease, mostly that
patients have the highest risk of cardiovascular disease. So many cardiovascular risk factors
are increased by declining kidney function. We can say that there is a direct relation between
CVD and CKD. In these patients, there are standard factors that only account for a small portion
that is observed in these patients.
27
Aging is an important determinant of kidney function. According to a study in the USA, more
than a third of the US has CKD in those people that have the age of 70. (78)
And this disease
increases with time. According to the postulate that older individuals that have CKD also have
the effect of CVD. In that case, some of the symptoms are diabetes, obesity, hypertension, and
other vascular diseases are present.
Blood Supply of the Heart
This Figure is taken from:
https://o.quizlet.com/xuwAGdOcf7jnc2YOQnTqPQ_b.jpg
28
DIAGNOSIS
Laboratory studies
Following lab tests in the diagnosis of MI are carried out:
• Cardiac enzymes/biomarkers: according to the cardiology society of Europe and
American Cardiology College in suspected patients of M.I. following tests are
recommended. The marker which is used to diagnose is troponin as it is sensitive and
specific. (79)
• Troponin levels rise in serum when necrosis of the myocardial occurs.
• CBC (complete blood count)
• Lipid profile
• Metabolic panel comprehensive
Electrocardiography
In initial evaluation and triage ECG is the most significant tool in those patients that have acute
coronary syndrome when MI is suspected. 80% of cases are confirmed by ECG(80)
. In M.I ECG
also identifying the site of occlusion in infarct-related arteries.
ECHOCARDIOGRAPHY
Useful for detecting wall motion abnormalities, LV function, and also see mechanical
complications of M.I.(81)
CARDIAC IMAGING (CORONARY ANGIOGRAPHY)
If patients have confirmed MI, then angiography is carried out to check the arteries of the heart.
29
MANAGEMENT
Pre-hospital care
Patients that have chest pain mostly include:
• Nitroglycerin for chest pain, given by the spray
• Non-enteric-coated chewable aspirin. Dose 325 mg stat
• Telemetry and pre-hospital ECG.
Emergency department and inpatient care
Design for medication and therapy include:
• Telemetry and ECG within 10 minutes After arrived in ER.
• Intravenous access, pulse oximetry supplemental oxygen when SaO2 Less than 94%
• Immediate giving of non-enteric-coated chewable aspirin. Dose 325 mg stat
• Oral p2y12 receptor antagonists
• Parenteral Antithrombotic Therapy.
• Recanalize infarct-related arteries within 90 minutes door to balloon time if PCI capability is
available. Primary PCI is the early goal to achieve. (82)
• Revascularize infarct-related arteries with fibrinolytic within 30 minutes door to injection time
in such patients where Primary PCI facility is not present. (83)
30
EPIDEMIOLOGY
United States statistics
In the United States, the main source of death is the coronary supply route, every year 500,000
to 700,000 deaths are occurred due to CAD. The cause of death due to M.I is approximately
one-third of all deaths in the population for those over the age of 35 years occurs annually
within the USA.
The yearly incidence death rate is about 600 cases per 100,000 individuals. The proportion of
patients diagnosed with NSTEMI has dynamically expanded as compared to ST-Elevation M.I.
Despite a decline in age-balanced deaths in the United States due to M.I. because of CAD-
related awareness is increased among peoples. since the mid-1970s, the total number of M.I-
related mortalities has not decreased.
The severity of M.I. in women is almost higher than in men. The CAD is more progress in the
dark population than white people at the age of 75 years. Among the Hispanic populace,
coronary artery disease mortality isn't as high as among dark people and white people. (84)
The
index mortality rate associated with acute M.I. is almost three times higher than that of men
compared to women.
European statistics
In European nations computer source design is the major source of death. CAD rate has
decreased by 30 percent in the European nation from the mid-1960s to the 1990s. eastern
European death expansion rate is intense. In the early 1900s, the MI death rate has decreased.
(85)
31
Cardiovascular disease in other developed countries and developing nations
A study of death statistics by the World Health Organization (WHO) found that in Japan, CAD
mortality was considerably lower, and WHO evident that about 30% mortality deceased by
mid-1990. CAD mortality is significantly lower than in the USA and Europe. because Japan
continues its strict control policies towards blood pressure and tobacco control and builds a
strategy to control BMI, Diabetes, and cholesterol level to prevent CAD deaths. (86)
(Ref.from
international Journal of Cardiology vol.291 Sep. 2019.
In China crucial rise in mortality associated with CAD is observed, which is likely due to
increased cardiovascular risk factors dyslipidemia and transcendent smoking. (87)
CAD levels
and related mortality are projected to rise significantly from an estimated 80 percent growth,
from approx.9 million in 1990 to 20 million by 2020, in other developing economics including
Asia, Latin America, the Middle East, and Sub-Saharan Africa.
It is suspected that these regional trends in the incidence of CAD and subsequent extreme MI
are potentially associated with consumption of high calories diet, reduce physical activity, and
higher smoking rates.
Notable Canadian-drove worldwide research has identified 9 efficient danger factors (smoking,
strange rates of blood lipids, obesity, diabetes, diet, physical activity, use of liquor, and
psychosocial factors) that are estimated to represent over 90%. across Africa, Asia, Australia,
Europe, Middle East, North and South America. (88)
The INTERHEART agents found that these hazard factors are the equivalent in pretty much
every geographic district and each racial/ethnic gathering around the world, and they are steady
in people. The INTERHEART preliminary demonstrated that smoking 1-5 cigarettes day by
32
day expanded the danger of an intense MI by 40%, and the hazard expanded with the measure
of tobacco smoked every day.
In the last few years, the study indicates that the approximate proportion of abdomen to hip
will supplant BMI as a sign of fitness, with the reason that all forms of tobacco – including
separate and unfiltered cigarettes, funneling and bites tobacco-are valuable and the stomach
robustness is a more important risk factor than weight gain (BMI).(89)
Patient Education
Patients with dynamic side effects of intense coronary disorder (ACS) ought to be told to call
crisis administrations, and they ought to be transported by crisis restorative administrations
faculty, not independent from anyone else, family, or companions. When suspected ACS
incidents last longer than 20 minutes, patients must be advised to reach the crisis office
immediately when closely associated syncope/ presyncope or hemodynamic shakiness is
present.
On the off chance that nitroglycerin is recommended to a patient with suspected ACS, if pain
not alleviates after taking nitroglycerin is experienced 5 minutes after the primary portion, the
patient should contact crisis administrations.
If help is experienced inside 5 minutes of the principal nitroglycerin portion, repeated dosages
can be allowed at regular intervals for a limit of 3 portions aggregate. If at that point, the
manifestations have not yet completely settled, the patient, a relative, or a parental figure should
contact crisis administrations.
Diet assumes a significant job in the improvement of coronary vessel diseases Instruct post-
myocardial dead tissue (MI) patients about the job of a low-cholesterol and low-salt eating
regimen. (90)
33
A dietitian should see and assess all patients before releasing them from the clinic. Moreover,
accentuation on exercise preparation ought to be made, because present proof exhibits that
heart diseases recovery after MI results in lower rates of repetitive cardiovascular occasions.
All patients ought to be instructed concerning the basic job of smoking in the improvement of
CAD. Smoking discontinuance classes ought to be offered to enable patients to abstain from
smoking after their MI. (91)
34
Chapter: 3
MATERIALS AND METHODS
Study Design:
Cross-Sectional Analytical Study
Sample Setting:
The study was conducted at Cardiology Department, Dr. Ruth Pfau Civil Hospital,
Karachi.From 15.3.2019 to 15.3.2020.
Sampling Technique:
Non-Probability Purposive Sampling
Sample Size:
Using open Epi 6, taking prevalence of 14% v/s 41% the highest in different studies for risk
factors, with a margin of error of 5%, the sample size will be 126 (63 in each group).
Inclusion Criteria:
• According to WHO criteria, all patients of recent MI of aged 25years and above of
either sex.
• Given consent to participate in the study.
• Exclusion criteria:
• Patients having any chronic co-morbid diseases. (PAH, CLD, Malignancy, etc)
• Patients already CABG, Most CABG Patients would be having prior MI
35
• Patients with congenital heart diseases (ASD, VSD, PDA, TOF) and valvular heart diseases
(Mitral, Tricuspid, pulmonary, and Aortic).
DATA COLLECTION PROCEDURE:
After getting approval from the scientific committee and IRB of DUHS, the study was conducted on
patients suffering from recent MI. Written consent was taken from all the participants for inclusion in
the study.
An equal number of patients i.e.,126 were taken for the study. The admitted patients <35 years of age
were placed in one group and the patients of >35 years were placed in another group.
A research proforma was developed for this study after pretest and validation were used to collect the
data from all the patients. The questionnaire had questions regarding socio-demographic aspects with
ST-elevation and risk factors like gender, family history of myocardial infarction, hypertension,
diabetics’ smoking, and lifestyle.
These factors with ECG and lab tests were compared to determine statistical significance in two groups.
(All tests and ECG are free at Civil Hospital Karachi)
DATA ANALYSIS PROCEDURE:
For data analysis, SPSS v25.0 was used. For qualitative data, frequencies along with percentages were
calculated. For quantitative data, mean with standard deviation were measured. To determine any
statistical difference, the Chi-square test was implemented in two groups. The significance was done
based on p<0.05. All these results were presented in the shape of tables and graphs. Confounding factors
and biases were controlled by strict follow-up of inclusion and exclusion criteria of the study.
36
Chapter: 4
RESULTS
This study was conducted to compare the risk factors of young adults with older adults with
recent myocardial infarctions. So, data collected and analyzed the results were as follows
The mean deviation age of young adults was 29.87 with a standard ± deviation of 5.85 and the
mean age of older adults was 58.58 with a standard deviation ± 10.13 in our study. When we
check statistical significance between these two groups the p-value showed a significant
difference as the p-value was less than the level of significance (p=<0.001).
The gender-wise distribution between groups showed differences as in young adults 44 out of
63(69.8%) were male and 19 out of 63(30.2%) were female. Similarly, in the older adults’
group, 48 out of 63(76.2%) were male and 15 out of 63(23.8%) were female (p=<0.422). These
also showed that males in both groups were more than females.
The smoking was more common in the young age group. 40 young patients were smokers out
of 63 (63.5%) as compared to the old adults group 20 patients were smokers out of 63 (31.7%).
The p-value also showed a significant difference in these two groups (p= < 0.001).
The diabetes risk factor was also more in the older adults’ group 53 out of 63 Patients (82.5%)
than young adults group in which 8 patients out of 63 (12.7%) were diabetics. P-value also
showed a significant difference in these groups (p=< 0.001).
The hypertension risk factor was more common in the older adults’ group 62 patients out of 63
(98.4%) and low in the young adults’ group 10 out of 63 (15.9%) were hypertensive. Chi-
square results also showed similar results (p=< 0.001).
37
The family history of IHD was more common in the young adults’ group 36 patients out of
63(57.1%) and less common in the older adults’ group 8 patients out of 63 (12.7%). Chi squares
results showed a significant difference in both groups (p<=0.001).
The sedentary lifestyle was more common in the older adults’ group 45 patients out of 63
(71.4%) and less in the young adults’ group 7 out of 63 (11.1%). Results showed significant
differences in both groups (p=< 0.001).
Obesity was also common in the older adults’ group 35 patients out of 63 (55.6%) than young
adult group 10 out of 63 (15.9%). The older adults’ group is a statistically significant difference
from young adults’ groups (p=< 0.001).
Dyslipidemia was also more in the older adults’ group 52 patients out of 63 were (82.5%) and
less in the young adults’ group 20 out of 63 (31.7%). Results showed a significant difference
in both groups (p=< 0.001).
Substance abuse use was more commonly seen in younger adult’s group compared to older
adults’ group. Substance abuse user younger adults were(84% v/s 58% older age group) with
or without smoking. In substance abuse material alcohol taken by the younger patients were 5
out of 63(7.93%) while 15 patients(23.80%) intake alcohol along with smoking while, in older
group 13 out of 63(20.63%) taking only alcohol, while 2 patients(3.17%) take alcohol along
with smoking, cocaine taking by the younger group were 3 out of 63(4.8%) along with smoking
charas taking more commonly by the younger group were 10 out of 63(15.9%) and the older
group were 7 out of 63(11.1%) in both groups all charas taker were smokers, only Gutka /
Betel nut chewing by young’s group were 12 out of 63(19.04%) and along with smoking were
8(12.69) and older groups who chewing were 12 out of 63 (19.04%) and 3 patients(4.76%)
uses both Gutka/Betel nut along with smoking overall P-value of 0.999 between two groups.
38
In young adults, the mean Deviation of blood urea was 28.11 mg/dl ± 11.72mg/dl Std Deviation
and in older adults, the mean Deviation of blood urea was 54.53 mg/dl ± 9.03 Std Deviation.
When we checked for statistical significance the p-value showed that there is a significant
difference between the two groups as the p-value was less than the level of significance
(p=0.001). Blood urea value is more in the older adults’ group.
The mean Deviation of serum creatinine in young adults was 1.10 ± 0.11 mg/dl Std Deviation
and in the older adults’ group, the mean Deviation of creatinine was 1.09 ± 0.10 mg/dl Std
Deviation. When checked statistical difference between these two groups, the p-value is greater
than the level of significance which showed no significant difference (p=< 0.736).
The mean Deviation of total cholesterol in young adults was 164.81 ± 21.44mg/dl Std
Deviation and in the older adults group mean Deviation was 212.68 ± 20.25 mg/dl Std
Deviation. The p-value showed a significant difference in both groups (p=< 0.001). Young
adults had normal range values while older adults had high cholesterol.
The level of TG was more in older adults’ groups and less in young adults’ groups. The mean
Deviation of young adults was 121.63 ± 45.78mg/dl Std Deviation and the mean Deviation of
older adults was 223.98±40.38 mg/dl Std Deviation. When the difference was checked
statistically the p-value showed a significant difference between these two groups. (p= <
0.001).
The value of LDL is also a significant difference in both groups as the mean Deviation of LDL
in young adults was 117.10±27.91 mg/dl Std Deviation and in older adults mean Deviation was
178.19±33.19 mg/dl Std Deviation. The value of p was also less than the level of significance
(p= < 0.001).
39
The mean and total Deviation of HDL in the young adults’ group was 55.52±12.34 with
standard deviation and the mean Deviation of HDL in older adults was 30.43 ± 8.31with
standard deviation. The value of HDL was more in the younger adults’ group than the older
group. The p-value was also less than the level of significance (p= < 0.001).
At the end of the results, it was seen that all risk factors of myocardial infarction in the older
adults’ group were more positive than young adults’ groups. Older people had more chance of
myocardial infarction as they had more risk factors.
40
Table-I: Comparison of age between groups
Variable Young Adults Older Adults p-value
Mean + SD Mean + SD
Age 29.87 + 5.85 58.58 + 10.13 < 0.001
Figure-1: Graphical presentation of gender
41
Table-II: Comparison of smoking distribution between groups
Smoking
Groups
Total p-value
Young Adults Older Adults
Yes
40 20 60
< 0.001
63.5% 31.7% 47.6%
No
23 43 66
36.5% 68.3% 52.4%
Total
63 63 126
100.0% 100.0% 100.0%
Table-III: Comparison of diabetes distribution between groups
Diabetes
Groups
Total p-value
Young
Adults
Older Adults
Yes
8 52 60
< 0.001
12.7% 82.5% 47.6%
No
55 11 66
87.3% 17.5% 52.4%
Total
63 63 126
100.0% 100.0% 100.0%
Table-IV: Comparison of hypertension distribution between groups
Hypertension
Groups
Total p-value
Young
Adults
Older
Adults
Yes
10 62 72
< 0.001
15.9% 98.4% 57.1%
No
53 1 54
84.1% 1.6% 42.9%
Total
63 63 126
100.0% 100.0% 100.0%
42
Table-V: Comparison of family history of IHD distribution between groups
Family
History of
IHD
Groups
Total p-value
Young Adults Older Adults
Yes
36 8 44
< 0.001
57.1% 12.7% 34.9%
No
27 55 82
42.9% 87.3% 65.1%
Total
63 63 126
100.0% 100.0% 100.0%
Table-VI: Comparison of sedentary lifestyle distribution between groups
Sedentary
Lifestyle
Groups
Total p-value
Young
Adults
Older Adults
Yes
7 45 52
<0.001
11.1% 71.4% 41.3%
No
56 18 74
88.9% 28.6% 58.7%
Total
63 63 126
100.0% 100.0% 100.0%
Table-VII: Comparison of obesity distribution between groups
Obesity
Groups
Total p-value
Young Adults Older Adults
Yes
10 35 45
< 0.001
15.9% 55.6% 35.7%
No
53 28 81
84.1% 44.4% 64.3%
Total
63 63 126
100.0% 100.0% 100.0%
43
Table-VIII: Comparison of dyslipidemia distribution between groups
Dyslipidaemia
Groups
Total p-value
Young
Adults
Older
Adults
Yes
20 52 55
< 0.001
31.7% 82.5% 43.7%
No
43 11 71
68.3% 17.5% 56.3%
Total
63 63 126
100.0% 100.0% 100.0%
Table-IX: Comparison of substance abuse distribution between groups
Substance Abuse
Groups
Total p-value
Young
Adults
Older Adults
No Substance
Abuse
10 26 36
0.999
15.87% 41.26% 28.57%
Only Alcohol 5 13 18
7.93% 20.63% 14.28%
Alcohol + Smoker
15 2 17
23.80% 3.17% 13.49%
Cocaine + Smoker
3 0 3
4.76% 0.0% 2.38%
Chars + Smoker
10 7 17
15.87% 11.11% 13.49%
Only Gutka/Betel Nut 12 12 24
19.4% 19.4% 19.4%
Gutka/Betel nut +
Smoker
8 3 11
12.69% 4.76% 8.73%
Total
63 63 126
100.0% 100.0% 100.0%
Use of Substance Abuse with smoking in Young Group is 84 % in my data
Use of substance abuse with smoking in older group is 58 % in my data
44
Comparison of laboratory investigation between groups.
Table-X: Comparison of blood urea distribution between groups
Variable
Young Adults Old Adults
P-value
Mean + SD Mean + SD
Blood Urea(mg/dl) 28.11+ 11.72 54.53+ 9.03 <0.001
Table-XI: Comparison of serum creatinine distribution between groups
Variable
Young Adults Old Adults
P-value
Mean + SD Mean + SD
Serum Creatinine (mg/dl) 1.10 + 0.11 1.09 + 0.10 0.736
45
Table-XII: Comparison of lipid profile distribution between group
Variable
Young Adults Old Adults
P-value
Mean + SD Mean + SD
Cholesterol(mg/dl) 164.81 + 21.44 212.68 + 20.25 < 0.001
TG (mg/dl) 121.63 + 45.78 223.98 + 40.38 < 0.001
LDL (mg/dl) 137.10 + 27.91 198.19 + 33.19 < 0.001
HDL (mg/dl) 55.52 + 12.34 30.43 + 8.31 < 0.001
46
Chapter: 5
DISCUSSION
MI is an old age disease however it is also seen in young age adults, but the young age group
has fewer conventional risk factors. Same in my study the young adults have fewer
conventional risk factors of myocardial infarction than older adult groups. below 40 years of
age cholesterol accumulated in less amount within arteries resulting in less chances of coronary
atherosclerosis. Hypertension and diabetes are also less likely to occur at a young age(Table: III
and IV)
. However, young groups have different risk factors and complications as compared to old
age patients. That may be the reason why CAD is becoming prevalent in our part of world.
Myocardial infarction is a very serious disease for a patient and also for its family. If a patient
at a young age gets this disease then it carries significant morbidity, psychological effects, and
financial constraints for the patient and his family, and this way patient may loss their life years.
In my study, I took cut off age less than 35 years or equal to 35 in the young adults’ group of
recent M.I. from the study of Faisal et al (18).
I had take two groups one was below 35 years or
equal to 35 years called young adults’ groups and the second is above 35 years called older
adults’ groups. For both groups, 63 patients were selected. More conventional risk factors were
present in older adults’ group. I studied both the groups of patients with respect to the gender
distribution, presence of hypertension, and diabetes mellitus ,F.H. ,smoking ,substance abuse
etc
In the young adult group, 69.8% were male patients and 30.2% were female patients. In past,
there were very few studies that compare gender distributions also in these types of studies.
Similarly, in older adults’ groups, 76.2% were male and 23.8% were female. The gender
distribution is significant in our study. The male ratio was more than female in both groups.
47
Same in other studies Abdus Samad et al(92)
and Faisal et al(18)
showed male ratio was more
than the female ratio.
It was determined in my study that dyslipidemia, hypertension, and diabetes were the
predominant risk factors in old age patients of M.I. Similar to it, in different study(15)
In a studies (6,9)
in young age patients of MI, the risk factors like family history of CAD,
smoking, and substance abuse was found much higher. Same in my study the ratio of risk
factors like family history of CAD, smoking with substance abuse is higher (57.1%, 84%
respectively) compared to old age patients (12.7%, 58% respectively) which were alarming
finding.
A study (67)
done by Dhruv Mohtta et al showed that patients who developed the
atherosclerotic cardiovascular disease are those who use more substance abuse materials like
tobacco 62.9%, alcohol 31.8%, cocaine 12.9%, and cannabis 12.5% in his study this shows that
recreational substances users had increase chances of ASCVD.
Similarly in my study substance abuse materials like smoking, alcohol, cocaine, charas,
