Call Girls Whitefield Just Call 7001305949 Top Class Call Girl Service Available
Acute MI - NSTEMI
1. NON -ST ELEVATION
MYOCARDIAL INFARCTION
VAISHNAVI SURESH NAIR
GROUP:7
2. Case:
An 81-year-old African American female (AAF) with
a past medical history (PMH) of hypertension (HTN),
diabetes type 2 (DM2), coronary artery disease
status post myocardial infarction (CAD S/P MI) 5
years ago, and chronic abdominal pain for 2 years
without a clear reason, was admitted to the hospital
with a worsening of the same abdominal pain for 2-3
days.
No chest pain (CP) or shortness of breath (SOB).
She complains of nausea and vomiting.
Physical examination
38.8 C HR-78 bpm-210/100 mm/Hg
Abdomen: RLQ tenderness, no rebound, soft, +BS.
The rest of the examination was not remarkable.
3. What laboratory workup would you suggest?
CBC, Comprehensive Metabolic Panel, Amylase, Lipase,
Urinalysis were all normal.
KUB (Kidney Ureter Bladder) was nonspecific.
CT of abdomen showed a dilated stomach,
stable 3.6 cm AAA (the same size as 2 years ago) and old renal
cysts.
Patient was started on IVF,
Pain meds and Zosyn for T* 38.3.
Blood cx were taken.
4. What is the most likely diagnosis?
Diverticulitis?
Appendicitis? (no, appendectomy was
done years ago).
DM Gastro paresis?
Gastroenteritis?
5. What happened?
ECG on admission showed deep Qs
waves in the inferior leads - probably an
old MI.
Cardiac enzymes x 1 were ordered.
10. The catheterization showed a 99%
occlusion of one of the branches of the
circumflex artery (Cx). Two stents were
placed. The right coronary artery (RCA)
had a 90% proximal stenosis but both
stent placement and PTCA
(percutaneous transluminal coronary
angioplasty) were unsuccessful. The
patient was scheduled for a repeated
catheterization for stent placement in
RCA within 2-3 weeks.
A diagram of the stent placement in the Cx artery
TREATMENT IN THIS CASE:
11. SO???!!!
Always keep the possibility of an acute myocardial infarction (AMI) in
patients with risk factors, even with atypical symptoms. MI can be
completely painless in diabetics and women. We do not need the
symptoms of chest pain (CP) to diagnose an MI.
In this case, the RLQ pain was not related to the MI
but with the previously diagnosed renal cyst.
12. NSTEMI:
It may be defined as a development of heart muscle necrosis (a form of cell death) without the ECG
(electrocardiography) change of ST-segment elevation, resulting from an acute interruption of blood
supply to a part of the heart and can be demonstrated by an elevation of cardiac markers (CK-MB or
troponin) in the blood.
ST-segment elevation indicates full thickness injury of heart muscle. Absence of ST-segment elevation
in NSTEMI involve (partial thickness) damage of heart muscle. Therefore, NSTEMI is less severe type
of heart attack compared to STEMI in which full thickness damage of heart muscle develops.
NSTEMI usually occurs by developing a partial occlusion of a major coronary artery or a complete
occlusion of a minor coronary artery previously affected by atherosclerosis. Atherosclerosis is a disease
of artery in which mainly cholesterol deposition occur within the wall of the artery. This deposited
cholesterol ultimately forms a plaque called atherosclerotic plaque. Many years are required to establish
an atherosclerotic plaque.
The most common mechanism of NSTEMI is rupture or erosion of an atherosclerotic plaque that triggers
platelet aggregation, which lead to formation of a thrombus (blood clot) in a coronary artery. This arterial
thrombus causes interruption of blood supply to part of the heart muscle; profound changes take place in
the heart muscle that lead to irreversible changes and death of myocardial cells. Usually, partial
thickness damage of heart muscle occurs.
13. Major risk factors:
1.High serum cholesterol level
2.Hypertension
3.Diabetes mellitus
4.Cigarette smoking
Minor risk factors:
1.Increasing age
2.Male gender
3.Family history
4.Physical inactivity
5.Obesity
6.Excess alcohol consumption
7.Excess carbohydrates intake
8.Social deprivation
9.Competitive and stressful lifestyle with type A personality
10.Diets deficient in fresh vegetables, fruit and polyunsaturated
fatty acids.
