This document discusses ischaemic heart disease and angina pectoris. It defines IHD as a condition where there is inadequate blood supply and oxygen to the myocardium. Angina pectoris is defined as a clinical syndrome characterized by precordial discomfort due to myocardial ischemia, typically brought on by exertion and relieved by rest. The document covers the epidemiology, risk factors, pathophysiology, clinical manifestations, diagnosis and treatment of these conditions. It emphasizes that risk factor identification and modification are important for managing patients with known or suspected IHD.
IHD also known as coronary artery diseases is a condition in which there is inadequate supply of blood and oxygen to a portion of myocardium. Imbalance between myocardial oxygen supply and demand causes Angina, MI, Hear failure, and Arrhythmia
Angina pectoris is a medical condition resulting in chest pain or discomfort. Angina pectoris occurs when the heart is not getting enough blood supply. the pain related to angina is temporary, but if left untreated can make serious heart complications inevitable.
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Myocardial infarction (MI), commonly known as a heart attack. MI is a blockage of blood flow to the heart muscle. Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease.
Angina also known as angina pectoris is a medical condition characterized by chest pain usually left sided due to inadequate blood supply (ischemia) to the heart muscles due to obstruction (like presence of blood clot), narrowing or contraction (vasospasm) of the supplying coronary arteries.
IHD also known as coronary artery diseases is a condition in which there is inadequate supply of blood and oxygen to a portion of myocardium. Imbalance between myocardial oxygen supply and demand causes Angina, MI, Hear failure, and Arrhythmia
Angina pectoris is a medical condition resulting in chest pain or discomfort. Angina pectoris occurs when the heart is not getting enough blood supply. the pain related to angina is temporary, but if left untreated can make serious heart complications inevitable.
Study Material
Myocardial infarction (MI), commonly known as a heart attack. MI is a blockage of blood flow to the heart muscle. Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease.
Angina also known as angina pectoris is a medical condition characterized by chest pain usually left sided due to inadequate blood supply (ischemia) to the heart muscles due to obstruction (like presence of blood clot), narrowing or contraction (vasospasm) of the supplying coronary arteries.
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6. Common cause of myocardial
ischaemia is atherosclerotic
disease of epicardial coronary
artery.
That cause a regional
reduction in myocardial blood
flow and inadequate perfusion of
myocardium supplied by involved
coronary artery.
Also known as coronary artery
disease.
Chest pain is the cardinal
symptom of IHD due to CAD.
6
10. Definition
A clinical syndrome due to
myocardial ischaemia characterized
by precordial discomfort or
pressure, typically precipitated by
exertion and relieved by rest or
sub-lingual nitroglycerine.
Tightness or
squeezing sensation.
The pain radiate to
the neck, chin, or
down the left arm to
the elbow. Lasts 2-3
min .Crescendo -
decrescendo nature.
Literally means
“strangled chest “,
a severe pain that
usually
accompanies with
MI.
10
13. classification
class
New York heart
association
functional
classification
Specific activity
scale
I Symptoms occurs
with unusual
activity.
Minimal or no
functional
impairment.
Patients can
perform to
completion any
activity involving
or equal to 7
metabolic
equivalents
II
Symptoms occurs
with prolonged or
slightly more than
usual activity.
Mild functional
impairment.
Patients can
perform to
completion any
activity involving
or equal to 5
metabolic
equivalents but
cannot perform
to completion any
activity involving
or equal to 7
13
14. III
Symptoms occurs
with usual
activities of daily
living.
Moderate
functional
impairment.
Patients can
perform to
completion any
activity involving
or equal to 2
metabolic
equivalents but
cannot perform
to completion any
activity involving
or equal to 5
metabolic
equivalents.
IV
Symptoms occurs
at rest.
Severe functional
impairment.
Patients can
perform to
completion any
activity involving
or equal to 2
metabolic
equivalents .
14
15. Some other forms of angina…
15
Unstable angina
Characterized by a progressive increase
in anginal symptoms, new onset of rest
(angina decubitus) or nocturnal angina, or
onset of prolonged angina.