gutka/betel nut takers were more commonly seen in young adults (84%), compared to the older
adults’ group (58% respectively).
All these substance abuse materials cause atherosclerosis, coronary spasm, atherogenesis,
thrombosis, increases fibrinogen level, LDLC, triglycerides, decreases HDLC, and also
increase C-reactive protein, increases heart rate and SBP which causes myocardial oxygen
supply-demand mismatch all of these effects contribute to causing Myocardial Infarction in
young people.
It was determined in a study(14)
that smoking, CVD family history, and male gender were the
predominating risk factors in young age patients of MI, whereas hypertension, and diabetes
were the predominating risk factors in old age patients of MI.(15)
48
It was determined in a study done by Faisal(18)
et al that smoking (76.6%), family history of
CVD (33.3%), and male gender (90%) were dominating risk factors in young age patients of
M.I. same in my study it showed that smoking(63%), family history CVD(57%) and male
gender(70%) were more prevalent in young age patients of recent M.I .than older age patients.
Another big AAUS study done in Pakistan by Abdus Samad(92)
et al showed that male gender
(68.1%) hypertension (55.2%) smoking (52%) and diabetes (37.8%) were major risk factors.
My study shows that smoking with substance abuse(84%) was the main risk factor in the young
adult group and risk factors hypertension(98%), diabetes(82%), and dyslipidemia(82%) were
more prevalent in the old age group patients of recent M.I.
Similar to it, in different studies,(6,9,14,16)
smoking (58.7% -76.7%) was the most common risk
factor in young age patients as compared to old age group patients with MI (31.7%-59.4%).
Almost similarly in my study smoking was (63.5% in young v/s 31.7 in older age group
patients) another study,(17)
showed relative risks in the young age population were
hypertension, CAD family history, and dyslipidemia. One study by A. LIUQAT PMC 6284873
reported that dyslipidemia was high in the younger population (49.7% v/s 38.85), whereas other
study,(8)
reported it is higher in old age patients (43.3% v/s 49.5% and 20.0% v/s 29.0%).
My study, shows that diabetes was less common in young patients (12.7% in young v/s 82.5 %
in older group) and similarly obesity was also less common in young patients (15.9% in young
v/s 55.6 % in older group). Other studies(20)
also shown that diabetes (3.3- 5% in young v/s 30-
38.6% in older) and obesity (6.6% in young vs. 21.4% in older) as fewer risk factors in the
young age population. According to a study(21),
there was a significant gender difference for
CAD in the short and long-term clinical outcomes of young patients with MI. Therefore,
preventive strategies should be taken to reduce the gender-different risk factor in young adults.
(Ref. Epidemiol community health 2016 Nov 70(11)1057-1064).
49
My study mainly focused is to compare the risk factors of myocardial infarction in young and
older adults. The level of blood urea, serum creatinine, total cholesterol, and TG were high in
older adults’ groups than young adults’ group(8)
. But HDL was high in young adults. These
values are significantly different between these two groups.
LIMITATIONS OF STUDY
• Single-center study
• Selection bias
• Limited sample size
RECOMMENDATIONS
• Multi-center study.
• The probability Sampling Technique will be helpful for the generalization of results to
the larger population.
In the future Community should be educated about the harmful effects of smoking and
substance abuse materials’ also control other modifiable risk factors along with routine
screening which would help in preventing coronary artery disease in them, who belong to the
highly productive group in the community.
50
CONCLUSION
I concluded in this study that the risk factors like diabetes, hypertension, obesity, dyslipidemia,
and sedentary lifestyle were more prevalent in the older adults group than young adults group,
and Smoking, Family history of IHD and Substance abuse materials like alcohol, charas,
cocaine, gutka/betel nut were more common risk factors in young adults that causing M.I.
Hence, we recommend at the national level to stop smoking, do physical activities, chose
healthy and better lifestyle to promote good health in society and according to my study 84%
of young patients are using some form of substance abuse. Hence I recommend to our
policymakers to introduce and implement some expend kinds of law and enforce them properly
to protect our young population from potentially deadly IHD disease. spread awareness through
electronic, print media and arrange seminars on how to avoid substance abuse materials in
young peoples. There is also a need for screening of blood sugar, blood pressure, dyslipidemia,
and control of these atherosclerotic risk factors to reduce CVD risk in the population.
51
References
1. Sai Krishna Patibandla; Kush Gupta; Khalid Alsayouri Cardiac Enzymes used in the
diagnosis of acute myocardial ischemia StatPearls Publishing; 2021 Jan.2020 Aug 14.
2. James Beckerman, What's Causing My Chest Pain? Reviewed by on March 08, 2021
3. Scheen AJ. [From atherosclerosis to atherothrombosis: from a silent chronic pathology to
an acute critical event]. Rev Med Liege. 2018 May;73(5-6):224-228.
4. Choudhury L, Marsh JD, Myocardial infarction in young patients, The American Journal
of Medicine 1999;107(3):254-61,
5. Gupta M, Singh N, Verma S. South Asians, and cardiovascular risk: what clinicians should
know? Circulation. 2006; 113:924–29
6. Ahmed I, Qaiser S, Myocardial Infarction under age 40: Risk factors and Coronary
Arteriographic findings. Annals of King Edward Medical University, 2016; 9(4)
7. Siddique MA, Shrestha P, Salman M, Haque KMHSS, Ahmed MK, Sultan MAU, et al,
Age-related differences of risk profile and angiographic findings in patients with coronary
heart disease, BSMMU J, 2010;3(1): 13-7Perviz Asaria, Prof Paul Elliott, Margaret
Douglass, Meng, Ziad Obermeyer, Michael Soljak Azeem Majeed, et al Published:
February 28, 2017
8. Francisco J. Félix-Redondo,* Maria Grau, and Daniel Fernández-Bergés Cholesterol and
Cardiovascular Disease in the Elderly. Facts and Gaps, Aging Dis. 2013 Jun; 4(3): 154–
169. Published online 2013 Mar 1.
9. Kaur R, Das R, Ahluwalia J, Kumar RM, Talwar KK, Genetic polymorphisms,
Biochemical Factors, and Conventional Risk Factors in Young and Elderly North Indian
Patients with Acute Myocardial Infarction,2014;22(2):178-83
52
10. Sharma A, Kumar R, Ashotra S, Thakur S, comparative evaluation of clinical profile, risk
factors and outcome of acute myocardial infarction in elderly and non-elderly patients,
Heart India, 2016;4:96-9
11. Jing M, Gao F, Chen Q, Carvalho LPD, Sim LL, Koh TH, et al, Comparison of Long-
Term Mortality of Patients Aged ≤40 Versus >40 Years With Acute Myocardial
Infarction The AmericanJournalofCardiology2016;118(3):319-25,
12. Amann U, Kirchberger I, Heier M, Thilo C, Kuch B, Peter A, et al, Predictors of non-
invasive therapy and 28-day-case fatality in elderly compared to younger patients with
acute myocardial infarction: an observational study from the MONICA/KORA
Myocardial Infarction; Registry BMC; Cardiovascular; Disorders BMC 2016;16:151
13. Hosseini SK, Soleimani A, Karimi AA, Sadeghian S, Arabian S, Abbasi SH, et al,
Clinical features, management and in-hospital outcome of ST-elevation myocardial
infarction (STEMI) in young adults under 40 years of age, International Journal of
cardiopulmonary medicine and rehabilitation, Monaldi Arch Chest Dis. 2009
Jun;72(2):71-6.
14. Das PK, Kamal SM, Murshed M, Acute myocardial infarction in young Bangladeshis: A
comparison with older patients, Journal of Indian College of Cardiology, 2015;5(1): 20-4
15. Shan Lu, Ming-Yang Bao, Shu-Mei Miao, Xin Zhang, Qing-Qing Jia, Shen-Qi Jing, Tao
Shan, Xiao-Hong Wu, and Yun Liu Prevalence of hypertension, diabetes, and dyslipidemia,
and their additive effects on myocardial infarction corresponding author 2019 Sep; 7(18):
436
16. Pathak V, Ruhela M, Chadha N, Jain S, Risk factors angiographic characterization and
prognosis in young adults presenting with the acute coronary syndrome at a tertiary care
center in north India, BMR Medicine, 2016;1(1):1-5.
17. Srikanth Yandrapalli, Christopher Nabors, Abhishek Goyal, Wilbert S Aronow, William H
Frishman Modifiable Risk Factors in Young Adults With First Myocardial Infarction 2019
Feb 12;73(5):573-584
18. Faisal AWK, Ayub M, Waseem T, Shahzad R, khan AT, Hasnain SS, Risk factors in
young patients of acute myocardial infarction, Ayub Med Coll Abbottabad, 2011;23 (3):
10-3
53
19. Adrian Rosada, Ursula Kassner, Felix Weidemann, Maximilian König, Nikolaus
Buchmann,Elisabeth Steinhagen-Thiessen, and Dominik Spira Hyperlipidemias in elderly
patients Published online 2020 May 14.
20. Shilpa N. Bhupathiraju1 and Frank B. Hu Epidemiology of Obesity and Diabetes and Their
Cardiovascular Disease Circ Res. 2016 May 27; 118(11): 1723–1735.
21. Cho KI, Shin E, Ann SH, Garg, Her AY, Kim JS, et al Gender differences in risk factors
and clinical outcomes in young patients with acute myocardial infarction, J Epidemiol
Community Health Published Online 2016.
22. David L Coven, Eric H Yang, What is the spectrum of clinical presentations of the acute
coronary syndrome (ACS)? Updated: Sep 30, 2020
23. Hina Akbar; Christopher Foth; Rehan A. Kahloon; Steven Mountfort Acute ST-Elevation
Myocardial Infarction. Last Update: August 8, 2020
24. Eugene Braunwald and David A. Morrow Unstable Angina Published 18 Jun 2013
Circulation. 2013;127:2452–2457
25. Oren J. Mechanic; Michael Gavin; Shamai A Acute Myocardial Infarction. Grossman
Last Update: March 9, 2021
26. Hyun Ju Yoon, Kye Hun Kim and Jong Yoon Kim Impaired Diastolic Recovery after
Acute Myocardial Infarction as a Predictor of Adverse Events J Cardiovasc
Ultrasound. 2015 Sep; 23(3): 150–157. Published online 2015 Sep 24.
27. Amit Kumar, and Christopher P. Cannon, Acute Coronary Syndromes: Diagnosis and
Management 2009 Nov; 84(11): 1021–1036.
28. Rathore SS, Gersh BJ, Weinfurt KP, Oetgen WJ, Schulman KA, Solomon AJ. The role of
reperfusion therapy in paced patients with acute myocardial infarction. Am Heart J. 2001
Sep. 142(3):516-9
29. Suzanne Falck and Linda Hepler Do I Have Prediabetes or Diabetes? Guide to Diagnosis
and Management Updated on June 29, 2018
54
30. Sungha Park Ideal Target Blood Pressure in Hypertension Korean Circ J. 2019 Nov;
49(11): 1002–1009. Published online 2019 Sep 20
31. Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Bernard R. Chaitman, Jeroen J. Bax,
David A. Morrow, Harvey D Fourth Universal Definition of Myocardial Infarction
(2018). White, Originally published24 Aug 2018 Circulation. 2018;138:e618–e651
32. Falk E, Nakano M, Bentzon JF, Finn AV, Virmani R. Update on acute coronary
syndromes: the pathologists’ view.Eur Heart J. 2013; 34:719–728
33. Bugiardini R, Manfrini O, Pizzi C, Fontana F, Morgagni G. Endothelial function
predicts the future development of coronary artery disease: a study on women with chest
pain and normal angiograms, Circulation, 2004, vol. 109 (pg. 2518-2523)
34. Wayne L. Miller, Kirk N. Garratt, Mary F. Burritt, Guy S. ReederAllan S. Jaffe Timing of
Peak Troponin T and Creatine Kinase-MB Elevations After Percutaneous Coronary
Intervention European Heart Journal, Volume 27, Issue 9, May 2006
35. A Maziar Zafari, Eric H Yang, What is an acute coronary syndrome (ACS) Updated:
May 07, 2019
36. O'Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. 2013
ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a
report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. Circulation. 2013 Jan 29. 127 (4):e362-425.
37. Peter J. Sabia, ., Eric R. Powers, Michael Ragosta, Ian J. Sarembock,., Ch.B., M
Lawrence R. Burwell et al December 24, 1992, recent myocardial infarction N Engl J
Med 1992; 327:1825-1831
38. Burchfield JS, Xie M, Hill JA. Pathological ventricular remodeling: mechanisms: part 1
of 2. Circulation. 2013 Jul 23. 128 (4):388-400.
55
39. Marban E. Myocardial stunning and hibernation. The physiology behind the
colloquialisms. Circulation. 1991 Feb. 83 (2):681-8.
40. McGill HC Jr, McMahan CA, Zieske AW, et al. Associations of coronary heart disease
risk factors with the intermediate lesion of atherosclerosis in youth. The Pathobiological
Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb
Vasc Biol. 2000 Aug. 20 (8):1998-2004
41. Kolodgie FD, Virmani R, Burke AP, et al. Pathologic assessment of the vulnerable
human coronary plaque. Heart. 2004 Dec. 90 (12):1385-91.
42. Soares AAS, Tavoni TM, de Faria EC, Remaley AT, Maranhao RC, Sposito AC, et al.
HDL acceptor capacities for cholesterol efflux from macrophages and lipid transfer are
both acutely reduced after myocardial infarction. Clin Chim Acta. 2018 Mar. 478:51-6.
43. Holmes MV, Millwood IY, Kartsonaki C, et al, for the China Kadoorie Biobank
Collaborative Group. Lipids, lipoproteins, and metabolites and risk of myocardial
infarction and stroke. J Am Coll Cardiol. 2018 Feb 13. 71 (6):620-32
44. Yusuf S, Hawken S, Ounpuu S, et al, for the INTERHEART Study Investigators. Effect
of potentially modifiable risk factors associated with myocardial infarction in 52
countries (the INTERHEART study): a case-control study. Lancet. 2004 Sep 11-17. 364
(9438):937-52.
45. Mehta Saif Rathore Martha JRadford, YongfeiWangYunWangHarlan MKrumholz Acute
myocardial infarction in the elderly differences by age Rajendra September 2001
46. Ali Yazdanyar, Anne B. Newman, The Burden of Cardiovascular Disease in the Elderly:
Morbidity, Mortality, and Costs Med. 2009 Nov; 25(4): 563–vii.
47. Throughout life, heart attacks are twice as common in men than women Published:
November 2016 https://www.health.harvard.edu/heart-health/throughout-life-heart-
attacks-are-twice-as-common-in-men-than-women
56
48. Zhang H, Sun S, Tong L, Li R, Cao XH, Zhang BH, et al. Effect of cigarette smoking on
clinical outcomes of hospitalized Chinese male smokers with acute myocardial infarction.
Chin Med J (Engl) 2010;123:2807–11.
49. S Tonstad and J L Cowan C-reactive protein as a predictor of disease in smokers 2009
Nov; 63(11): 1634–1641.
50. Rockville, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for
Smoking-Attributable Disease: A Report of the Surgeon General.Centers for Disease
Control and Prevention (US); National Center for Chronic Disease Prevention and Health
Promotion (US); Office on Smoking and Health (US). Atlanta (GA): Centers for Disease
Control and Prevention (US); 2010
51. Thomas R. Einarson, Annabel Acs, Craig Ludwig & Ulrik H. Panton Prevalence of
cardiovascular disease in type 2 diabetes: a systematic literature review of scientific
evidence from across the world in 2007–2017 Published: 08 June 2018
52. Tomas Kovarnik, Zhi Chen, Gary S. Mintz, Andreas Wahle, Kristyna Bayerova, Ales
Kral, Martin Chval, Karel Kopriva, John Lopez, et al, Plaque volume and plaque risk
profile in diabetic vs. non-diabetic patients undergoing lipid-lowering therapy: a study
based on 3D intravascular ultrasound and virtual histology 2017; 16: 156. Published
online 2017 Dec 7
53. David J. Schneider, and Burton E. Sobel, Diabetes and Thrombosis
54. Mirjana Cubrilo-Turek, Hypertension and Coronary Heart Disease EJIFCC. 2003 Jul;
14(2): 67–73. Published online 2003 Jul 3.
55. Oladipupo Olafiranye, Ferdinand Zizi, Perry Brimah, Girardin Jean-Louis, Amgad N.
Makaryus Samy McFarlane, and Gbenga Ogedegbe Management of Hypertension among
Patients with Coronary Heart Disease 6 2011; 2011: 653903. Published online 2011 Jul
13.
57
56. Mattis Flyvholm Ranthe, Jonathan Aavang Petersen, Henning Bundgaard, Jan
Wohlfahrt, Mads Melbye, and Heather A. Boyd A Detailed Family History of
Myocardial Infarction and Risk of Myocardial Infarction – A Nationwide Cohort Study
2015; 10(5): e0125896. Published online 2015 May 26
57. Dr. Trine Moholdt Trondheim, Norway Sedentary lifestyle for 20 years linked to doubled
mortality risk compared to being active 31 Aug
58. Danyang Tian 1 and Jinqi Meng Exercise for Prevention and Relief of Cardiovascular
Disease corresponding author 22019; 2019: 3756750. Published online 2019 Apr 9
59. Mashhad Hedayatnia, Zahra Asadi, Reza Zare-Feyzabadi, Mahdiyeh Yaghooti-Khorasani
Dyslipidemia, and cardiovascular disease risk among the MASHAD study population
Published: 16 March 2020
60. Cohort Norway Grace M Egeland 1, Jannicke England 2, Gerhard Sulo 2, Ottar Nygård 3,
Marta Ebbing 4, Grethe S Tell non-fasting triglycerides to predict incident acute
myocardial infarction among those with favorable HDL-cholesterol 5 2015 Jul;22(7):872-
81
61. The incidence of acute myocardial infarction about overweight and obesity: a meta-
analysis 2014 Oct 27; 10(5): 855–862. Published online 2014 Oct 23
62. Qinqin Cao, Shui Yu, Wenji Xiong, Yuewei Lin, Huimin Li, Jinwei Li, and Feng Li,
Waist-hip ratio as a predictor of myocardial infarction risk 2018 Jul; 97(30): e11639.
Published online 2018 Jul 27.
63. Susanna C. Larsson, Stephen Burgess, Amy M. Mason, Karl Michaëlsson Alcohol
Consumption and Cardiovascular Disease Originally published 5 May 2020
64. Sung Tae Kim and Taehwan Park Acute and Chronic Effects of Cocaine on
Cardiovascular Health Feb; 20(3): 584. Published online 2019 Jan 29.
58
65. Mary Rodriguez Ziccardi; Jason D. Hatcher Prinzmetal Angina. Last Update: August 16,
2020.
66. Muhammad Shahzeb Khan, Faizan Imran Bawany, Muhammad Umer Ahmed, Mehwish
Hussain, Asadullah Khan & Muhammad Nawaz Lashari Betel Nut Usage Is a Major Risk
Factor for Coronary Artery Disease Global Journal of Health Science; Vol. 6, No. 2; 2014
67. Dhruv Mehta, David Ramsey, Chayakrit Krittanawong, Mahmoud Al Rifa Recreational
substance use among patients with premature atherosclerotic cardiovascular disease
68. Concheiro-Guisan A, Sousa-Rouco C, Fernandez-Santamarina I, Gonzalez-Carrero J.
Intrauterine myocardial infarction: unsuspected diagnosis in the delivery room. Fetal
Pediatr Pathol. 2006 Jul-Aug. 25(4):179-84.
69. Muhammad Ajmal Malik,1 Shahzad Alam Khan,2 Sohail Safdar,3 and Ijaz-Ul-Haque
Taseer4 Chest Pain as a presenting complaint in patients with acute myocardial infarction
(AMI) 2013 Apr; 29(2): 565–568
70. A Maziar Zafari ,Eric H Yang, What is the role of heart rate in the evaluation of
symptoms of myocardial infarction (MI, heart attack)? Updated: May 07, 2019
71. Tomas Ondrus, Jan Kanovsky, Tomas Novotny, Irena Andrsova, Jindrich Spinar, and Petr
Kala, Right ventricular myocardial infarction: From pathophysiology to prognosis 2013
Winter; 18(1): 27–30.
72. Daanish Aijaz Chhapra,∗ Sanket Kaushik Mahajan, and Sanjay Tukaram Thorat A study
of the clinical profile of right ventricular infarction in context to inferior wall myocardial
infarction in a tertiary care center 2013 Sep; 4(3): 170–176. Published online 2013 Nov
13.
73. Walker HK, Hall WD, Hurst JW, Clinical Methods: The History, Physical, and
Laboratory Examinations. 3rd edition.: Butterworths; 1990.
59
74. Oren J. Mechanic; Michael Gavin; Shamai A Acute Myocardial Infarction. Grossman.
Last Update: March 9, 2021.
75. A Maziar Zafari Eric H Yang, What are the characteristics of typical chest pain in acute
myocardial infarction (MI, heart attack)? Updated: May 07, 2019
76. National Center for Chronic Disease Prevention and Health Promotion, Division for Heart
Disease and Stroke Prevention Page last reviewed: September 8, 2020, Heart Disease
Facts https://cutt.ly/Wc4LTyN
77. Mark A. Williams, Jerome L. Fleg, Philip A. Ades, Bernard R. Chaitman Secondary
Prevention of Coronary Heart Disease in the Elderly (With Emphasis on Patients ≥75
Years of Age) Originally published9 Apr 2002
78. Chronic Kidney Disease in the United States Centers for Disease Control and Prevention
Page last reviewed: March 4, 2021, https://cutt.ly/1c4ZU5C
79. Kamal (Komo) Gursahani and Barry E Brenner Cardiac Markers Updated: Jul 30, 2021
80. B. B. L. M. IJkema, J. J. R. M. Bonnier, D. Schoors, M. J. Schalij and C. A. Swenne
Role of the ECG in initial acute coronary syndrome triage: primary PCI regardless
presence of ST elevation or of non-ST elevation Neth Heart J. 2014 Nov; 22(11): 484–
490. Published online 2014 Sep 9.1968
81. Azin Alizadehasl , Anita Sadeghpour and Mohaddeseh Behjati The role of
echocardiography in acute myocardial infarction Indian Heart J. 2017 Jul-Aug; 69(4):
563. Published online 2017 Jun 30.
82. O'Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. 2013
ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a
report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. Circulation. 2013 Jan 29. 127 (4):e362-425.
60
83. Wanda L Rivera-Bou, Erik D Schraga, Thrombolytic Therapy Author: Updated: Dec 31,
2017.
84. Lloyd-Jones D, Adams RJ, Brown TM, et al, for the American Heart Association
Statistics Committee and Stroke Statistics Subcommittee. Executive summary: heart
disease and stroke statistics--2010 update: a report from the American Heart Association.
Circulation. 2010 Feb 23. 121 (7):948-54
85. Levi F, Lucchini F, Negri E, La Vecchia C. Trends in mortality from cardiovascular and
cerebrovascular diseases in Europe and other areas of the world. Heart. 2002 Aug. 88
(2):119-24.
86. International Journal of Cardiology Volume 291 http://gestyy.com/ey4E6R
87. Critchley J, Liu J, Zhao D, Wei W, Capewell S. Explaining the increase in coronary heart
disease mortality in Beijing between 1984 and 1999. Circulation. 2004 Sep 7. 110
(10):1236-44.
88. Yusuf S, Hawken S, Ounpuu S, et al, for the INTERHEART Study Investigators. Effect
of potentially modifiable risk factors associated with myocardial infarction in 52
countries (the INTERHEART study): a case-control study. Lancet. 2004 Sep 11-17. 364
(9438):937-52
89. Sibu P Saha, Deepak K Bhalla, Thomas F Whayne, Jr, and CG Gairola Cigarette smoke
and adverse health effects: An overview of research trends and future needs Int J
Angiol. 2007 Autumn; 16(3): 77–83.
90. Smith SC Jr, Allen J, Blair SN, et al, AHA/ACC guidelines for secondary prevention for
patients with coronary and another atherosclerotic vascular disease: 2006 update:
endorsed by the National Heart, Lung, and Blood Institute. Circulation. 2006 May 16. 113
(19):2363-72
61
91. Nancy A Rigotti, James K Stoller, D Aronson, Lisa Kunins, Patient education: Quitting
smoking Author: Published: 1-Jan-2021
92. Maqbool H. Jafary, Abdus Samad, Mohammad Ishaq, Shaukat Ali Jawaid, Mansoor
Ahmad, Ejaz Ahmad Vohra et al PROFILE OF ACUTE MYOCARDIAL INFARCTION
(AMI) IN PAKISTAN On behalf of AAUS Study.
93. Heather A. McGrane Minton, Kelly Thevenet-Morrison, and I. Diana Fernandez, Using
Television-Viewing Hours and Total Hours Sitting as Interchangeable Measures of
Sedentary Behavior Am J Lifestyle Med. 2019 Jan-Feb; 13(1): 98–105. Published online
2016 Nov 30
62