14. Symptoms:
(1)Chest pain: Chest pain is the main symptom. It is constricting, tightening, choking or heavy in character,
usually located in the centre of the chest, but may radiate to neck, jaw, shoulder, back, and arms (most
commonly left arms). Occasionally, pain may be felt only at the sites of radiation. In older patients or those with
diabetes mellitus, painless attack may occur (pain conducting autonomic nerve of the heart are degenerated in
old age and in diabetes).
(2) Difficulty in breathing: Breathing difficulty occur when the damage to the heart muscle limits the pumping
action of the left ventricle, causing acute left heart failure and consequent lung congestion.
(3) Nausea, vomiting, and sweating: These are due to autonomic nervous system upset.
(4) Palpitation: It is due to sympathetic nervous system activation.
(5) Cardiogenic shock: If NSTEMI involve a large territory of heart, patients may present with shock due to
impaired myocardial function.
15. Diagnosis:
Initially, patients with suspected NSTEMI, ECG and cardiac markers estimation are mandatory
Electrocardiography (ECG): The usual ECG findings of NSTEMI are ST-segment depression
or T-wave inversion.
16. Cardiac markers:
Cardio-specific isoenzyme CK-MB (creatine kinase myocardial band), and cardiospecific proteins
troponin T and troponin I are rises in blood in NSTEMI. These are released from damaged heart muscle
cells during and after attack. CK-MB starts to rise at 4-6 hours and falls to normal within 48-72 hours.
Troponin T and troponin I start to rise at 4-6 hours and remain high for up to two weeks.
Full blood count:
WBC (white blood cell) count is usually elevated. ESR (Erythrocyte sedimentation rate) and CRP (C-reactive
protein) may also elevate.
Chest X-ray:
Assess for signs of lung edema.
Echocardiography:
It is done for assessing the function of heart chamber and for detecting important complications.
17. Complications:
NSTEMI can lead to several complications immediately following an attack or later in recovery. Usually,
complications depend on what part of the heart is damaged and the extent of damage.
Immediate complications
(A) Heart arrhythmia – Heart arrhythmia is a disturbance of the electrical rhythm of the heart. In
NSTEMI, damaged heart muscle disrupts electrical signals and produces arrhythmia in which
heartbeat may be too fast, too slow or irregular. It is the most common complication following an
attack. The following types of arrhythmia may develop:
1.Ventricular fibrillation
2.Ventricular tachycardia
3.Ventricular ectopics
4.Accelerated idioventricular rhythm
5.Atrial fibrillation
6.Atrial tachycardia
7.Atrioventricular block
8.Sinus bradycardia
In majority of cases arrhythmia is mild and transient. It is controlled by rest, pain relief and medication.
But, life threatening arrhythmia may develop that is the major cause of death during the first 24 hours
after an attack.
18. In majority of cases arrhythmia is mild and transient. It is controlled by rest, pain relief and medication.
But, life threatening arrhythmia may develop that is the major cause of death during the first 24 hours
after an attack.
(B) Acute heart failure – It may develop when the damage area of the heart muscle is large. Suddenly,
this damaged heart cannot pump enough blood to meet the body’s demand and developed acute heart
failure.
(C) Cardiogenic shock – It may develop after the large territory heart muscle damage. It leads to failure
of the pumping action of the heart. The end results are very low blood pressure with an inadequate supply
of oxygen rich blood to the tissues of the body.
(D) Mitral regurgitation – Papillary muscle damage sometimes causes mitral regurgitation.
Late complications
(A)Dressler’s syndrome – This syndrome is characterized by fever, pleuritis and percarditis. It is caused
by an autoimmune reaction to damage heart muscle. It occurs a few weeks or even months after an
NSTEMI.
(B) Chronic heart failure – It occurs slowly over time after an attack in which the heart cannot pump
enough blood to meet the body’s demand.
19. Treatment:
Patients should be admitted immediately to hospital, preferably to a cardiac care unit because there
is a significant risk of death.
(1) Bed rest with continuous monitoring by ECG.
(2) Inhaled oxygen therapy.