It is precipitated by an acute increase in
coronary obstruction due to rupture of the
fibrous plaque covering an atheroma with
consequent platelet adhesion.
Pain is more when compared to stable
angina.
16. 16
Variant angina
• Angina pectoris i.e.
usually secondary to
large vessel spasm.
• Characterized by
discomfort at rest
and by ST segment
elevation during the
attack.
• Have significant
obstruction of at
least one major
coronary artery.
Also known as
prinzmetal’s
angina.
18. 18
Epidemiology and
prevalence
Leading cause of death
, disability and incurs
world wide.
Major cause of death in
both developed and
developing countries.
Greater economic costs
than any other illness
in the developed
countries. Most
common in us 13
million.
6 million angina and
7 million MI.
In USA and Europe
more among low
income groups than
high income group.
Prevalence is more in
low and middle income
countries.
Predominant in male
and increase with age.
Annual incidence rate
of angina is 1.5%
depending on the age,
gender and risk factor
profile.
Angina is more in
women than in men.
Female to male ratio is
1.7:1.
Prevalence of 4.6
million in women and
3.3 million in men.
19. 19
High rate of STEMI (61%)
than high income countries
(15-25%).
Highest burden of acute
coronary syndrome in the
world.
Common risk factors include
smoking (40%), high BP
(38%), and diabetes (30%) .
The mean age the patient is
58 yrs.
53 % of lower middle class
and 20% were from poor
middle class.
In India 98 % receiving anti
platelet drugs.
51-61% receiving ACE
inhibitors or ARB.
57-54 % receiving lipid
lowering therapy .
20. 20
Mortality rate per 100,000, 382 for
men and 128 for women.
60 % death in men and 40 % death in
women . It occur before the age of
68 yrs.
CAD results in high economic
burden.
Prevalence of heart disease in rural
Kerala is 7%.
24. 24
Etiology and risk factors
When cardiac workload and
MVO2 demand exceed, the
ability of coronary arteries
to supply an adequate
amount of oxygenated blood
decrease.
Atherosclerosis ,
Coronary artery spasm,
rarely coronary artery
embolism.
Increased age, male sex,
family history of CAD,
smoking, diabetes mellitus,
HT.
Soft factors include stress,
anxious personality, obesity,
alcohol consumption.
causes
26. 26
Prime determinants
of myocardial
oxygen demand.
Heart rate,
Contractility, and Wall
stress .
Increase in HR
contractility,
ventricular vol or
pressure will increase
MVO2.upset the
demand results in
angina .
Coronary blood
flow.
Depends on a pressure
gradient b/w aorta and
intra myocardial
coronary arteriole.
Reduction of the
coronary gradient will
reduce coronary flow
and result angina.
pathophysiology
29. 29
Clinical
manifestation
Angina presents as
substernal, retrosternal, or
transsternal discomfort.
Pain radiates to the left
jaw, shoulder, and arm.
Discomfort is a dull pain,
strangling or constricting
sensation.
Patient describes the
discomfort as pressure,
heaviness, fullness,
squeezing, burning,
aching, gas or anxiety.
Severity of discomfort
ranges from slight to
disabling pain. It have a
gradual onset and lasts
from0.5 to 30 mins.
Provocation of anginal
episodes include physical
exertion, emotion,
exposure to cold, heat and
humidity, meals.
33. 33
Exercise
tolerance testing
ETT
• Test of choice for evaluating most patients of intermediate
risk for CAD.
BRUCE
PROTOC
OL
• Consist of 3-min stages of increasing treadmill speed and
incline. BP, HR, and ECG are monitored throughout the
study and the recovery period.
observa
tions
• study is considered positive if,
• New ST segment depression of 1 mm in multiple leads
• Hypotensive response to exercise
• Sustained ventricular arrhythmias are precipitated by
exercise.
39. 39
MOA : Indirectly via reduction in the MVO2 secondary
to venodilation and arterial- arteriolar dilation, leading to
a reduction in wall stress from reduced ventricular vol
and pressure.