More Related Content

Similar to COMPARISON OF RISK FACTORS IN YOUNG ADULTS WITH OLDER ADULT PATIENTS WITH RECENT MYOCARDIAL INFARCTION AT DR RUTH PFAU CIVIL HOSPITAL KARACHI

Clinical Profile of Acute Coronary Syndrome among Young Adults
Clinical Profile of Acute Coronary Syndrome among Young AdultsClinical Profile of Acute Coronary Syndrome among Young Adults
Clinical Profile of Acute Coronary Syndrome among Young AdultsPremier Publishers
 
Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...
Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...
Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...M. Luisetto Pharm.D.Spec. Pharmacology
 
Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...
Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...
Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...asclepiuspdfs
 
Dyslipidemia & ayurveda
Dyslipidemia & ayurvedaDyslipidemia & ayurveda
Dyslipidemia & ayurvedaAmit Sharma
 
CVD Egypt Clinical Diabetes Reprint Summer 2010
CVD Egypt Clinical Diabetes Reprint Summer 2010CVD Egypt Clinical Diabetes Reprint Summer 2010
CVD Egypt Clinical Diabetes Reprint Summer 2010Mahmoud IBRAHIM
 
The Use of Artificial Neural Network and Logistic Regression to Predict the I...
The Use of Artificial Neural Network and Logistic Regression to Predict the I...The Use of Artificial Neural Network and Logistic Regression to Predict the I...
The Use of Artificial Neural Network and Logistic Regression to Predict the I...Crimsonpublisherscojnh
 
Cardiovascular.pptx slide for detection cancer
Cardiovascular.pptx slide for detection cancerCardiovascular.pptx slide for detection cancer
Cardiovascular.pptx slide for detection cancerJafarHussain48
 
Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology a new ...
Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology   a new ...Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology   a new ...
Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology a new ...M. Luisetto Pharm.D.Spec. Pharmacology
 
Luisetto m, khan fa, mashori gr (2017) sudden heart pathology a new researc...
Luisetto m, khan fa, mashori gr (2017) sudden heart pathology   a new researc...Luisetto m, khan fa, mashori gr (2017) sudden heart pathology   a new researc...
Luisetto m, khan fa, mashori gr (2017) sudden heart pathology a new researc...M. Luisetto Pharm.D.Spec. Pharmacology
 
Epidemiology of Cardiovascular Diseases
Epidemiology of Cardiovascular DiseasesEpidemiology of Cardiovascular Diseases
Epidemiology of Cardiovascular DiseasesSarinkumar P S
 
Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...
Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...
Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...Erwin Chiquete, MD, PhD
 
M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...
M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...
M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...M. Luisetto Pharm.D.Spec. Pharmacology
 
ECG changes in anorexia nervosa
ECG changes in anorexia nervosaECG changes in anorexia nervosa
ECG changes in anorexia nervosaSimon Daley
 
https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...
https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...
https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...Samuel Oche
 
CIR.0000000000000921.pdf
CIR.0000000000000921.pdfCIR.0000000000000921.pdf
CIR.0000000000000921.pdfcikKahadi
 
Newsletter July07
Newsletter July07Newsletter July07
Newsletter July07robwear
 
CVD Risk Managemnt- Focus on HTN & Dys.pdf
CVD Risk Managemnt- Focus on HTN & Dys.pdfCVD Risk Managemnt- Focus on HTN & Dys.pdf
CVD Risk Managemnt- Focus on HTN & Dys.pdfDr. Nayan Ray
 
Introduction to ncd, coronary heart disease online lecture slides 2020 april 1
Introduction to ncd, coronary heart disease online lecture slides 2020 april 1Introduction to ncd, coronary heart disease online lecture slides 2020 april 1
Introduction to ncd, coronary heart disease online lecture slides 2020 april 1Animesh Jain
 
Copyright 2016 American Medical Association. All rights reserv.docx
Copyright 2016 American Medical Association. All rights reserv.docxCopyright 2016 American Medical Association. All rights reserv.docx
Copyright 2016 American Medical Association. All rights reserv.docxmelvinjrobinson2199
 

Similar to COMPARISON OF RISK FACTORS IN YOUNG ADULTS WITH OLDER ADULT PATIENTS WITH RECENT MYOCARDIAL INFARCTION AT DR RUTH PFAU CIVIL HOSPITAL KARACHI (20)

Clinical Profile of Acute Coronary Syndrome among Young Adults
Clinical Profile of Acute Coronary Syndrome among Young AdultsClinical Profile of Acute Coronary Syndrome among Young Adults
Clinical Profile of Acute Coronary Syndrome among Young Adults
 
Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...
Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...
Luisetto m, luca c, f. a. khan, g. r. mashori. sudden heart pathology a new r...
 
Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...
Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...
Diagnosis of Early Risks, Management of Risks, and Reduction of Vascular Dise...
 
Dyslipidemia & ayurveda
Dyslipidemia & ayurvedaDyslipidemia & ayurveda
Dyslipidemia & ayurveda
 
CVD Egypt Clinical Diabetes Reprint Summer 2010
CVD Egypt Clinical Diabetes Reprint Summer 2010CVD Egypt Clinical Diabetes Reprint Summer 2010
CVD Egypt Clinical Diabetes Reprint Summer 2010
 
The Use of Artificial Neural Network and Logistic Regression to Predict the I...
The Use of Artificial Neural Network and Logistic Regression to Predict the I...The Use of Artificial Neural Network and Logistic Regression to Predict the I...
The Use of Artificial Neural Network and Logistic Regression to Predict the I...
 
Cardiovascular.pptx slide for detection cancer
Cardiovascular.pptx slide for detection cancerCardiovascular.pptx slide for detection cancer
Cardiovascular.pptx slide for detection cancer
 
Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology a new ...
Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology   a new ...Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology   a new ...
Luisetto m, luca c, farhan a, ghulam r. sudden death heart pathology a new ...
 
Luisetto m, khan fa, mashori gr (2017) sudden heart pathology a new researc...
Luisetto m, khan fa, mashori gr (2017) sudden heart pathology   a new researc...Luisetto m, khan fa, mashori gr (2017) sudden heart pathology   a new researc...
Luisetto m, khan fa, mashori gr (2017) sudden heart pathology a new researc...
 
Epidemiology of Cardiovascular Diseases
Epidemiology of Cardiovascular DiseasesEpidemiology of Cardiovascular Diseases
Epidemiology of Cardiovascular Diseases
 
Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...
Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...
Atherothrombotic Disease, Traditional Risk Factors, and 4-Year Mortality in a...
 
Vasudha main
Vasudha mainVasudha main
Vasudha main
 
M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...
M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...
M. luisetto (2017) sudden death heart pathology – a new research hipotesys in...
 
ECG changes in anorexia nervosa
ECG changes in anorexia nervosaECG changes in anorexia nervosa
ECG changes in anorexia nervosa
 
https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...
https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...
https://nationalreporters.wordpress.com/2023/08/23/guidelines-forprevention-a...
 