(3) Relief of pain by opiate analgesic:
Intravenous morphine 10 mg or diamorphine 5 mg is usually used and may have to be repeated to
relieve severe pain.
(4) Antiplatelet therapy:
Antiplatelet drugs prevent platelet aggregation within coronary artery. A 300 mg tablet of aspirin should
be given orally as early as possible then 75 mg daily should be continued indefinitely if there are no
side effects occur. Aspirin reduces the mortality rate of NSTEMI by approximately 25%. In combination
of aspirin, clopidogrel 600 mg should be given orally as early as possible, followed by 150 mg daily for 7
days and 75 mg daily thereafter, gives a further reduction in mortality. Ticagrelor 150 mg followed by 90
mg two times daily is more effective than clopidegrol. High risk patients, especially patients with
diabetes mellitus or patients who undergo percutaneous coronary intervention (PCI), should also be
considered for intake of glycoprotein IIb/IIIa receptor blocker (block the final common pathway of
platelet aggregation), such as tirofiban, abciximab, or eptifibatide.
20. (5) Anticoagulant therapy:
Anticoagulant drugs prevent reinfarction, and reduces the risk of thromboembolic complications.
Anticoagulation can be achieved by using unfractionated heparin, low molecular weight heparin (also
called fractionated heparin and includes enoxaparin, dalteparin) or a pentasaccharide (fondaparinux).
Comparatively low molecular weight heparin is more safety and efficacious than unfractionated heparin,
and pentasaccharide is more safety and efficacious than low molecular weight heparin. The dose
regimens are:
1.Enoxaparin: 1 mg/kg body weight two times daily usually for 8 days by subcutaneous injection.
2.Dalteparin: 120 units/kg body weight two times daily usually for 8 days by subcutaneous injection.
3.Fondaparinux: 2.5 mg daily usually for 8 days by subcutaneous injection.
(6) Beta-blockers:
Beta-blockers reduce arrhythmias, heart rate, blood pressure and myocardial oxygen demand, and relive
pain. Oral beta-blocker atenolol 25-50 mg twice daily, metoprolol 25-50 mg twice daily, or bisoprolol 5 mg
once daily are usually adequate. Patients with heart rate more than 90 beats/minute or patients with
hypertension (systolic blood pressure more than 150 mmHg or diastolic more than 90 mmHg),
intravenous beta-blockers (atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes) can be given. Beta-blockers
should be avoided if there is heart failure, heart block, hypotension, or bradycardia.
21. (7) Nitrates:
Nitrates act as a vasodilator and relief pain. Nitrates should first be given buccally or by sublingual (under
tongue) spray. If the patient experiencing persistent ischemic chest pain after 3 doses given 5 minutes
apart, then intravenous glyceryl trinitrate 0.6-1.2 mg/hour or isosorbide dinitrate 1-2 mg/hour can be given
until pain relieved or systolic blood pressure falls to less than 100 mgHg. Oral or sublingual nitrates can be
used once the pain has resolved.
(8) Statins:
Irrespective of serum cholesterol level, all patients should receive statin such as atorvastatin, simvastatin,
or rosuvastatin after NSTEMI.
(9) ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensive receptor blockers):
An ACE inhibitor such as ramipril, enalapril, captopril, or lisinopril is started 1 or 2 days after NSTEMI.
ACE inhibitor therapy reduces ventricular remodeling, prevent the onset of heart failure, and reduce
recurrent infarction. An ARB (valsartan, candesartan, losartan or olmesartan) is suitable alternatives in
patients who are intolerant of ACE inhibitors (ACE inhibitors can cause dry cough).
22. (10) Coronary angiography and revascularization:
Before giving revascularization treatment, risk analysis in patients with NSTEMI should be done
immediately after hospital admission. Several systems are available for risk stratification, but TIMI
score and GRACE score are the best. These systems categorized the patients into low, medium
and high risk groups.
Medium to high risk patients should be considered for early coronary angiography and
revascularization, either by PCI (percutaneous coronary intervention) or by CABG (coronary artery
bypass grafting). Early medical treatment is appropriate in low risk patients, and coronary
angiography and revascularization are reserved for those who fail to settle with medical treatment.