• Dosage SL : 0.4 mg every 5 min, Topical: 0.5-2 iv :
10-200 mcg/min .
NTG is contraindicated in sildenafil due to severe risk of
hypotension .
• Nitrates are contraindicated in patients with severe
aortic stenosis and hypertrophic obstructive
cardiomyopathy.
Nitrates
Pharmacological TREATMENT
40. 40
Dose
2-4 mg
IV.
Patient whose symptoms are
not relieved after three serial
sublingual nitroglycerine
tablets or whose symptoms
recur with adequate anti-
ischemic therapy.
Contraindicated in hypotension, respiratory
depression, confusion, obtundation .
Morphine
41. 41
MOA of beta blocker is it decrease HR,
contractility, and BP reduce MVO2 and
oxygen demand in patients with effort
induced angina.
Dose :
Metoprolol : 5 mg IV or 25 mg PO qid.
Atenolol : 50-200 mg PO daily.
Propranolol : 20-80 mg PO bid.
Beta blockers reduce s the risk of
recurrent ischemia, myocardial infarction
and mortality in patients with
UA/NSTEMI.
BETA
BLOCKERS
42. 42
MOA : Direct actions include vasodilation of
systemic arterioles and coronary arteries,
leading to a reduction of arterial pressure and
coronary vascular resistance and myocardial
contractility.
Dose : amlodipine 5-10 mg daily.
Verampamil 80-160 mg tid.
Nifidipine 30 -180 mg daily.
Short acting nifidipine should use along with
beta blocker otherwise risk of myocardial
infarction and death.
Verampamil should be avoided in patients with
severe LV dysfunction, pulmonary congestion,
or AV block.
Calcium channel
blockers
43. 43
It reduces the risk
for formations of
a clot in the
narrowed artery
by interrupting
the clotting
process
Once daily
therapy treatment
with low dose
aspirin,75-325mg
is recommended.
Aspirin
48. 48
Diet
A diet low in saturated and trans unsaturated fatty acids and a
caloric intake to achieve optimal body weight is essential in the
management of chronic IHD.
Dyslipidaemia
For long term relief from angina treatment of dyslipidaemia is
essential. Control of lipids can be achieved by the combination
of low fatty diet, exercise and weight loss.
obesity
The treatment of obesity and accompanying risk factors is an
important component of management plan.
Modification of risk factors
49. 49
Diabetes mellitus
It accelerates coronary and peripheral atherosclerosis, it frequently
associated with dyslipidemia and increase in the risk of angina.
Control of dyslipidemia and HT is essential for diabetic patient.
Smoking
Cigarette smoking accelerates coronary atherosclerosis in both sexes
and at all ages. So patient must be strongly advised to give up smoking
completely.
Hypertension
Long term, effective treatment of HT can decrease the occurrence of
adverse coronary events.
55. 55
CAD can be
managed by
pharmacological
and non
pharmacological
treatment.
Risk factor
identification
and
modification.
Chest pain is
cardinal
symptom.
IHD is caused
due to coronary
atherosclerosis.
Conclusion
57. 57
Davidson’s Principle and Practice of Medicine by
Nicholas.N.Boon, Niki. R.colledge, Brain. R. Walker Page
No: 424 – 434,20 th edition.
Text book of therapeutics- Drug and Disease
Management, by Eric. T. Herfintal, Dick .R.Gourley; page
no : 917 – 934,7th edition.
Pharmacotherapy- A pathophysiological approach, by
Joseph. T. Dipiro, Robert. L. Talbert, Gary. C. Yee, Gary. R.
Matzke , Barbara. G. Wells, L. Michael Posey; Page No: 261
– 287,6 th edition.
Harrison’s Principle of Internal Medicine ,Vol 1 by Longo,
Fauci Kasper, Hasper, Jamesoli Page No: 1514 – 1531,18 th
edition.
Oxford text book of medicine , vol 3 , David . A . Warrell ,
Timothy . M . Cox , John . Difirth. Page no : 2318 -2331,4th
editon.
References