CIR.0000000000000921.pdf
CIR.0000000000000921.pdfCIR.0000000000000921.pdf
CIR.0000000000000921.pdf
 
Newsletter July07
Newsletter July07Newsletter July07
Newsletter July07
 
CVD Risk Managemnt- Focus on HTN & Dys.pdf
CVD Risk Managemnt- Focus on HTN & Dys.pdfCVD Risk Managemnt- Focus on HTN & Dys.pdf
CVD Risk Managemnt- Focus on HTN & Dys.pdf
 
Introduction to ncd, coronary heart disease online lecture slides 2020 april 1
Introduction to ncd, coronary heart disease online lecture slides 2020 april 1Introduction to ncd, coronary heart disease online lecture slides 2020 april 1
Introduction to ncd, coronary heart disease online lecture slides 2020 april 1
 
Copyright 2016 American Medical Association. All rights reserv.docx
Copyright 2016 American Medical Association. All rights reserv.docxCopyright 2016 American Medical Association. All rights reserv.docx
Copyright 2016 American Medical Association. All rights reserv.docx
 

Recently uploaded

Physiochemical properties of nanomaterials and its nanotoxicity.pptx
Physiochemical properties of nanomaterials and its nanotoxicity.pptxPhysiochemical properties of nanomaterials and its nanotoxicity.pptx
Physiochemical properties of nanomaterials and its nanotoxicity.pptxAArockiyaNisha
 
Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...
Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...
Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...Sérgio Sacani
 
Unlocking the Potential: Deep dive into ocean of Ceramic Magnets.pptx
Unlocking  the Potential: Deep dive into ocean of Ceramic Magnets.pptxUnlocking  the Potential: Deep dive into ocean of Ceramic Magnets.pptx
Unlocking the Potential: Deep dive into ocean of Ceramic Magnets.pptxanandsmhk
 
CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service 🪡
CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service  🪡CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service  🪡
CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service 🪡anilsa9823
 
Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.
Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.
Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.aasikanpl
 
SOLUBLE PATTERN RECOGNITION RECEPTORS.pptx
SOLUBLE PATTERN RECOGNITION RECEPTORS.pptxSOLUBLE PATTERN RECOGNITION RECEPTORS.pptx
SOLUBLE PATTERN RECOGNITION RECEPTORS.pptxkessiyaTpeter
 
Caco-2 cell permeability assay for drug absorption
Caco-2 cell permeability assay for drug absorptionCaco-2 cell permeability assay for drug absorption
Caco-2 cell permeability assay for drug absorptionPriyansha Singh
 
Botany 4th semester file By Sumit Kumar yadav.pdf
Botany 4th semester file By Sumit Kumar yadav.pdfBotany 4th semester file By Sumit Kumar yadav.pdf
Botany 4th semester file By Sumit Kumar yadav.pdfSumit Kumar yadav
 
Presentation Vikram Lander by Vedansh Gupta.pptx
Presentation Vikram Lander by Vedansh Gupta.pptxPresentation Vikram Lander by Vedansh Gupta.pptx
Presentation Vikram Lander by Vedansh Gupta.pptxgindu3009
 
Bentham & Hooker's Classification. along with the merits and demerits of the ...
Bentham & Hooker's Classification. along with the merits and demerits of the ...Bentham & Hooker's Classification. along with the merits and demerits of the ...
Bentham & Hooker's Classification. along with the merits and demerits of the ...Nistarini College, Purulia (W.B) India
 
Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...
Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...
Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...jana861314
 
Spermiogenesis or Spermateleosis or metamorphosis of spermatid
Spermiogenesis or Spermateleosis or metamorphosis of spermatidSpermiogenesis or Spermateleosis or metamorphosis of spermatid
Spermiogenesis or Spermateleosis or metamorphosis of spermatidSarthak Sekhar Mondal
 
Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...
Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...
Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...anilsa9823
 
GFP in rDNA Technology (Biotechnology).pptx
GFP in rDNA Technology (Biotechnology).pptxGFP in rDNA Technology (Biotechnology).pptx
GFP in rDNA Technology (Biotechnology).pptxAleenaTreesaSaji
 
Biological Classification BioHack (3).pdf
Biological Classification BioHack (3).pdfBiological Classification BioHack (3).pdf
Biological Classification BioHack (3).pdfmuntazimhurra
 
PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...
PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...
PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...Sérgio Sacani
 
Biopesticide (2).pptx .This slides helps to know the different types of biop...
Biopesticide (2).pptx  .This slides helps to know the different types of biop...Biopesticide (2).pptx  .This slides helps to know the different types of biop...
Biopesticide (2).pptx .This slides helps to know the different types of biop...RohitNehra6
 
Types of different blotting techniques.pptx
Types of different blotting techniques.pptxTypes of different blotting techniques.pptx
Types of different blotting techniques.pptxkhadijarafiq2012
 

Recently uploaded (20)

Physiochemical properties of nanomaterials and its nanotoxicity.pptx
Physiochemical properties of nanomaterials and its nanotoxicity.pptxPhysiochemical properties of nanomaterials and its nanotoxicity.pptx
Physiochemical properties of nanomaterials and its nanotoxicity.pptx
 
Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...
Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...
Discovery of an Accretion Streamer and a Slow Wide-angle Outflow around FUOri...
 
Unlocking the Potential: Deep dive into ocean of Ceramic Magnets.pptx
Unlocking  the Potential: Deep dive into ocean of Ceramic Magnets.pptxUnlocking  the Potential: Deep dive into ocean of Ceramic Magnets.pptx
Unlocking the Potential: Deep dive into ocean of Ceramic Magnets.pptx
 
CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service 🪡
CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service  🪡CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service  🪡
CALL ON ➥8923113531 🔝Call Girls Kesar Bagh Lucknow best Night Fun service 🪡
 
Engler and Prantl system of classification in plant taxonomy
Engler and Prantl system of classification in plant taxonomyEngler and Prantl system of classification in plant taxonomy
Engler and Prantl system of classification in plant taxonomy
 
Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.
Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.
Call Girls in Mayapuri Delhi 💯Call Us 🔝9953322196🔝 💯Escort.
 
SOLUBLE PATTERN RECOGNITION RECEPTORS.pptx
SOLUBLE PATTERN RECOGNITION RECEPTORS.pptxSOLUBLE PATTERN RECOGNITION RECEPTORS.pptx
SOLUBLE PATTERN RECOGNITION RECEPTORS.pptx
 
Caco-2 cell permeability assay for drug absorption
Caco-2 cell permeability assay for drug absorptionCaco-2 cell permeability assay for drug absorption
Caco-2 cell permeability assay for drug absorption
 
Botany 4th semester file By Sumit Kumar yadav.pdf
Botany 4th semester file By Sumit Kumar yadav.pdfBotany 4th semester file By Sumit Kumar yadav.pdf
Botany 4th semester file By Sumit Kumar yadav.pdf
 
Presentation Vikram Lander by Vedansh Gupta.pptx
Presentation Vikram Lander by Vedansh Gupta.pptxPresentation Vikram Lander by Vedansh Gupta.pptx
Presentation Vikram Lander by Vedansh Gupta.pptx
 
Bentham & Hooker's Classification. along with the merits and demerits of the ...
Bentham & Hooker's Classification. along with the merits and demerits of the ...Bentham & Hooker's Classification. along with the merits and demerits of the ...
Bentham & Hooker's Classification. along with the merits and demerits of the ...
 
Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...
Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...
Traditional Agroforestry System in India- Shifting Cultivation, Taungya, Home...
 
Spermiogenesis or Spermateleosis or metamorphosis of spermatid
Spermiogenesis or Spermateleosis or metamorphosis of spermatidSpermiogenesis or Spermateleosis or metamorphosis of spermatid
Spermiogenesis or Spermateleosis or metamorphosis of spermatid
 
Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...
Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...
Lucknow 💋 Russian Call Girls Lucknow Finest Escorts Service 8923113531 Availa...
 
GFP in rDNA Technology (Biotechnology).pptx
GFP in rDNA Technology (Biotechnology).pptxGFP in rDNA Technology (Biotechnology).pptx
GFP in rDNA Technology (Biotechnology).pptx
 
Biological Classification BioHack (3).pdf
Biological Classification BioHack (3).pdfBiological Classification BioHack (3).pdf
Biological Classification BioHack (3).pdf
 
PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...
PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...
PossibleEoarcheanRecordsoftheGeomagneticFieldPreservedintheIsuaSupracrustalBe...
 
Biopesticide (2).pptx .This slides helps to know the different types of biop...
Biopesticide (2).pptx  .This slides helps to know the different types of biop...Biopesticide (2).pptx  .This slides helps to know the different types of biop...
Biopesticide (2).pptx .This slides helps to know the different types of biop...
 
9953056974 Young Call Girls In Mahavir enclave Indian Quality Escort service
9953056974 Young Call Girls In Mahavir enclave Indian Quality Escort service9953056974 Young Call Girls In Mahavir enclave Indian Quality Escort service
9953056974 Young Call Girls In Mahavir enclave Indian Quality Escort service
 
Types of different blotting techniques.pptx
Types of different blotting techniques.pptxTypes of different blotting techniques.pptx
Types of different blotting techniques.pptx
 

COMPARISON OF RISK FACTORS IN YOUNG ADULTS WITH OLDER ADULT PATIENTS WITH RECENT MYOCARDIAL INFARCTION AT DR RUTH PFAU CIVIL HOSPITAL KARACHI