Prognosis:
Early death in NSTEMI is usually due to an arrhythmia. Long term mortality is high in those who have
extensive damage of heart muscle, poor left ventricular function and persistent ventricular arrhythmia.
Depression, social isolation and old age are also associated with a higher mortality. According to GRACE
score, in-hospital death is less than 1% in low risk, 1-9% in medium risk and more than 9% in high risk
patients with non-ST segment elevation myocardial infarction. After hospital discharge, more than 80%
patients survive for a further year, approximately 75% for 5 years, 50% for 10 years and 25% for 20
years.
23. Lifestyle after NSTEMI:
► Restrict physical activities for four to six weeks after attack – death tissue in damage heart muscle
takes 4-6 weeks to be healed with fibrous tissue.
► Cessation of cigarette smoking.
► Maintaining an ideal body weight.
► Eating a Mediterranean style diet (diet rich in monounsaturated fatty acids and omega-3 fatty acids,
but low in saturated fatty acids).
► Achieving well control of high pressure and diabetes mellitus if present.
► Taking regular exercise up to, but not beyond, the point of chest discomfort.
► Continue secondary prevention drugs therapy including aspirin, clopidogrel, beta-blocker, ACE
inhibitor, and statin.
24. GRACE SCORE:
GRACE (Global Registry of Acute Coronary Events) score is used for risk assessment in ACS
(acute coronary syndrome) which includes NSTEMI, STEMI and unstable angina. This score
is more accurate because it is derived from a multinational registry of unselected patients and
includes hospitals in Europe, Asia, North America, South America, Australia and New Zealand.
Risk assessment should be performed at the time of hospital admission and is important
because it gives an idea about probability of in-hospital death and also guides the appropriate
treatment plan in NSTEMI and unstable angina.
Calculation of GRACE score:
Eight parameters are used for calculating GRACE score that include patient’s age,
heart rate, systolic blood pressure, Killip class, serum creatinine level, cardiac
arrest at hospital admission, ST-segment deviation in ECG and elevated
cardiac marker.
25. Treatment plan according to GRACE risk stratification:
In low risk patients with NSTEMI or unstable angina, medical treatment is appropriate and surgical
intervention is reserved for those who fail to settle with medical treatment. By contrast, medium and
high risk patients with NSTEMI or unstable angina should be treated with multiple drugs and
considered for early coronary angiography and revascularization. Revascularization can be done
either by percutaneous coronary intervention (PCI) or by coronary artery bypass grafting (CABG).
Treatment plan in STEMI is not depend on risk stratification. All patients with STEMI should be
treated immediately with reperfusion therapy by primary percutaneous coronary intervention (PCI)
along with multiple drugs. Where PCI cannot be achieved within 120 minutes of diagnosis or PCI is
not available, thrombolytic therapy (streptokinase, alteplase, tenecteplase, or reteplase) may be
given.
27. 4. Killip class:
Killip class Score
I (No heart failure) 0
II (Crackles audible in lower half of lung field) 20
III (Crackles audible in whole lung field) 39
IV (Cardiogenic shock) 59
5. Serum creatinine level:
Serum
creatinine
(μmol/L)
Serum creatinine
(mg/dl)
Score
0-34 0-0.38 1
35-70 0.39-0.79 4
71-105 0.80-1.19 7
106-140 1.20-1.58 10
141-176 1.59-1.90 13
177-353 2.0-3.99 21
≥ 354 ≥ 4 28
6. Cardiac arrest at hospital admission:
Cardiac arrest at hospital admission Score
Absent 0
Present 39
7. ST-segment deviation in ECG:
ST-segment deviation in ECG Score
Absent 0
Present 28
8. Elevated serum cardiac marker (Troponin or
CK-MB):
Elevated cardiac
marker
Score
Absent 0
Present 14
28. Risk assessment by GRACE score:
We can assess risk by summation of score for all eight parameters.