  • 1. COMPARISON OF RISK FACTORS IN YOUNG ADULTS WITH OLDER ADULT PATIENTS WITH RECENT MYOCARDIAL INFARCTION AT DR RUTH PFAU CIVIL HOSPITAL KARACHI A RESEARCH THESIS Submitted to the Board of Advanced Studies and Research Dow University of Health Sciences Karachi By Dr Sajad Ahmed Badvi MBBS, DIPLOMA IN CARDIOLOGY (DIPCARD), DOCTOR OF MEDICINE IN CARDIOLOGY (MD) {DUHS}
  • 2. Table of Contents Abstract ....................................................................................................I Background...............................................................................................I Objective...................................................................................................I Methods....................................................................................................I Results ...................................................................................................I-II Conclusion................................................................................................II Chapter 1 ................................................................................................... 1. Introduction......................................................................................1 1.1 Background......................................................................................4 1.2 Objective of Study.............................................................................6 1.3 Hypothesis.......................................................................................6 1.4 Operational Definitions ......................................................................6 Chapter 2 ................................................................................................... 2. Review of Literature ...........................................................................9 2.1 Definition of M.I and Types of M.I ...................................................9-10 2.2 Pathophysiology of M.I ....................................................................12 2.3 Causes of M.I .................................................................................15 2.4 Diagnosis of M.I .............................................................................28 2.5 Management of M.I ........................................................................29 2.6 Epidemiology of M.I ........................................................................30 Chapter 3 ................................................................................................... 3. Materials and Methods.....................................................................34 3.1 Research Design and Settings............................................................34 3.2 Study Duration ...............................................................................34 3.3 Inclusion Criteria ............................................................................34 3.4 Exclusion Criteria ............................................................................34 3.5 Sampling Techniques ......................................................................34 3.6 Sample Size Estimation ....................................................................34 3.7 Data Collection...............................................................................35 3.8 Data Analysis..................................................................................35
  • 3. Chapter 4 ................................................................................................... 4. Results...........................................................................................36 Chapter 5 .................................................................................................. 5. Discussion ......................................................................................46 5.1 Limitations.....................................................................................49 5.2 Recommendations ..........................................................................49 5.3 Conclusion.....................................................................................50 References .............................................................................................51
  • 4. LIST OF TABLES: Table 1: Comparison of age between groups Page:40 Bar Graph 1: Comparison of gender between groups Page:4o Table 2: Comparison of smoking between groups Page:41 Table 3: Comparison of diabetes between groups Page:41 Table 4: Comparison of hypertension between groups Page:41 Table 5: Comparison of family history of IHD between groups Page:42 Table 6: Comparison of sedentary lifestyle between groups Page:42 Table 7: Comparison of obesity between groups Page:42 Table 8: Comparison of dyslipidemia between groups Page:43 Table 9: Comparison of substance abuse between groups Page:43 Table 10: Comparison of blood urea between groups Page:44 Table 11: Comparison of serum creatinine between groups Page:44 Table 12: Comparison of lipid profile between groups Page:45 FIGURE  Figure: Blood supply of heart Page:27
  • 5. LIST OF ABBREVIATIONS ACS = Acute Coronary Syndrome AHA = American Heart Association ACEI = Angiotensin Converting Enzyme Inhibitors AMI = Acute Myocardial Infarction ATP = Adenosine Triphosphate ADP = Adenosine Diphosphate BMI = Body Mass Index CABG = Coronary Artery Bypass Grafting CAD = Coronary Artery Disease CHD = Coronary Heart Disease CBC = Complete Blood Count CKD = Chronic Kidney Disease DM = Diabetes Mellitus ECG = Electrocardiography ESC = European Society of Cardiology FH = Family History FBS = Fasting Blood Sugar HBP = High Blood Pressure HDL = High Density Lipoprotein IHD = Ischemic Heart Disease LBBB = Left Bundle Branch Block LDL = Low Density Lipoprotein PCI = Percutaneous Coronary Intervention RBS = Random Blood Sugar SD = Standard Deviation WHO = World Health Organization
  • 6. i ABSTRACT BACKGROUND: Myocardial infarction occurs when a rise or fall recorded in troponin and one of the values must be 99th percentile of upper reference limit along with ischemia evidence. There is a common factor in young patients having a family history of coronary artery disease. More young patients were smokers, and drug abusers. However, a history of previous MI or angina was found less in younger age patients. Similarly, major risk factors of coronary artery disease like diabetes and obesity were also found less in young age group, compared to the older age group. OBJECTIVE: To compare the risk factors in young adults with older adults’ patients suffering from recent myocardial infarction admitted in the cardiology unit of civil hospital Karachi. METHODOLOGY: The patients admitted in the cardiology department having age <35 years or equal to 35 years were placed in one group and patients age >35 years were placed in another group. The questionnaire has questions regarding socio- demographic aspects with ST-elevation and risk factors like gender, family history of myocardial infarction, hypertension, diabetes, smoking, substance abuse, and lifestyle. These factors with ECG and lab tests were compared to determine statistical significance in two groups. The collected data were analyzed through SPSS v25.0. To find the statistical significance between the two groups Chi-square test is used. The significance was done labelled as p<0.05. All these results were presented in tables and graphs. My study showed that young adult group(69.8% were males v/s 3o.2% females) older adult group(76.2% were males v/s 23.3% were females), smoking was common in young patients (63.5% in young v/s 31.7% in older group) similarly family history of IHD was common in young patients (57.1% in young v/s 12.7% in older group),
  • 7. ii similarly substance abuse intake without smoking were (26.9% in young v/s 39.6% in the older group) and substance abuse used with smoking 57.1% were young v/s 19.0% were older), diabetes mellitus was less common in young patients (12.7% in young v/s 82.5% in older group), similarly hypertension was less common in young patients(15.9% in young v/s 98.5% in older group), sedentary lifestyle was more common in older patients (11.1% in young v/s71.4% in older group), again obesity was more common seen in older patients (15.9% in young v/s 55.6% in older group), similarly dyslipidemia was also common in older group (31.7% in young v/s 82.5% in older groups). CONCLUSION: Smoking, Substance abuse and Family History of IHD were the more common risk factors among young age group patients of M.I. While conventional risk factors are common in older age group .Hence more effort is required to protect young population. Hence, we recommend at the national level to stop smoking, have physical activities, chose healthy and better life style to promote good health in society and advise policy makers to spread awareness through electronic, print media and arrange seminars in societies to avoid substance abuse materials. KEYWORDS: Coronary Atherosclerosis, Risk factors, Young v/s Old adults, Myocardial Infarction.
  • 8. 1 Chapter: 1 INTRODUCTION Myocardial Infarction (MI) occurs when rise and fall are recorded in troponin(1) and one of the values above 99th percentile of upper reference limit along with evidence of ischemia. The main symptoms of MI are chest pain(2) , shortness of breath, feeling of discomfort with heart burning, cold sweat, and nausea. The pain mostly travels from chest to arm, shoulder, jaws, neck, and back. M.I. is an old age disease however it can also develop in young age grown-ups. However, it has different risk factors and complications as compared to old age patients. M.I. occurs due to plaque rupture which reduces the supply of blood to the heart. (3) In a study (4) conducted in the USA, it was determined that the prevalence of M.I. in the younger age group (<45 years) was 6 to 10 percent. In a study(5) of India, it was observed that in South Asians, the occurrence of MI in the young population is high as compared to other regions. According to the study, the incidence of coronary arterial disease was determined as 12 to 16 percent. According to a study,(6) conducted in Pakistan, AMI in<40 years of age accounts for approximately 19%. It is more common in men who were smokers. However, in 10% of cases, the cause was not related to atherosclerosis. Another study(92) Abdul Samad et al. performed in Pakistan shows that the rising profile of patients with AMI is that the bulk is male, comparatively younger were <45 years, have smoked 52%, hypertension 55% and diabetes 36% and IHD 44% were major risk factors. higher management of risk factors and the awareness of preventive ways are needed. Study(18) Faisal et al. Smoking 76.66%, hypertension 6.6%, diabetes 3.3% and dyslipidemia 43.3% are common modifiable risk factors in our young adults<35 years. Three or additional risk factors in a personal incline to CAD at comparatively in younger age.
  • 9. 2 Study, (7) concluded that clinical findings and major risk factors of acute MI are quite different in young age patients as in old age patients. In the US, the main cause of mortality in either sex was M.I. Similarly, myocardial infarction was the major reason for hospitalization worldwide. The most common risk factor which contributed to the narrowing of coronary arteries was high cholesterol in older age. (8) Another study determined that elevated homocysteine and alcohol are major risk factors for developing AMI among young patients whereas in old age patient’s hypertension is the main risk factor. (9) Another Study concluded that the risk profile of CAD is different in old age group as compared to young age patients and mortality is much higher in the old age group compared to young age group. (10) Mortality in long term is fivefold less in young age people suffering from M.I, compared to old age people. (11) According to a study, it was determined that predictors of non-invasive therapy were the same for all ages but different in AMI cases. (12) However, in young age CAD patients, the potential remains more for improvement in the cardiovascular risk profile. (13) In a study,(14) in young age patients of M.I, the risk factors, such as the family history of CAD, smoking, and dyslipidemia were found to be much higher (28.6%, 64.5%, and 49.7% respectively) compared to old age patients (19.8%, 59.4%, and 38.8% respectively). However, M.I. history and angina history were found less in young age patients of M.I. (17.4% and 9.2%) as compared to old age patients (26.7% and 26,1%). It was determined in a study that dyslipidemia, hypertension, and diabetes were the predominant risk factors in old age patients of MI. Similar to it, in different studies, (15) smoking (58.7% -76.7%) was the most common risk factor in young age patients as compared to old age group patients with MI (31.7%- 59.4%). (16) In another study, (17) SRIKANTH YANDRRAPALLI and CHRISTOPHER NABORS 2019 by Journal of American College of Cardiology the relative risk factors in the young age population were determined that smoking, hypertension, and dyslipidemia were more prevalent. One study,(18) reported
  • 10. 3 that dyslipidemia was high in younger population (49.7% v/s 38.85), whereas other studies (19) reported it higher in old age patients (43.3% v/s 49.5% and 20.0% v/s 29.0%). The risk factors such as DM and obesity were found less in the young age group. Other studies (20) also shown diabetes (3.3- 5% in young v/s 30-38.6% in older) and obesity (6.6% in young vs. 21.4% in older) as fewer risk factors in the young age population. According to a study, (21) the risk factors of MI have significant gender differences in short and long- term clinical outcomes of young patients. Therefore, preventive strategies should be taken to reduce the risk factor in young adults. The aim of my study was to find out risk factors that are causing M.I.in young population so through preventive measures reduce chances of IHD and protecting the patients from huge expensive heart disease treatment. Since last more than five years no research occurred on such topic. Further aim of my study was to determine the effects of substance abuse drugs on heart how these substances causes IHD .because nowadays the tendency of our young population to take drugs has increased especially they use alcohol,Gutka/ Betelnut more frequently. Most of the cases registered in my study were also found to be addictive of smoking, alcohol, gutka/betelnut.
  • 11. 4 BACKGROUND The main reason behind myocardial infarction (MI) is an imbalance of oxygen supply and demand which is caused by the formation of plaque rupture in an epicardial coronary artery, as a result, acute reduction of blood supply in the myocardium occurs. The findings of an acute MI are presented below in the electrocardiographic (ECG). ECG shows Acute Inferior Wall Myocardial Infarction Taken from: https://emedicine.medscape.com/article/155919-overview In acute coronary syndrome, MI is considered a part of the spectrum (ACS). The spectrum of ACS(22) consists of ST-segment elevation M.I, non-ST-segment elevation M.I and unstable angina that is collectively known as an acute coronary syndrome. Patients with non-ST- segment elevation M.I might have T-wave or ST-segment changes that occur on the surface (ECG), Persistent and continuing transmural myocardial injury shows ST-segment elevation MI seen on the ECG(23) . Many patients who develop Q-waves have already dead myocardial area or myocardium at risk of death unless immediate reperfusion therapy has been given.
  • 12. 5 In the presence of cardiac enzymes, the patients are diagnosed to have NSTEMI with the absence of raised cardiac enzymes indicates UNSTABLE ANGINA.(24) Both these conditions produce ST and T wave morphological changes on surface ECG. Due to MI systolic and diastolic impairment can occur and this leads to long-term complications. (25,26) Primary treatment of acute MI includes coronary thrombolysis and percutaneous revascularization. (27) Benefit of the open infarct-related artery with percutaneous route is more pronounced when the door to balloon time is kept within 90 minutes after first medical contact in same way benefit with fibrinolytic is achieved when the door to injection time within 30 minutes after first medical contact. Ventricular functions, collateral blood flow, prevention of ventricular remodeling improves by the opening of an infarct-related artery. (28)
  • 13. 6 OBJECTIVE To compare the risk factors in young adults with older adult patients suffering from recent myocardial infarction admitted in the cardiology unit of civil hospital Karachi. Null Hypothesis: There is no difference in risk factors of young adults and older adults’ patients suffering from recent myocardial infarction. Alternate Hypothesis: The risk factors of young adults are different from the risk factors of older adults’ patients suffering from recent myocardial infarction OPERATIONAL DEFINITIONS Myocardial Infarction Myocardial Infarction (MI) occurs when a rise or fall in cardiac troponin levels recorded with one value must be above the 99th percentile of upper reference level along with ischemia evidence. ST-Elevation MI: It is defined as 1mm ST-segment elevation in two or more adjoining leads often with reciprocal ST depression in contra lateral leads. Except in leads V2, V3 where criteria for men is 2.5mm of ST elevation<40 years and 2mmST elevation >40 years and in female 1.5mm ST-segment elevation on ECG is considered diagnostic.(4,13)
  • 14. 7 NST Elevation MI: It is distinguished from unstable angina by the presence of elevated serum levels of cardiac biomarkers, serial measurements in patients presenting with ACS should be performed. In patients of NST elevation, MI and unstable angina both produce ST and T wave changes on ECGs. Hyperlipidemia: It is a condition in which total cholesterol is >200 mg/dl, LDLC >100mg/dl, and HDL goes to <40mg/dl or they are on statin therapy.(19,59) Young adult age: <35 years of age or equal to 35 years.(18) Old adult age: >35 years of age Diabetes Mellitus: All the patients having HbA1c more than 6.5% or fasting blood sugar more than 126 mg/dl and random blood sugar more than 200 mg/dl or they are on anti-diabetic therapy will be counted as diabetics.(29) Hypertension: In patients with blood pressure >130/80mmHg or patients taking antihypertensive therapy for control of blood pressure.(30)
  • 15. 8 Smoker: Patients taking minimum five cigarettes per day for at least one-year duration is called a smoker.(48) • Current < 1 month • Recent 1month to 1 year • Ex-smoker More than 1 year • Non-smoker Obesity: If BMI is exceeded to 30 Kg/m2. .(61) Normal 18.5 to 24.9 Kg/m2 . Overweight 25 to 27.8 Kg/m2 . Obese > 30Kg/m2 Sedentary Lifestyle The patient achieved a METS score <1.5 Oxygen cost ml/kg /min. watching the T.V, playing video games, sitting in the office between 6.7 to 8 hours /day.(93)
  • 16. 9 Chapter: 2 REVIEW OF LITERATURE DEFINITIONS The fourth universal definition of myocardial infarction(31) Heart attack's second name is myocardial infarction (MI) which is defined pathologically when myocardial cells are dead due to ischemia. Clinically myocardial infarction is a condition apparent in most cases from major symptoms such as chest pain. It is supported by electrocardiographic changes, elevated cardiac biomarkers that indicate myocardial necrosis. Detection of an increase or decrease in cardiac markers while using troponin may be associated with the following findings. By autopsy or angiographic the identification of thrombus intracoronary. • Ischemia symptoms • New wave (ST-T) or LBBB significant. • In ECG formation of Q waves (pathologic) • Evidence by imaging with regional wall motion abnormality.
  • 17. 10 Types of MI According to the joint WHF/ESC/AHA task force, MI has the following 5 types. • Type 1 includes atherosclerotic plaque rupture. Dissection, erosion fissuring in the coronary artery leads to decrease myocardial blood flow that nearly is myocyte necrosis resulting. The patient may have CAD. (32) • Type 2 leads to ischemic imbalance, at this stage cell demand more oxygen, but has less supply. (33) • Type 3 leads to patient death when biomarkers values are unavailable. Sudden before blood sample to biomarker has taken when unexpected cardiac death can happen. d) Type 4a MI is associated with PCI (34) e) Type 4b MI is associated with stent thrombosis f) Type 5 MI is associated with CABG
  • 18. 11 ACUTE CORONARY SYNDROME The expression "intense coronary disorder" (ACS) alludes to a range of conditions that occur because of intense myocardial ischemia or potentially localized necrosis because of a sudden decrease in blood supply to the myocardium. (35) STEMI The major segregating highlight of STEMI is the nearness of indications of myocardial ischemia/damage alongside tenacious ECG ST-Segment height not necessarily elevation of cardiovascular biomarkers. (36) RECENT M.I Ongoing myocardial localized necrosis characterized that had happened two days to five weeks after M.I. (37)
  • 19. 12 PATHOPHYSIOLOGY Cellular effects of myocardial infarction (MI) A normal heart needs a blood supply to work properly and delivers blood to the entire body. Oxygen is also needed to work properly. Hearts need oxygen supply properly and also need supplements for their functioning by coronary dissemination. Ischemia is a condition when blood supply to the myocardium is inadequate. If this event persists then it damages heart cells and becomes it's fiery and biochemically, in the long run, heart muscles cells become irreversibly damaged. The progression of this disorder first indicates necrosis of coagulation and then a healing phase of myocardial scar formation called myocardial fibrosis. That is a serious health concern. These all things slowly build changes to contractile capacity and shape of the myocardium, especially in the left ventricle. That all reduced heart contractile capacity. Later over time heart's left ventricle becomes widens and changes to a round shape in a process called redesigning of the left ventricle. With time serious health problems occur with this condition of the heart. Ventricular redesigning is a regulated process so specific treatment strategy particularly ACE inhibitors or ARB should be used in AMI management to reduce the occurrence and seriousness of ventricular redesigning. (38) Myocardial stunning and hibernation are both triggered by the loss of fundamental metabolites, for example, adenosine, necessary for adenosine triphosphate (ATP)-dependent contraction, which is needed for normal myocardial contractility (39)
  • 20. 13 Plaque Atherosclerotic plaques which cause M. I. Plaques occur in multiple stages in a dynamic process. The process can be seen immediately after birth, initially, intima thickening occur which comprise of vascular smooth muscle with very few or no inflammatory cells, subsequently, a fibrous cap atheroma with a lipid-rich necrotic core surrounded by fibrous tissue develops and finally a thin cap atheroma develop, which is with a large necrotic core mainly isolated from blood vessels known as vulnerable plaque that are penetrated by inflammatory cells and are susceptible to rupture due to lack of smooth muscle cells (40,41) The course of acute coronary thrombosis leading to ACS involves a pathogenic mechanism of plaque rupture and less frequent plaque erosion. When complete obstruction of the coronary artery occurs by thrombus it causes ST-Segment elevation M.I and when partial obstruction occurs it causes either NSTEMI or unstable angina. The Brasilia Heart Study Group shows that the antiatherogenic capacity of (HDL) to transport blood vessels lipids can be altered by modification of high-thickening lipoprotein (HDL) in the MI. Specialists observed simultaneous lipid substitution to HDL and the limit HDL to efflux cell cholesterol. (42) Settled case-control study examining plasma metabolic markers relationships with the risk of MI, ischemic and intra-cerebral bleeding showed that lipoproteins and lipids were in a favorable relationship with MI and ischemic stroke but were not with intracerebral hemorrhage. (43)
  • 21. 14 Non-modifiable risk factors for atherosclerosis include the following: • Sex • Age • Family history of CHD • baldness Male-pattern Modifiable Risk Factors (44) • Dyslipidemia • Diabetes mellitus • Obesity (abdominal obesity) • Smoking • Psychosocial stress • Type A personality • Elevated homocysteine levels • lack of exercise • Presence of peripheral vascular disease
  • 22. 15 COMMON RISK FACTORS OF MYOCARDIAL INFARCTION There are various risk factors of AMI. Among them, some are modifiable (treatable) and others are non-modifiable (cannot be changed). The major risk factors of AMI are described below. Age Old age increases mortality in acute myocardial infarction. (45) The mechanism by which elevated age contributes to increased mortality is unknown. About 80% of heart disease deaths occur in people aged 65 or older. (46) Gender Men have more lifetime heart attacks than females. (47) Women's heart problems occur primarily after menopause. And now, both men and women face heart disease as the leading cause of death. Smoking Smoking is an important risk factor for myocardial infarction. Smoking causes early atherosclerosis and sudden cardiac death. Smoking primarily affects unhealthy patients with early STEMI. (48) Cigarette smoking by atherogenesis raises the risk of AMI. Smoking raises serum LDL cholesterol, triglyceride and decreases serum HDL- cholesterol levels. The cigarette smoke does not do radical damage to LDL so that the arterial wall can absorb oxidized LDL-cholesterol Smoking induces traditional artery inflammation atherosclerosis, with higher serum levels of C-reactive protein in smokers than in non-smokers. (49) Smoking stimulates the sympathetic nervous system (SNS), increases heart rate and systolic blood pressure through the content of nicotine. This rise in levels and pressure causes myocardial oxygen demand to rise. Increasing SNS activity also contributes to coronary arterial
  • 23. 16 vasoconstriction that decreases myocardial oxygen supply and increases myocardial oxygen demand this effect contributes to causing ischemia. (50) Diabetes Mellitus Diabetes mellitus is an important risk factor for cardiovascular disease (CVD). The cardiovascular mortality and morbidity in people with type 2 diabetes mellitus are higher. (51) Diabetes patients have a greater risk of atherosclerotic vascular disease in both the heart and other vascularized regions. Atheromatous plaques in diabetic patients are more vulnerable to rupture. (52) Diabetes raises the risk of myocardial infarction as it raises the rate of atherosclerotic progression and influences the lipid profile and plaque formation. Diabetes reduces the synthesis of nitric oxide resulting in increased platelet aggregation and activation of thrombosis. Platelet function is also irregular in Diabetes, which raises the risk of thrombosis at the site of the plaque break, resulting in up-regulation of factor VII, thrombin, tissue factor, PAI-1 clotting for diabetes individuals,(53) myocardial infarction is often fatal in contrast to Non-diabetic patients. Hypertension All systolic and diastolic hypertension increase the risk of myocardial infarction. This is a significant risk factor in coronary blood vessels causing atherosclerosis contributing to cause myocardial infarction. (54) In old age, hypertension is much greater in the heart and responsible for at least 70 percent of heart disease. Hypertension accelerates atheroma symptoms, increases shear stress on plaques, adversely affects coronary circulation, and degrades endothelial function and. Hypertension management with strict compliance with proper medication and dietary changes greatly decreases the risk of myocardial infarction. (55)
  • 24. 17 Family history The family history of myocardial infarction (MI) is an independent risk factor of MI. Many genetic variations are associated with an increased risk of MI. (56) The strongest genetic effect on the risk of myocardial infarction is that of a variant found on chromosome 9p21. Only a few of the myocardial infarction genes are associated with classic risk factors. The history of AMI due to acute myocardial infarction in a first degree raises the risk for men by around two times and almost three times the risk for women. If a father has a heart attack before age 55 years and a mother before 65 years, good family history may become very important to prevent a premature myocardial infarction in the next generation. Sedentary Lifestyle In a sedentary lifestyle, people with multiple cardiac risk factors are more likely to develop AMI. Sedentary lifestyle persons have double the risk for CAD death as that of active people. (57) Up to 20%-30% reduced risk of coronary heart disease through physical activity like Brisk walking, climbing, and cycling activities provide safety from CVD. The AHA recommends that 30 minutes or more of moderate-intensity activity on most days of the week improves glucose tolerance, insulin sensitivity, increases fibrinolysis, HDL and improves oxygen uptake in the heart, and increases coronary artery diameter. (58) Dyslipidemia Overall, Dyslipidemia, which is a significant risk factor in cardiovascular disease was generally referred to as total cholesterol, LDL, triglycerides or rates above the 90th percentile or HDL-C below the 10th percentile in the general population. (59) The level of non-fasting triglyceride appears to be a strong and independent predictor of potential AMI risk, especially when the levels of total cholesterol also increase. The explanation
  • 25. 18 for this is that reduced levels of HDL-C and increased levels of triglyceride cause metabolic worries and potentially adverse consequences. (60) Framingham's study established the relationship between dyslipidemia and coronary artery disease. The main risk factors for coronary atherosclerosis are elevated total cholesterol, LDL, and low HDL levels. Dyslipidemia correction can reduce the risk of myocardial disease. Obesity Increased BMI is directly related to increased incidence of myocardial infarction. (61) Elevated BMI increase total cholesterol and triglyceride also decrease the level of HDL- C. Although BMI and waist to hip ratios have a linear relation between obesity and CAD. The waist to hip ratio is a more accurate predictor of CAD. (62) Among Abdominal obesity increased the risk of AMI. Obesity causes hyperinsulinemia which is associate with lipid derangement, increase plasminogen activator inhibitor and enhanced proliferation of cells in atherosclerotic plaque enhance chances of CAD. Obese are those with a BMI of > 30kg/m2 . Alcohol Consumption Alcohol consumption increased the risk of myocardial infarction among those people who drink alcohol daily. Heavy alcohol drinking enhances cardio-vascular risk. (63) Heavy drinking has been shown to increase low-density lipoproteins, which increase cardiovascular morbidity and mortality. Binge drinking has been associated with an increased risk of thrombosis. Most researches showed that alcohol consumption could increase LDL-C, triglyceride, heart rate, blood pressure and thus increase the risks of atherosclerosis, atrial fibrillation resulting in damaging cardiac muscle cells and cardiovascular system and producing fibrinolytic enzyme inhibitors. Moderate drinking is not associated with any serious
  • 26. 19 morbidity; however, hypertriglyceridemias, cardiomyopathies, hypertension, and M.I. are associated more often in those who drinks alcohol three or more times a day. COCAINE USE Cocaine increases the incidence of CAD also cocaine raises heart rate, blood pressure, and enhances oxygen demand in heart muscle, and reduced coronary blood flow causes ischemia. Cocaine abuse causes coronary spasm or thrombus formation by a-adrenergic stimulation. (64) Chest pain caused by infarction after 3 hours of cocaine ingestion and also depends on the route of intake ( chest pain caused by M.I. after 30 min. with intravenous use, 90 min with smoking , more than 80% of persons who use cocaine are also cigarette smokers, and pain caused 135 minutes after nasal inhalation). Even single use of cocaine caused Prinzmetals Angina which is due to coronary arterial vasospasm (65) Gutka/ Betel Nut: People who chewed ten edible seeds each day were 4 times the additional possible risk to induce CAD as compared to people who do not take it. Previously, mastication betel nut was the reason behind several risk factors for CAD. One study established that chewing betel nut was related to central blubber (Lin et al., 2009). However, Betel nut chewing increase blood pressure in patients with D.M. It is also seen a positive association between edible seed mastication and metabolic syndrome. It will so be projected that chewing betel nut could either be a freelance factor associated with CAD(66) or be an element by influencing renowned risk factors for hypertension or diabetes. Several mechanisms justify that edible seed chewing, causes narrowing of coronary arteries, and causes CAD. Arecoline, the compound found in true pepper nut, has been reported to cause induction of cyclooxygenase expression. The compound hydroxychavicol was found to induce the reactive oxygen species and thereby mediating cells. Further more, the extracts of betel nut modify LDL towards artery epithelium cells. These facts facilitate that the rationale for CAD in betel nut mastication people may be specifically attributed to atherosclerosis.
  • 27. 20 Betel nut chewing could be an important risk factor for the event of CAD. it was found that betel nut chewing increased the probability of CAD by almost 6 times. Furthermore, it was established that those chewing edible seed for ten years had an eight-fold increase in the risk of developing CAD. This shows that future betel nut chewing considerably vital risk issue in conjunction with cardiovascular disease and polygenic disorder for CAD. All these substance abuse materials like smoking, alcohol, charas, cocaine, and Gutka/betel nut causes atherosclerosis, coronary spasm, atherogenesis, thrombosis, increases fibrinogen level, LDLC, triglycerides, decreased HDLC, and increased C- reactive protein .substance abuse also increases heart rate and SBP which causes myocardial oxygen supply-demand mismatch all of these effects to contribute to causing M.I. A study was done by Dhruv Mohtta(67) et al showed that patients who developed atherosclerotic cardiovascular disease are those who use more substance abuse materials like tobacco 62.9%, alcohol 31.8%, cocaine 12.9%, and cannabis 12.5% in his study shows that recreational substances users had increase chances of ASCVD. MI occurs by Non-atherosclerosis reasons are as below • auxiliary to vasculitis coronary impediment • hypertrophy of Ventricular (e.g., hypertrophic cardiomyopathy, left ventricular hypertrophy) • Coronary cholesterol, vein emboli, air, or sepsis. • Injury to coronary arteries • Vasospasm (angina variation) • Arteritis
  • 28. 21 • Use of drugs (e.g., cocaine, ephedrine, amphetamines) • Coronary courses aneurysms • oxygen necessity factors expansion, for example, overwhelming effort or hyperthyroidism, fever • Factors that decline oxygen conveyance, for example, hypoxemia of extreme pallor • Inclusion of the coronary courses with retrograde aortic analysis, • Respiratory diseases Moreover, because harmful effects of carbon monoxide or extreme aspiration problems can lead to hypoxia which causes M.I. While not rare, diseases like Marfan, Kawasaki, Takayasu arteritis, progeria, and cystic medial necrosis may be occur in child coronary supply. In youth and immaturity, acute M.I is caused by acute inflammation of the coronary arteries or irregular coronary artery origin is more common in adults with coronal corridors due to deep- rooted affidavit of the atheroma and the plaque, which causes coronary artery spasm and thrombosis. Intrauterine M.I, sometimes associated with coronary artery stenosis, also occurs. (68) SIGNS AND SYMPTOMS In the case of acute MI, there are the following symptoms. • Crushing Substernal chest pain. Pain is typically more severe of longer duration usually more than 20 minutes. (69) • Chest pain radiates to the neck, shoulder, jaw, back, left, &right arm and epigastrium.
  • 29. 22 • Sometimes it is due to pressure feeling that is characterized by aching, as squeezing or constricting nature. • Most patients have the feeling of indigestion, gas, fullness-like symptoms. Patients that have myocardial infarction have fatigue, chest discomfort, and malaise as symptoms. These symptoms can show in days and even in weeks. Sometimes symptoms may occur suddenly or sometimes it happens without warning In MI the patient’s vital signals may demonstrate as: • The heartbeat of the patients is increased in case of high sympathoadrenal discharge. (70) • Sometimes due to atrial fibrillation, pulse rhythm can be irregular. • Due to peripheral arterial vasoconstriction patient's blood pressure is initially elevated, which can cause pain. • When MI is in the right ventricular, cardiogenic shock can happen. (71) • Due to pulmonary congestion or anxiety respiratory rate enhance. • Sometimes wheezing, coughing, and the production of frothy sputum can occur. • Sometimes patients develop respiratory distress for which they need ventilatory support.
  • 30. 23 PHYSICAL EXAMINATION While examining a patient with myocardial infarction, various clinical findings are sought out which are described below. Vital signs Heart rate Usually, heart rate is increased in AMI, Because during M. I heart muscles receive a small amount of blood from arteries that supply blood to muscle, which are blocked. In M.I. the pulse may be regular or irregular. Irregular pulse is seen in ventricular ectopy, atrial fibrillation, sometimes ventricular tachycardia, flutter and accelerated idioventricular rhythm or other supraventricular arrhythmias are seen. Blood pressure The blood pressure of M.I. patients is elevated initially, due to pain, anxiety, and agitation. Also due to large infract area or impaired global cardiac contractility. As well as systolic blood pressure may be decreased in M.I due to tachycardia which impairs stroke volume. Respiratory rate Due to pain, anxiety, or congestion the respiratory rate is increased. Patients with pulmonary Oedema may have a respiratory rate of more than 40 breaths/min. Temperature Fever is a non-specific response to tissue necrosis. In between 24-48 hours fever usually develops and the curve is generally parallel with the time that elevates creatine kinase level in blood. Mostly body temperature does not exceed 102°F.
  • 31. 24 Neck veins In the case of acute inferior-wall MI with RV infarct, the patients have right ventricular immersion, the failure of the right ventricle makes the vein visible. (72) Hepatomegaly, edema, hypotension is caused by impaired right ventricular function. Heart Sounds An S3and S4 gallop sounds are audible in patients with large MI.(73) Ruptured, mitral postero medial, papillary muscle produce a state that is known as mitral regurgitation, produces a pan systolic murmur. Pericardial friction rub that is produced through sliding contact of inflammation-roughed surfaces of pericardium due to post-MI pericarditis. Chest Auscultation Wheezes and rales are auscultated, these conditions can occur from secondary to respiratory venous hypertension. Extensive acute left ventricular MI is associated with this condition. (74) Abdomen MI Patient develops abdominal pain along with nausea, vomiting, and abdominal distension, hepatomegaly, and positive Hepatojugular reflux are elicited in RV INFARCTION.
  • 32. 25 HISTORY In the case of the initial diagnosis of MI, only some clues are obtaining from physical examination while patients’ history is crucial in-patient presentations. The patient that has acute MI, they usually have chest pain that led to prodromal symptoms of fatigue, malaise, chest discomfort is symptoms of typical ST-elevation M.I. happen without warning. In the case of acute MI typical chest pain can happen and it remains more than 20 minutes. It also radiates to the shoulder, neck, and jaw and down to the left arm, this pain is retrosternal. In the case of M.I. substernal pressure sensation can occur, which is also perceiving as aching, burning, squeezing. Some patients have symptoms as epigastric condition, feeling of indigestion, and fullness or gas. (75) Sometimes many patients, do not recognize chest pain, and suddenly high pain threshold happens to them. These patients have a disorder that impairs pain perception so this may result in a defective anginal warning system. Moreover, some patients can have high threshold pain due to mental status that is caused by medication. MI mostly occurs in the daytime in the morning hours, as the morning increases the sympathetic tone, this may increase the heart rate, high blood pressure, myocardial contractility, coronary vascular tone, all these factors can explain better the whole circadian variation. Morning is important because at that time blood viscosity is also high, and coagulation can occur. Rapid evaluation in case of initial state a brief history and focused physical examination is included. Other symptoms of myocardial infarction include the following: Myocardial infarction symptoms are as follows:
  • 33. 26 • Anxiety • Profuse sweating • Cough • Nausea, with or without vomiting. • Shortness of breath • Wheezes • Rapid or irregular heart rate • indigestion, Fullness In United State, most deaths are due to heart disease. Heart diseases increase as age increase, so it is an important, risk, albeit non-modifiable factor for cardiovascular disease in the general population.(76) It is also common in those patients that have chronic kidney disease. In 1995 in the USA chronic heart disease in men and women was prevalent at the age of 65. And the incidence in women was 90 per 1000 and in men, it was 83 per 1000. And the cumulative prevalence was 217 per 1000 for men and 129 per 1000 women. It was proved that the elderly had a high rate of chronic heart disease(77) . Patients that have chronic kidney disease have more chances to carry heart disease, mostly that patients have the highest risk of cardiovascular disease. So many cardiovascular risk factors are increased by declining kidney function. We can say that there is a direct relation between CVD and CKD. In these patients, there are standard factors that only account for a small portion that is observed in these patients.
  • 34. 27 Aging is an important determinant of kidney function. According to a study in the USA, more than a third of the US has CKD in those people that have the age of 70. (78) And this disease increases with time. According to the postulate that older individuals that have CKD also have the effect of CVD. In that case, some of the symptoms are diabetes, obesity, hypertension, and other vascular diseases are present. Blood Supply of the Heart This Figure is taken from: https://o.quizlet.com/xuwAGdOcf7jnc2YOQnTqPQ_b.jpg