Total score Risk assessment
≤ 100
Low risk patients– In-hospital death
rate less than 1%
101-170
Medium risk patients – In-hospital
death rate 1-9%
≥ 171
High risk patients – In-hospital death
rate more than 9%
29. Probability of in-hospital death by GRACE score:
Total score In-hospital death (%)
≤ 60 ≤ 0.2
70 0.3
80 0.4
90 0.6
100 0.8
110 1.1
120 1.6
130 2.1
140 2.9
150 3.9
160 5.4
170 7.3
180 9.8
190 13
200 18
210 23
220 29
230 36
240 44
≤ 250 ≤ 52
30. TIMI score
TIMI (Thrombolysis In Myocardial Infarction) score is used in patients with NSTEMI (Non ST-segment
elevation myocardial infarction), STEMI (ST-segment elevation myocardial infarction) and unstable
angina to define risk. TIMI Study Group established this risk score. TIMI Study Group is an Academic
Research Organization affiliated with Harvard Medical School, and Brigham and Women’s Hospital in
Boston. This score was derived from patients enlisted to randomized controlled trials of low molecular
weight heparins. The main advantages of TIMI score are its simplicity and ease of use.
TIMI risk score for patients with NSTEMI or unstable angina:
Seven variables are used to assess risk in NSTEMI or unstable angina including age of patient, risk
factors for coronary artery disease, prior coronary artery stenosis, ST-segment deviation on ECG, prior
aspirin intake, severe anginal chest pain within 24 hours and elevated cardiac markers. It is done
immediately after an attack.
31. 1. Age of patient:
Age of patient Score
Less than 65
0
years
65 years or more 1
2. Risk factors for coronary artery disease:
Five risk factors are included. These are:
•Hypertension (high blood pressure)
•Hypercholesterolemia (high blood cholesterol level)
•Family history of coronary artery disease
•Diabetes
•Smoking
Number of risk factors for coronary
artery disease
Score
Presence of less than three 0
Presence of three or more 1
3. Prior coronary artery stenosis:
Coronary angiography is done to see the stenosis.
Prior coronary artery
stenosis
Score
Less than 50% 0
50% or more 1
4. ST-segment deviation on ECG:
It includes horizontal ST-segment depression or transient
ST-segment elevation more than 1 mm.
ST-segment deviation
on ECG
Score
Absent 0
Present 1
32. 5. Prior aspirin intake:
Prior aspirin intake Score
No aspirin intake in the
0
last 7 days
Aspirin intake in the last
7 days
1
6. Severe anginal chest pain:
Severe anginal chest pain Score
No or one episode in last
0
24 hours
Two or more episodes in
last 24 hours
1
7. Elevated cardiac markers (CK–MB or troponin):
Elevated cardiac markers Score
Absent 0
Present 1
Risk stratification by TIMI score in patients
with NSTEMI or unstable angina:
Risk stratification Score
Low risk patients 0 – 2
Medium risk patients 3 – 4
High risk patients 5 – 7
33. Plan of treatment according to TIMI score:
In low risk patients with NSTEMI or unstable angina, drug therapy is appropriate and surgical
intervention is reserved for those who fail to settle with drug therapy. By contrast, medium to high risk
patients with NSTEMI or unstable angina should be treated with multiple drugs and considered for early
coronary angiography and revascularization.
Interpretation of TIMI score in NSTEMI or unstable angina:
Total score
Rate of death, or new or recurrent
myocardial infarction, or severe recurrent
anginal chest pain requiring urgent
revascularization in 14 days
0 – 1 4.7%
2 8.3%
3 13.2%
4 19.9%
5 26.2%
6 – 7 40.9%
34. TIMI risk score for patients with STEMI:
Eleven variables are used to assess risk in STEMI that are age of patient, history of anginal chest pain,
history of hypertension, history of diabetes, systolic blood pressure, heart rate, Killip class, weight of
patient, anterior myocardial infarction in ECG, left bundle branch block (LBBB) in ECG and delay to
treatment after an attack.
Interpretation of TIMI score in STEMI:
Total score Risk of death at 30 days
0 0.8%
1 1.6%
2 2.2%
3 4.4%
4 7.3%
5 12.4%
6 16.1%
7 23.4%
8 26.8%
9 – 16 35.9%
35. NSTEMI VS STEMI
PAHOPHYSIOLOGY OF NSTEMI:
NSTEMI occurs by developing a complete occlusion
of a minor coronary artery or a partial occlusion of a
major coronary artery previously affected by
atherosclerosis. This causes a partial thickness
damage of heart muscle.