  • 35. 28 DIAGNOSIS Laboratory studies Following lab tests in the diagnosis of MI are carried out: • Cardiac enzymes/biomarkers: according to the cardiology society of Europe and American Cardiology College in suspected patients of M.I. following tests are recommended. The marker which is used to diagnose is troponin as it is sensitive and specific. (79) • Troponin levels rise in serum when necrosis of the myocardial occurs. • CBC (complete blood count) • Lipid profile • Metabolic panel comprehensive Electrocardiography In initial evaluation and triage ECG is the most significant tool in those patients that have acute coronary syndrome when MI is suspected. 80% of cases are confirmed by ECG(80) . In M.I ECG also identifying the site of occlusion in infarct-related arteries. ECHOCARDIOGRAPHY Useful for detecting wall motion abnormalities, LV function, and also see mechanical complications of M.I.(81) CARDIAC IMAGING (CORONARY ANGIOGRAPHY) If patients have confirmed MI, then angiography is carried out to check the arteries of the heart.
  • 36. 29 MANAGEMENT Pre-hospital care Patients that have chest pain mostly include: • Nitroglycerin for chest pain, given by the spray • Non-enteric-coated chewable aspirin. Dose 325 mg stat • Telemetry and pre-hospital ECG. Emergency department and inpatient care Design for medication and therapy include: • Telemetry and ECG within 10 minutes After arrived in ER. • Intravenous access, pulse oximetry supplemental oxygen when SaO2 Less than 94% • Immediate giving of non-enteric-coated chewable aspirin. Dose 325 mg stat • Oral p2y12 receptor antagonists • Parenteral Antithrombotic Therapy. • Recanalize infarct-related arteries within 90 minutes door to balloon time if PCI capability is available. Primary PCI is the early goal to achieve. (82) • Revascularize infarct-related arteries with fibrinolytic within 30 minutes door to injection time in such patients where Primary PCI facility is not present. (83)
  • 37. 30 EPIDEMIOLOGY United States statistics In the United States, the main source of death is the coronary supply route, every year 500,000 to 700,000 deaths are occurred due to CAD. The cause of death due to M.I is approximately one-third of all deaths in the population for those over the age of 35 years occurs annually within the USA. The yearly incidence death rate is about 600 cases per 100,000 individuals. The proportion of patients diagnosed with NSTEMI has dynamically expanded as compared to ST-Elevation M.I. Despite a decline in age-balanced deaths in the United States due to M.I. because of CAD- related awareness is increased among peoples. since the mid-1970s, the total number of M.I- related mortalities has not decreased. The severity of M.I. in women is almost higher than in men. The CAD is more progress in the dark population than white people at the age of 75 years. Among the Hispanic populace, coronary artery disease mortality isn't as high as among dark people and white people. (84) The index mortality rate associated with acute M.I. is almost three times higher than that of men compared to women. European statistics In European nations computer source design is the major source of death. CAD rate has decreased by 30 percent in the European nation from the mid-1960s to the 1990s. eastern European death expansion rate is intense. In the early 1900s, the MI death rate has decreased. (85)
  • 38. 31 Cardiovascular disease in other developed countries and developing nations A study of death statistics by the World Health Organization (WHO) found that in Japan, CAD mortality was considerably lower, and WHO evident that about 30% mortality deceased by mid-1990. CAD mortality is significantly lower than in the USA and Europe. because Japan continues its strict control policies towards blood pressure and tobacco control and builds a strategy to control BMI, Diabetes, and cholesterol level to prevent CAD deaths. (86) (Ref.from international Journal of Cardiology vol.291 Sep. 2019. In China crucial rise in mortality associated with CAD is observed, which is likely due to increased cardiovascular risk factors dyslipidemia and transcendent smoking. (87) CAD levels and related mortality are projected to rise significantly from an estimated 80 percent growth, from approx.9 million in 1990 to 20 million by 2020, in other developing economics including Asia, Latin America, the Middle East, and Sub-Saharan Africa. It is suspected that these regional trends in the incidence of CAD and subsequent extreme MI are potentially associated with consumption of high calories diet, reduce physical activity, and higher smoking rates. Notable Canadian-drove worldwide research has identified 9 efficient danger factors (smoking, strange rates of blood lipids, obesity, diabetes, diet, physical activity, use of liquor, and psychosocial factors) that are estimated to represent over 90%. across Africa, Asia, Australia, Europe, Middle East, North and South America. (88) The INTERHEART agents found that these hazard factors are the equivalent in pretty much every geographic district and each racial/ethnic gathering around the world, and they are steady in people. The INTERHEART preliminary demonstrated that smoking 1-5 cigarettes day by
  • 39. 32 day expanded the danger of an intense MI by 40%, and the hazard expanded with the measure of tobacco smoked every day. In the last few years, the study indicates that the approximate proportion of abdomen to hip will supplant BMI as a sign of fitness, with the reason that all forms of tobacco – including separate and unfiltered cigarettes, funneling and bites tobacco-are valuable and the stomach robustness is a more important risk factor than weight gain (BMI).(89) Patient Education Patients with dynamic side effects of intense coronary disorder (ACS) ought to be told to call crisis administrations, and they ought to be transported by crisis restorative administrations faculty, not independent from anyone else, family, or companions. When suspected ACS incidents last longer than 20 minutes, patients must be advised to reach the crisis office immediately when closely associated syncope/ presyncope or hemodynamic shakiness is present. On the off chance that nitroglycerin is recommended to a patient with suspected ACS, if pain not alleviates after taking nitroglycerin is experienced 5 minutes after the primary portion, the patient should contact crisis administrations. If help is experienced inside 5 minutes of the principal nitroglycerin portion, repeated dosages can be allowed at regular intervals for a limit of 3 portions aggregate. If at that point, the manifestations have not yet completely settled, the patient, a relative, or a parental figure should contact crisis administrations. Diet assumes a significant job in the improvement of coronary vessel diseases Instruct post- myocardial dead tissue (MI) patients about the job of a low-cholesterol and low-salt eating regimen. (90)
  • 40. 33 A dietitian should see and assess all patients before releasing them from the clinic. Moreover, accentuation on exercise preparation ought to be made, because present proof exhibits that heart diseases recovery after MI results in lower rates of repetitive cardiovascular occasions. All patients ought to be instructed concerning the basic job of smoking in the improvement of CAD. Smoking discontinuance classes ought to be offered to enable patients to abstain from smoking after their MI. (91)
  • 41. 34 Chapter: 3 MATERIALS AND METHODS Study Design: Cross-Sectional Analytical Study Sample Setting: The study was conducted at Cardiology Department, Dr. Ruth Pfau Civil Hospital, Karachi.From 15.3.2019 to 15.3.2020. Sampling Technique: Non-Probability Purposive Sampling Sample Size: Using open Epi 6, taking prevalence of 14% v/s 41% the highest in different studies for risk factors, with a margin of error of 5%, the sample size will be 126 (63 in each group). Inclusion Criteria: • According to WHO criteria, all patients of recent MI of aged 25years and above of either sex. • Given consent to participate in the study. • Exclusion criteria: • Patients having any chronic co-morbid diseases. (PAH, CLD, Malignancy, etc) • Patients already CABG, Most CABG Patients would be having prior MI
  • 42. 35 • Patients with congenital heart diseases (ASD, VSD, PDA, TOF) and valvular heart diseases (Mitral, Tricuspid, pulmonary, and Aortic). DATA COLLECTION PROCEDURE: After getting approval from the scientific committee and IRB of DUHS, the study was conducted on patients suffering from recent MI. Written consent was taken from all the participants for inclusion in the study. An equal number of patients i.e.,126 were taken for the study. The admitted patients <35 years of age were placed in one group and the patients of >35 years were placed in another group. A research proforma was developed for this study after pretest and validation were used to collect the data from all the patients. The questionnaire had questions regarding socio-demographic aspects with ST-elevation and risk factors like gender, family history of myocardial infarction, hypertension, diabetics’ smoking, and lifestyle. These factors with ECG and lab tests were compared to determine statistical significance in two groups. (All tests and ECG are free at Civil Hospital Karachi) DATA ANALYSIS PROCEDURE: For data analysis, SPSS v25.0 was used. For qualitative data, frequencies along with percentages were calculated. For quantitative data, mean with standard deviation were measured. To determine any statistical difference, the Chi-square test was implemented in two groups. The significance was done based on p<0.05. All these results were presented in the shape of tables and graphs. Confounding factors and biases were controlled by strict follow-up of inclusion and exclusion criteria of the study.
  • 43. 36 Chapter: 4 RESULTS This study was conducted to compare the risk factors of young adults with older adults with recent myocardial infarctions. So, data collected and analyzed the results were as follows The mean deviation age of young adults was 29.87 with a standard ± deviation of 5.85 and the mean age of older adults was 58.58 with a standard deviation ± 10.13 in our study. When we check statistical significance between these two groups the p-value showed a significant difference as the p-value was less than the level of significance (p=<0.001). The gender-wise distribution between groups showed differences as in young adults 44 out of 63(69.8%) were male and 19 out of 63(30.2%) were female. Similarly, in the older adults’ group, 48 out of 63(76.2%) were male and 15 out of 63(23.8%) were female (p=<0.422). These also showed that males in both groups were more than females. The smoking was more common in the young age group. 40 young patients were smokers out of 63 (63.5%) as compared to the old adults group 20 patients were smokers out of 63 (31.7%). The p-value also showed a significant difference in these two groups (p= < 0.001). The diabetes risk factor was also more in the older adults’ group 53 out of 63 Patients (82.5%) than young adults group in which 8 patients out of 63 (12.7%) were diabetics. P-value also showed a significant difference in these groups (p=< 0.001). The hypertension risk factor was more common in the older adults’ group 62 patients out of 63 (98.4%) and low in the young adults’ group 10 out of 63 (15.9%) were hypertensive. Chi- square results also showed similar results (p=< 0.001).
  • 44. 37 The family history of IHD was more common in the young adults’ group 36 patients out of 63(57.1%) and less common in the older adults’ group 8 patients out of 63 (12.7%). Chi squares results showed a significant difference in both groups (p<=0.001). The sedentary lifestyle was more common in the older adults’ group 45 patients out of 63 (71.4%) and less in the young adults’ group 7 out of 63 (11.1%). Results showed significant differences in both groups (p=< 0.001). Obesity was also common in the older adults’ group 35 patients out of 63 (55.6%) than young adult group 10 out of 63 (15.9%). The older adults’ group is a statistically significant difference from young adults’ groups (p=< 0.001). Dyslipidemia was also more in the older adults’ group 52 patients out of 63 were (82.5%) and less in the young adults’ group 20 out of 63 (31.7%). Results showed a significant difference in both groups (p=< 0.001). Substance abuse use was more commonly seen in younger adult’s group compared to older adults’ group. Substance abuse user younger adults were(84% v/s 58% older age group) with or without smoking. In substance abuse material alcohol taken by the younger patients were 5 out of 63(7.93%) while 15 patients(23.80%) intake alcohol along with smoking while, in older group 13 out of 63(20.63%) taking only alcohol, while 2 patients(3.17%) take alcohol along with smoking, cocaine taking by the younger group were 3 out of 63(4.8%) along with smoking charas taking more commonly by the younger group were 10 out of 63(15.9%) and the older group were 7 out of 63(11.1%) in both groups all charas taker were smokers, only Gutka / Betel nut chewing by young’s group were 12 out of 63(19.04%) and along with smoking were 8(12.69) and older groups who chewing were 12 out of 63 (19.04%) and 3 patients(4.76%) uses both Gutka/Betel nut along with smoking overall P-value of 0.999 between two groups.
  • 45. 38 In young adults, the mean Deviation of blood urea was 28.11 mg/dl ± 11.72mg/dl Std Deviation and in older adults, the mean Deviation of blood urea was 54.53 mg/dl ± 9.03 Std Deviation. When we checked for statistical significance the p-value showed that there is a significant difference between the two groups as the p-value was less than the level of significance (p=0.001). Blood urea value is more in the older adults’ group. The mean Deviation of serum creatinine in young adults was 1.10 ± 0.11 mg/dl Std Deviation and in the older adults’ group, the mean Deviation of creatinine was 1.09 ± 0.10 mg/dl Std Deviation. When checked statistical difference between these two groups, the p-value is greater than the level of significance which showed no significant difference (p=< 0.736). The mean Deviation of total cholesterol in young adults was 164.81 ± 21.44mg/dl Std Deviation and in the older adults group mean Deviation was 212.68 ± 20.25 mg/dl Std Deviation. The p-value showed a significant difference in both groups (p=< 0.001). Young adults had normal range values while older adults had high cholesterol. The level of TG was more in older adults’ groups and less in young adults’ groups. The mean Deviation of young adults was 121.63 ± 45.78mg/dl Std Deviation and the mean Deviation of older adults was 223.98±40.38 mg/dl Std Deviation. When the difference was checked statistically the p-value showed a significant difference between these two groups. (p= < 0.001). The value of LDL is also a significant difference in both groups as the mean Deviation of LDL in young adults was 117.10±27.91 mg/dl Std Deviation and in older adults mean Deviation was 178.19±33.19 mg/dl Std Deviation. The value of p was also less than the level of significance (p= < 0.001).
  • 46. 39 The mean and total Deviation of HDL in the young adults’ group was 55.52±12.34 with standard deviation and the mean Deviation of HDL in older adults was 30.43 ± 8.31with standard deviation. The value of HDL was more in the younger adults’ group than the older group. The p-value was also less than the level of significance (p= < 0.001). At the end of the results, it was seen that all risk factors of myocardial infarction in the older adults’ group were more positive than young adults’ groups. Older people had more chance of myocardial infarction as they had more risk factors.
  • 47. 40 Table-I: Comparison of age between groups Variable Young Adults Older Adults p-value Mean + SD Mean + SD Age 29.87 + 5.85 58.58 + 10.13 < 0.001 Figure-1: Graphical presentation of gender
  • 48. 41 Table-II: Comparison of smoking distribution between groups Smoking Groups Total p-value Young Adults Older Adults Yes 40 20 60 < 0.001 63.5% 31.7% 47.6% No 23 43 66 36.5% 68.3% 52.4% Total 63 63 126 100.0% 100.0% 100.0% Table-III: Comparison of diabetes distribution between groups Diabetes Groups Total p-value Young Adults Older Adults Yes 8 52 60 < 0.001 12.7% 82.5% 47.6% No 55 11 66 87.3% 17.5% 52.4% Total 63 63 126 100.0% 100.0% 100.0% Table-IV: Comparison of hypertension distribution between groups Hypertension Groups Total p-value Young Adults Older Adults Yes 10 62 72 < 0.001 15.9% 98.4% 57.1% No 53 1 54 84.1% 1.6% 42.9% Total 63 63 126 100.0% 100.0% 100.0%
  • 49. 42 Table-V: Comparison of family history of IHD distribution between groups Family History of IHD Groups Total p-value Young Adults Older Adults Yes 36 8 44 < 0.001 57.1% 12.7% 34.9% No 27 55 82 42.9% 87.3% 65.1% Total 63 63 126 100.0% 100.0% 100.0% Table-VI: Comparison of sedentary lifestyle distribution between groups Sedentary Lifestyle Groups Total p-value Young Adults Older Adults Yes 7 45 52 <0.001 11.1% 71.4% 41.3% No 56 18 74 88.9% 28.6% 58.7% Total 63 63 126 100.0% 100.0% 100.0% Table-VII: Comparison of obesity distribution between groups Obesity Groups Total p-value Young Adults Older Adults Yes 10 35 45 < 0.001 15.9% 55.6% 35.7% No 53 28 81 84.1% 44.4% 64.3% Total 63 63 126 100.0% 100.0% 100.0%
  • 50. 43 Table-VIII: Comparison of dyslipidemia distribution between groups Dyslipidaemia Groups Total p-value Young Adults Older Adults Yes 20 52 55 < 0.001 31.7% 82.5% 43.7% No 43 11 71 68.3% 17.5% 56.3% Total 63 63 126 100.0% 100.0% 100.0% Table-IX: Comparison of substance abuse distribution between groups Substance Abuse Groups Total p-value Young Adults Older Adults No Substance Abuse 10 26 36 0.999 15.87% 41.26% 28.57% Only Alcohol 5 13 18 7.93% 20.63% 14.28% Alcohol + Smoker 15 2 17 23.80% 3.17% 13.49% Cocaine + Smoker 3 0 3 4.76% 0.0% 2.38% Chars + Smoker 10 7 17 15.87% 11.11% 13.49% Only Gutka/Betel Nut 12 12 24 19.4% 19.4% 19.4% Gutka/Betel nut + Smoker 8 3 11 12.69% 4.76% 8.73% Total 63 63 126 100.0% 100.0% 100.0% Use of Substance Abuse with smoking in Young Group is 84 % in my data Use of substance abuse with smoking in older group is 58 % in my data
  • 51. 44 Comparison of laboratory investigation between groups. Table-X: Comparison of blood urea distribution between groups Variable Young Adults Old Adults P-value Mean + SD Mean + SD Blood Urea(mg/dl) 28.11+ 11.72 54.53+ 9.03 <0.001 Table-XI: Comparison of serum creatinine distribution between groups Variable Young Adults Old Adults P-value Mean + SD Mean + SD Serum Creatinine (mg/dl) 1.10 + 0.11 1.09 + 0.10 0.736
  • 52. 45 Table-XII: Comparison of lipid profile distribution between group Variable Young Adults Old Adults P-value Mean + SD Mean + SD Cholesterol(mg/dl) 164.81 + 21.44 212.68 + 20.25 < 0.001 TG (mg/dl) 121.63 + 45.78 223.98 + 40.38 < 0.001 LDL (mg/dl) 137.10 + 27.91 198.19 + 33.19 < 0.001 HDL (mg/dl) 55.52 + 12.34 30.43 + 8.31 < 0.001
  • 53. 46 Chapter: 5 DISCUSSION MI is an old age disease however it is also seen in young age adults, but the young age group has fewer conventional risk factors. Same in my study the young adults have fewer conventional risk factors of myocardial infarction than older adult groups. below 40 years of age cholesterol accumulated in less amount within arteries resulting in less chances of coronary atherosclerosis. Hypertension and diabetes are also less likely to occur at a young age(Table: III and IV) . However, young groups have different risk factors and complications as compared to old age patients. That may be the reason why CAD is becoming prevalent in our part of world. Myocardial infarction is a very serious disease for a patient and also for its family. If a patient at a young age gets this disease then it carries significant morbidity, psychological effects, and financial constraints for the patient and his family, and this way patient may loss their life years. In my study, I took cut off age less than 35 years or equal to 35 in the young adults’ group of recent M.I. from the study of Faisal et al (18). I had take two groups one was below 35 years or equal to 35 years called young adults’ groups and the second is above 35 years called older adults’ groups. For both groups, 63 patients were selected. More conventional risk factors were present in older adults’ group. I studied both the groups of patients with respect to the gender distribution, presence of hypertension, and diabetes mellitus ,F.H. ,smoking ,substance abuse etc In the young adult group, 69.8% were male patients and 30.2% were female patients. In past, there were very few studies that compare gender distributions also in these types of studies. Similarly, in older adults’ groups, 76.2% were male and 23.8% were female. The gender distribution is significant in our study. The male ratio was more than female in both groups.
  • 54. 47 Same in other studies Abdus Samad et al(92) and Faisal et al(18) showed male ratio was more than the female ratio. It was determined in my study that dyslipidemia, hypertension, and diabetes were the predominant risk factors in old age patients of M.I. Similar to it, in different study(15) In a studies (6,9) in young age patients of MI, the risk factors like family history of CAD, smoking, and substance abuse was found much higher. Same in my study the ratio of risk factors like family history of CAD, smoking with substance abuse is higher (57.1%, 84% respectively) compared to old age patients (12.7%, 58% respectively) which were alarming finding. A study (67) done by Dhruv Mohtta et al showed that patients who developed the atherosclerotic cardiovascular disease are those who use more substance abuse materials like tobacco 62.9%, alcohol 31.8%, cocaine 12.9%, and cannabis 12.5% in his study this shows that recreational substances users had increase chances of ASCVD. Similarly in my study substance abuse materials like smoking, alcohol, cocaine, charas, gutka/betel nut takers were more commonly seen in young adults (84%), compared to the older adults’ group (58% respectively). All these substance abuse materials cause atherosclerosis, coronary spasm, atherogenesis, thrombosis, increases fibrinogen level, LDLC, triglycerides, decreases HDLC, and also increase C-reactive protein, increases heart rate and SBP which causes myocardial oxygen supply-demand mismatch all of these effects contribute to causing Myocardial Infarction in young people. It was determined in a study(14) that smoking, CVD family history, and male gender were the predominating risk factors in young age patients of MI, whereas hypertension, and diabetes were the predominating risk factors in old age patients of MI.(15)
  • 55. 48 It was determined in a study done by Faisal(18) et al that smoking (76.6%), family history of CVD (33.3%), and male gender (90%) were dominating risk factors in young age patients of M.I. same in my study it showed that smoking(63%), family history CVD(57%) and male gender(70%) were more prevalent in young age patients of recent M.I .than older age patients. Another big AAUS study done in Pakistan by Abdus Samad(92) et al showed that male gender (68.1%) hypertension (55.2%) smoking (52%) and diabetes (37.8%) were major risk factors. My study shows that smoking with substance abuse(84%) was the main risk factor in the young adult group and risk factors hypertension(98%), diabetes(82%), and dyslipidemia(82%) were more prevalent in the old age group patients of recent M.I. Similar to it, in different studies,(6,9,14,16) smoking (58.7% -76.7%) was the most common risk factor in young age patients as compared to old age group patients with MI (31.7%-59.4%). Almost similarly in my study smoking was (63.5% in young v/s 31.7 in older age group patients) another study,(17) showed relative risks in the young age population were hypertension, CAD family history, and dyslipidemia. One study by A. LIUQAT PMC 6284873 reported that dyslipidemia was high in the younger population (49.7% v/s 38.85), whereas other study,(8) reported it is higher in old age patients (43.3% v/s 49.5% and 20.0% v/s 29.0%). My study, shows that diabetes was less common in young patients (12.7% in young v/s 82.5 % in older group) and similarly obesity was also less common in young patients (15.9% in young v/s 55.6 % in older group). Other studies(20) also shown that diabetes (3.3- 5% in young v/s 30- 38.6% in older) and obesity (6.6% in young vs. 21.4% in older) as fewer risk factors in the young age population. According to a study(21), there was a significant gender difference for CAD in the short and long-term clinical outcomes of young patients with MI. Therefore, preventive strategies should be taken to reduce the gender-different risk factor in young adults. (Ref. Epidemiol community health 2016 Nov 70(11)1057-1064).
  • 56. 49 My study mainly focused is to compare the risk factors of myocardial infarction in young and older adults. The level of blood urea, serum creatinine, total cholesterol, and TG were high in older adults’ groups than young adults’ group(8) . But HDL was high in young adults. These values are significantly different between these two groups. LIMITATIONS OF STUDY • Single-center study • Selection bias • Limited sample size RECOMMENDATIONS • Multi-center study. • The probability Sampling Technique will be helpful for the generalization of results to the larger population. In the future Community should be educated about the harmful effects of smoking and substance abuse materials’ also control other modifiable risk factors along with routine screening which would help in preventing coronary artery disease in them, who belong to the highly productive group in the community.
  • 57. 50 CONCLUSION I concluded in this study that the risk factors like diabetes, hypertension, obesity, dyslipidemia, and sedentary lifestyle were more prevalent in the older adults group than young adults group, and Smoking, Family history of IHD and Substance abuse materials like alcohol, charas, cocaine, gutka/betel nut were more common risk factors in young adults that causing M.I. Hence, we recommend at the national level to stop smoking, do physical activities, chose healthy and better lifestyle to promote good health in society and according to my study 84% of young patients are using some form of substance abuse. Hence I recommend to our policymakers to introduce and implement some expend kinds of law and enforce them properly to protect our young population from potentially deadly IHD disease. spread awareness through electronic, print media and arrange seminars on how to avoid substance abuse materials in young peoples. There is also a need for screening of blood sugar, blood pressure, dyslipidemia, and control of these atherosclerotic risk factors to reduce CVD risk in the population.
  • 58. 51 References 1. Sai Krishna Patibandla; Kush Gupta; Khalid Alsayouri Cardiac Enzymes used in the diagnosis of acute myocardial ischemia StatPearls Publishing; 2021 Jan.2020 Aug 14. 2. James Beckerman, What's Causing My Chest Pain? Reviewed by on March 08, 2021 3. Scheen AJ. [From atherosclerosis to atherothrombosis: from a silent chronic pathology to an acute critical event]. Rev Med Liege. 2018 May;73(5-6):224-228. 4. Choudhury L, Marsh JD, Myocardial infarction in young patients, The American Journal of Medicine 1999;107(3):254-61, 5. Gupta M, Singh N, Verma S. South Asians, and cardiovascular risk: what clinicians should know? Circulation. 2006; 113:924–29 6. Ahmed I, Qaiser S, Myocardial Infarction under age 40: Risk factors and Coronary Arteriographic findings. Annals of King Edward Medical University, 2016; 9(4) 7. Siddique MA, Shrestha P, Salman M, Haque KMHSS, Ahmed MK, Sultan MAU, et al, Age-related differences of risk profile and angiographic findings in patients with coronary heart disease, BSMMU J, 2010;3(1): 13-7Perviz Asaria, Prof Paul Elliott, Margaret Douglass, Meng, Ziad Obermeyer, Michael Soljak Azeem Majeed, et al Published: February 28, 2017 8. Francisco J. Félix-Redondo,* Maria Grau, and Daniel Fernández-Bergés Cholesterol and Cardiovascular Disease in the Elderly. Facts and Gaps, Aging Dis. 2013 Jun; 4(3): 154– 169. Published online 2013 Mar 1. 9. Kaur R, Das R, Ahluwalia J, Kumar RM, Talwar KK, Genetic polymorphisms, Biochemical Factors, and Conventional Risk Factors in Young and Elderly North Indian Patients with Acute Myocardial Infarction,2014;22(2):178-83
  • 59. 52 10. Sharma A, Kumar R, Ashotra S, Thakur S, comparative evaluation of clinical profile, risk factors and outcome of acute myocardial infarction in elderly and non-elderly patients, Heart India, 2016;4:96-9 11. Jing M, Gao F, Chen Q, Carvalho LPD, Sim LL, Koh TH, et al, Comparison of Long- Term Mortality of Patients Aged ≤40 Versus >40 Years With Acute Myocardial Infarction The AmericanJournalofCardiology2016;118(3):319-25, 12. Amann U, Kirchberger I, Heier M, Thilo C, Kuch B, Peter A, et al, Predictors of non- invasive therapy and 28-day-case fatality in elderly compared to younger patients with acute myocardial infarction: an observational study from the MONICA/KORA Myocardial Infarction; Registry BMC; Cardiovascular; Disorders BMC 2016;16:151 13. Hosseini SK, Soleimani A, Karimi AA, Sadeghian S, Arabian S, Abbasi SH, et al, Clinical features, management and in-hospital outcome of ST-elevation myocardial infarction (STEMI) in young adults under 40 years of age, International Journal of cardiopulmonary medicine and rehabilitation, Monaldi Arch Chest Dis. 2009 Jun;72(2):71-6. 14. Das PK, Kamal SM, Murshed M, Acute myocardial infarction in young Bangladeshis: A comparison with older patients, Journal of Indian College of Cardiology, 2015;5(1): 20-4 15. Shan Lu, Ming-Yang Bao, Shu-Mei Miao, Xin Zhang, Qing-Qing Jia, Shen-Qi Jing, Tao Shan, Xiao-Hong Wu, and Yun Liu Prevalence of hypertension, diabetes, and dyslipidemia, and their additive effects on myocardial infarction corresponding author 2019 Sep; 7(18): 436 16. Pathak V, Ruhela M, Chadha N, Jain S, Risk factors angiographic characterization and prognosis in young adults presenting with the acute coronary syndrome at a tertiary care center in north India, BMR Medicine, 2016;1(1):1-5. 17. Srikanth Yandrapalli, Christopher Nabors, Abhishek Goyal, Wilbert S Aronow, William H Frishman Modifiable Risk Factors in Young Adults With First Myocardial Infarction 2019 Feb 12;73(5):573-584 18. Faisal AWK, Ayub M, Waseem T, Shahzad R, khan AT, Hasnain SS, Risk factors in young patients of acute myocardial infarction, Ayub Med Coll Abbottabad, 2011;23 (3): 10-3
  • 60. 53 19. Adrian Rosada, Ursula Kassner, Felix Weidemann, Maximilian König, Nikolaus Buchmann,Elisabeth Steinhagen-Thiessen, and Dominik Spira Hyperlipidemias in elderly patients Published online 2020 May 14. 20. Shilpa N. Bhupathiraju1 and Frank B. Hu Epidemiology of Obesity and Diabetes and Their Cardiovascular Disease Circ Res. 2016 May 27; 118(11): 1723–1735. 21. Cho KI, Shin E, Ann SH, Garg, Her AY, Kim JS, et al Gender differences in risk factors and clinical outcomes in young patients with acute myocardial infarction, J Epidemiol Community Health Published Online 2016. 22. David L Coven, Eric H Yang, What is the spectrum of clinical presentations of the acute coronary syndrome (ACS)? Updated: Sep 30, 2020 23. Hina Akbar; Christopher Foth; Rehan A. Kahloon; Steven Mountfort Acute ST-Elevation Myocardial Infarction. Last Update: August 8, 2020 24. Eugene Braunwald and David A. Morrow Unstable Angina Published 18 Jun 2013 Circulation. 2013;127:2452–2457 25. Oren J. Mechanic; Michael Gavin; Shamai A Acute Myocardial Infarction. Grossman Last Update: March 9, 2021 26. Hyun Ju Yoon, Kye Hun Kim and Jong Yoon Kim Impaired Diastolic Recovery after Acute Myocardial Infarction as a Predictor of Adverse Events J Cardiovasc Ultrasound. 2015 Sep; 23(3): 150–157. Published online 2015 Sep 24. 27. Amit Kumar, and Christopher P. Cannon, Acute Coronary Syndromes: Diagnosis and Management 2009 Nov; 84(11): 1021–1036. 28. Rathore SS, Gersh BJ, Weinfurt KP, Oetgen WJ, Schulman KA, Solomon AJ. The role of reperfusion therapy in paced patients with acute myocardial infarction. Am Heart J. 2001 Sep. 142(3):516-9 29. Suzanne Falck and Linda Hepler Do I Have Prediabetes or Diabetes? Guide to Diagnosis and Management Updated on June 29, 2018
  • 61. 54 30. Sungha Park Ideal Target Blood Pressure in Hypertension Korean Circ J. 2019 Nov; 49(11): 1002–1009. Published online 2019 Sep 20 31. Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Bernard R. Chaitman, Jeroen J. Bax, David A. Morrow, Harvey D Fourth Universal Definition of Myocardial Infarction (2018). White, Originally published24 Aug 2018 Circulation. 2018;138:e618–e651 32. Falk E, Nakano M, Bentzon JF, Finn AV, Virmani R. Update on acute coronary syndromes: the pathologists’ view.Eur Heart J. 2013; 34:719–728 33. Bugiardini R, Manfrini O, Pizzi C, Fontana F, Morgagni G. Endothelial function predicts the future development of coronary artery disease: a study on women with chest pain and normal angiograms, Circulation, 2004, vol. 109 (pg. 2518-2523) 34. Wayne L. Miller, Kirk N. Garratt, Mary F. Burritt, Guy S. ReederAllan S. Jaffe Timing of Peak Troponin T and Creatine Kinase-MB Elevations After Percutaneous Coronary Intervention European Heart Journal, Volume 27, Issue 9, May 2006 35. A Maziar Zafari, Eric H Yang, What is an acute coronary syndrome (ACS) Updated: May 07, 2019 36. O'Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Jan 29. 127 (4):e362-425. 37. Peter J. Sabia, ., Eric R. Powers, Michael Ragosta, Ian J. Sarembock,., Ch.B., M Lawrence R. Burwell et al December 24, 1992, recent myocardial infarction N Engl J Med 1992; 327:1825-1831 38. Burchfield JS, Xie M, Hill JA. Pathological ventricular remodeling: mechanisms: part 1 of 2. Circulation. 2013 Jul 23. 128 (4):388-400.
  • 62. 55 39. Marban E. Myocardial stunning and hibernation. The physiology behind the colloquialisms. Circulation. 1991 Feb. 83 (2):681-8. 40. McGill HC Jr, McMahan CA, Zieske AW, et al. Associations of coronary heart disease risk factors with the intermediate lesion of atherosclerosis in youth. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb Vasc Biol. 2000 Aug. 20 (8):1998-2004 41. Kolodgie FD, Virmani R, Burke AP, et al. Pathologic assessment of the vulnerable human coronary plaque. Heart. 2004 Dec. 90 (12):1385-91. 42. Soares AAS, Tavoni TM, de Faria EC, Remaley AT, Maranhao RC, Sposito AC, et al. HDL acceptor capacities for cholesterol efflux from macrophages and lipid transfer are both acutely reduced after myocardial infarction. Clin Chim Acta. 2018 Mar. 478:51-6. 43. Holmes MV, Millwood IY, Kartsonaki C, et al, for the China Kadoorie Biobank Collaborative Group. Lipids, lipoproteins, and metabolites and risk of myocardial infarction and stroke. J Am Coll Cardiol. 2018 Feb 13. 71 (6):620-32 44. Yusuf S, Hawken S, Ounpuu S, et al, for the INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): a case-control study. Lancet. 2004 Sep 11-17. 364 (9438):937-52. 45. Mehta Saif Rathore Martha JRadford, YongfeiWangYunWangHarlan MKrumholz Acute myocardial infarction in the elderly differences by age Rajendra September 2001 46. Ali Yazdanyar, Anne B. Newman, The Burden of Cardiovascular Disease in the Elderly: Morbidity, Mortality, and Costs Med. 2009 Nov; 25(4): 563–vii. 47. Throughout life, heart attacks are twice as common in men than women Published: November 2016 https://www.health.harvard.edu/heart-health/throughout-life-heart- attacks-are-twice-as-common-in-men-than-women
  • 63. 56 48. Zhang H, Sun S, Tong L, Li R, Cao XH, Zhang BH, et al. Effect of cigarette smoking on clinical outcomes of hospitalized Chinese male smokers with acute myocardial infarction. Chin Med J (Engl) 2010;123:2807–11. 49. S Tonstad and J L Cowan C-reactive protein as a predictor of disease in smokers 2009 Nov; 63(11): 1634–1641. 50. Rockville, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General.Centers for Disease Control and Prevention (US); National Center for Chronic Disease Prevention and Health Promotion (US); Office on Smoking and Health (US). Atlanta (GA): Centers for Disease Control and Prevention (US); 2010 51. Thomas R. Einarson, Annabel Acs, Craig Ludwig & Ulrik H. Panton Prevalence of cardiovascular disease in type 2 diabetes: a systematic literature review of scientific evidence from across the world in 2007–2017 Published: 08 June 2018 52. Tomas Kovarnik, Zhi Chen, Gary S. Mintz, Andreas Wahle, Kristyna Bayerova, Ales Kral, Martin Chval, Karel Kopriva, John Lopez, et al, Plaque volume and plaque risk profile in diabetic vs. non-diabetic patients undergoing lipid-lowering therapy: a study based on 3D intravascular ultrasound and virtual histology 2017; 16: 156. Published online 2017 Dec 7 53. David J. Schneider, and Burton E. Sobel, Diabetes and Thrombosis 54. Mirjana Cubrilo-Turek, Hypertension and Coronary Heart Disease EJIFCC. 2003 Jul; 14(2): 67–73. Published online 2003 Jul 3. 55. Oladipupo Olafiranye, Ferdinand Zizi, Perry Brimah, Girardin Jean-Louis, Amgad N. Makaryus Samy McFarlane, and Gbenga Ogedegbe Management of Hypertension among Patients with Coronary Heart Disease 6 2011; 2011: 653903. Published online 2011 Jul 13.
  • 64. 57 56. Mattis Flyvholm Ranthe, Jonathan Aavang Petersen, Henning Bundgaard, Jan Wohlfahrt, Mads Melbye, and Heather A. Boyd A Detailed Family History of Myocardial Infarction and Risk of Myocardial Infarction – A Nationwide Cohort Study 2015; 10(5): e0125896. Published online 2015 May 26 57. Dr. Trine Moholdt Trondheim, Norway Sedentary lifestyle for 20 years linked to doubled mortality risk compared to being active 31 Aug 58. Danyang Tian 1 and Jinqi Meng Exercise for Prevention and Relief of Cardiovascular Disease corresponding author 22019; 2019: 3756750. Published online 2019 Apr 9 59. Mashhad Hedayatnia, Zahra Asadi, Reza Zare-Feyzabadi, Mahdiyeh Yaghooti-Khorasani Dyslipidemia, and cardiovascular disease risk among the MASHAD study population Published: 16 March 2020 60. Cohort Norway Grace M Egeland 1, Jannicke England 2, Gerhard Sulo 2, Ottar Nygård 3, Marta Ebbing 4, Grethe S Tell non-fasting triglycerides to predict incident acute myocardial infarction among those with favorable HDL-cholesterol 5 2015 Jul;22(7):872- 81 61. The incidence of acute myocardial infarction about overweight and obesity: a meta- analysis 2014 Oct 27; 10(5): 855–862. Published online 2014 Oct 23 62. Qinqin Cao, Shui Yu, Wenji Xiong, Yuewei Lin, Huimin Li, Jinwei Li, and Feng Li, Waist-hip ratio as a predictor of myocardial infarction risk 2018 Jul; 97(30): e11639. Published online 2018 Jul 27. 63. Susanna C. Larsson, Stephen Burgess, Amy M. Mason, Karl Michaëlsson Alcohol Consumption and Cardiovascular Disease Originally published 5 May 2020 64. Sung Tae Kim and Taehwan Park Acute and Chronic Effects of Cocaine on Cardiovascular Health Feb; 20(3): 584. Published online 2019 Jan 29.
  • 65. 58 65. Mary Rodriguez Ziccardi; Jason D. Hatcher Prinzmetal Angina. Last Update: August 16, 2020. 66. Muhammad Shahzeb Khan, Faizan Imran Bawany, Muhammad Umer Ahmed, Mehwish Hussain, Asadullah Khan & Muhammad Nawaz Lashari Betel Nut Usage Is a Major Risk Factor for Coronary Artery Disease Global Journal of Health Science; Vol. 6, No. 2; 2014 67. Dhruv Mehta, David Ramsey, Chayakrit Krittanawong, Mahmoud Al Rifa Recreational substance use among patients with premature atherosclerotic cardiovascular disease 68. Concheiro-Guisan A, Sousa-Rouco C, Fernandez-Santamarina I, Gonzalez-Carrero J. Intrauterine myocardial infarction: unsuspected diagnosis in the delivery room. Fetal Pediatr Pathol. 2006 Jul-Aug. 25(4):179-84. 69. Muhammad Ajmal Malik,1 Shahzad Alam Khan,2 Sohail Safdar,3 and Ijaz-Ul-Haque Taseer4 Chest Pain as a presenting complaint in patients with acute myocardial infarction (AMI) 2013 Apr; 29(2): 565–568 70. A Maziar Zafari ,Eric H Yang, What is the role of heart rate in the evaluation of symptoms of myocardial infarction (MI, heart attack)? Updated: May 07, 2019 71. Tomas Ondrus, Jan Kanovsky, Tomas Novotny, Irena Andrsova, Jindrich Spinar, and Petr Kala, Right ventricular myocardial infarction: From pathophysiology to prognosis 2013 Winter; 18(1): 27–30. 72. Daanish Aijaz Chhapra,∗ Sanket Kaushik Mahajan, and Sanjay Tukaram Thorat A study of the clinical profile of right ventricular infarction in context to inferior wall myocardial infarction in a tertiary care center 2013 Sep; 4(3): 170–176. Published online 2013 Nov 13. 73. Walker HK, Hall WD, Hurst JW, Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition.: Butterworths; 1990.
  • 66. 59 74. Oren J. Mechanic; Michael Gavin; Shamai A Acute Myocardial Infarction. Grossman. Last Update: March 9, 2021. 75. A Maziar Zafari Eric H Yang, What are the characteristics of typical chest pain in acute myocardial infarction (MI, heart attack)? Updated: May 07, 2019 76. National Center for Chronic Disease Prevention and Health Promotion, Division for Heart Disease and Stroke Prevention Page last reviewed: September 8, 2020, Heart Disease Facts https://cutt.ly/Wc4LTyN 77. Mark A. Williams, Jerome L. Fleg, Philip A. Ades, Bernard R. Chaitman Secondary Prevention of Coronary Heart Disease in the Elderly (With Emphasis on Patients ≥75 Years of Age) Originally published9 Apr 2002 78. Chronic Kidney Disease in the United States Centers for Disease Control and Prevention Page last reviewed: March 4, 2021, https://cutt.ly/1c4ZU5C 79. Kamal (Komo) Gursahani and Barry E Brenner Cardiac Markers Updated: Jul 30, 2021 80. B. B. L. M. IJkema, J. J. R. M. Bonnier, D. Schoors, M. J. Schalij and C. A. Swenne Role of the ECG in initial acute coronary syndrome triage: primary PCI regardless presence of ST elevation or of non-ST elevation Neth Heart J. 2014 Nov; 22(11): 484– 490. Published online 2014 Sep 9.1968 81. Azin Alizadehasl , Anita Sadeghpour and Mohaddeseh Behjati The role of echocardiography in acute myocardial infarction Indian Heart J. 2017 Jul-Aug; 69(4): 563. Published online 2017 Jun 30. 82. O'Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Jan 29. 127 (4):e362-425.
  • 67. 60 83. Wanda L Rivera-Bou, Erik D Schraga, Thrombolytic Therapy Author: Updated: Dec 31, 2017. 84. Lloyd-Jones D, Adams RJ, Brown TM, et al, for the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Executive summary: heart disease and stroke statistics--2010 update: a report from the American Heart Association. Circulation. 2010 Feb 23. 121 (7):948-54 85. Levi F, Lucchini F, Negri E, La Vecchia C. Trends in mortality from cardiovascular and cerebrovascular diseases in Europe and other areas of the world. Heart. 2002 Aug. 88 (2):119-24. 86. International Journal of Cardiology Volume 291 http://gestyy.com/ey4E6R 87. Critchley J, Liu J, Zhao D, Wei W, Capewell S. Explaining the increase in coronary heart disease mortality in Beijing between 1984 and 1999. Circulation. 2004 Sep 7. 110 (10):1236-44. 88. Yusuf S, Hawken S, Ounpuu S, et al, for the INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): a case-control study. Lancet. 2004 Sep 11-17. 364 (9438):937-52 89. Sibu P Saha, Deepak K Bhalla, Thomas F Whayne, Jr, and CG Gairola Cigarette smoke and adverse health effects: An overview of research trends and future needs Int J Angiol. 2007 Autumn; 16(3): 77–83. 90. Smith SC Jr, Allen J, Blair SN, et al, AHA/ACC guidelines for secondary prevention for patients with coronary and another atherosclerotic vascular disease: 2006 update: endorsed by the National Heart, Lung, and Blood Institute. Circulation. 2006 May 16. 113 (19):2363-72
  • 68. 61 91. Nancy A Rigotti, James K Stoller, D Aronson, Lisa Kunins, Patient education: Quitting smoking Author: Published: 1-Jan-2021 92. Maqbool H. Jafary, Abdus Samad, Mohammad Ishaq, Shaukat Ali Jawaid, Mansoor Ahmad, Ejaz Ahmad Vohra et al PROFILE OF ACUTE MYOCARDIAL INFARCTION (AMI) IN PAKISTAN On behalf of AAUS Study. 93. Heather A. McGrane Minton, Kelly Thevenet-Morrison, and I. Diana Fernandez, Using Television-Viewing Hours and Total Hours Sitting as Interchangeable Measures of Sedentary Behavior Am J Lifestyle Med. 2019 Jan-Feb; 13(1): 98–105. Published online 2016 Nov 30
  • 69. 62