PATHOPHYSIOLOGY OF STEMI:
STEMI occurs by developing a complete occlusion
of a major coronary artery previously affected by
atherosclerosis. This causes a full thickness
damage of heart muscle.
36. ECG FINDINGS OF NSTEMI:
The usual ECG findings of NSTEMI are ST-segment
depression or T-wave inversion. NSTEMI does not
show ST segment elevation in ECG (due to partial
thickness injury of heart muscle) and later does not
progress to a Q-wave. For this reason, it is also
called a non–Q-wave myocardial infarction (NQMI).
ECG FINDINGS OF STEMI:
STEMI shows ST segment elevation in ECG (due to
full thickness injury of heart muscle) and later
progress to a Q-wave. For this reason, it is also
called a Q-wave myocardial infarction (QWMI). The
ultimate ECG findings of STEMI are ST-segment
elevation, pathological Q-wave formation and T-wave
inversion.
37. DDX OF NSTEMI & STEMI:
1) BY ECG:
The diagnosis of a NSTEMI is based on a
typical history of chest pain, no ST segment
elevation in ECG plus elevation of cardiac
markers in serum.
The diagnosis of a STEMI is based on a typical
history of chest pain, ST segment elevation in
ECG plus elevation of cardiac markers in
serum.
2) CARDIAC MARKERS:
Cardiac markers including CK-MB (creatine
kinase myocardial band), troponin I and
troponin T, all elevate both in cases. But the
elevation of these markers is often mild in
NSTEMI compared with STEMI
COMPLICATIONS:
Complications like cardiogenic shock, left ventricular
failure, severe mitral regurgitation due to papillary
muscle rupture, cardiac tamponade due to
ventricular wall rupture are more in STEMI (due to
full thickness heart muscle damage) than NSTEMI.
PROGNOSIS:
Long-term mortality is similar or higher in NSTEMI
compared to STEMI (two year mortality is
approximately 30% in both cases).
38. TREATMENT:
Antiplatelets (Aspirin, Clopidogrel, Ticagrelor), Anticoagulants (Enoxaparin, Dalteparin, Fondaparinux),
Beta-blockers (atenolol, metoprolol, bisoprolol), Nitrates (isosorbide dinitrate, glyceryl trinitrate), Statins
(atorvastatin, rosuvastatin, simvastatin, pitavastatin), ACE inhibitors (Ramipril, enalapril, captopril,
Lisinopril) or ARBs (valsartan, candesartan, losartan, olmesartan) are given both in NSTEMI and STEMI.
In case of reperfusion therapy, primary PCI (percutaneous coronary intervention) is the treatment of choice
for STEMI. Where primary PCI cannot be achieved within 120 minutes of diagnosis or PCI is not available,
thrombolytic therapy such as streptokinase, tenecteplase, alteplase or reteplase should be given.
On the other hand, early coronary angiography and revascularization, either by PCI or by CABG (coronary
artery bypass grafting) is the treatment of choice for medium to high risk patients with NSTEMI.
Drug treatment is appropriate in low risk patients with NSTEMI, and coronary angiography and
revascularization reserved for those who fail to settle with drug treatment (low, medium and high risk
patients are categorized in NSTEMI by GRACE score) . Thrombolytic therapy is harmful in NSTEMI. The
aggregate data suggest that patients with NSTEMI may be put at risk of re infarction if thrombolytic therapy
is used.
The Killip classification is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them. Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class
Patients were ranked by Killip class in the following way:
Killip class I includes individuals with no clinical signs of heart failure.
Killip class II includes individuals with rales or crackles in the lungs, an S3, and elevated jugular venous pressure.
Killip class III describes individuals with frank acute pulmonary edema.
Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).
Within a 95% confidence intervalthe patient outcome was as follows:
Killip class I:81/250 patients;32% (27–38%).Mortality rate was found to be 6%.(current 30 day mortality 2.8)Killip class II:96/250 patients;38% (32–44%).Mortality rate was found to be 17%.(current 30 day mortality 8.8)Killip class III:26/250 patients;10% (6.6–14%).Mortality rate was found to be 38%.(current 30 day mortality 14.4)Killip class IV:47/250 patients;19% (14–24%).Mortality rate was found to be 67%.
