2. • People of South Asian descent, including those from India, Pakistan,
Bangladesh, Nepal, Sri Lanka, Bhutan and the Maldives, have a higher
risk of ASCVD – fourfold higher than the general population.
Moreover, they develop heart disease up to a decade earlier
• South Asians represent approximately 25 percent of the world's
population – yet they account for 60 percent of the world's heart
disease patients.
• South Asians undergoing coronary angiography in the U.S. have been
noted to have smaller luminal diameters, higher-grade stenoses and a
higher prevalence of multivessel disease.
• 25% of heart attacks occur under age 40 for young South Asians, and
50% occur under age 50.
• There is a 40% higher chance of mortality from heart attacks among
South Asians than the average population.
3.
4. Acute Coronary Syndrome
• The clinical presentation of acute coronary syndromes (ACS) is broad
• It ranges from cardiac arrest, electrical or hemodynamic instability with cardiogenic shock (CS)
• The leading symptom initiating the diagnostic and therapeutic cascade in patients with
suspected ACS is acute chest discomfort described as pain, pressure, tightness, and burning.
Chest pain-equivalent symptoms may include dyspnea, epigastric pain, and pain in the left arm.
• Based on the electrocardiogram (ECG), two groups of patients should be differentiated
1. ST-segment elevation ACS : Patients with acute chest pain and persistent (>20 min) ST-
segment elevation. The mainstay of treatment in these patients is immediate reperfusion by
primary percutaneous coronary intervention (PCI) or, if not available in a timely manner, by
fibrinolytic therapy
2. Non-ST-segment elevation ACS (NSTE-ACS): patients with acute chest discomfort but no
persistent ST-segment elevation. exhibit ECG changes that may include transient ST-segment
elevation, persistent or transient ST-segment depression, T-wave inversion, flat T waves, or
pseudo-normalization of T waves; or the ECG may be normal.
5. Unstable angina in the era of high-sensitivity cardiac
troponin assays
• Unstable angina is defined as myocardial ischemia at rest or on minimal exertion
in the absence of acute cardiomyocyte injury/necrosis
• Among unselected patients presenting to the emergency department with
suspected NSTE-ACS, the introduction of hs-cTn measurements in place of
standard troponin assays resulted in an increase in the detection of MI (∼4%
absolute and 20% relative increases) and a reciprocal decrease in the diagnosis of
unstable angina.
• Compared with NSTEMI patients, individuals with unstable angina do not
experience acute cardiomyocyte injury/necrosis, have a substantially lower risk
of death, and appear to derive less benefit from intensified antiplatelet therapy,
as well as an invasive strategy within 72 h
6. High sensitivity cardiac
troponin
• Have higher NPV for AMI
• Reduce the ‘troponin-blind’ interval leading to
earlier detection of AMI
• Result in ∼4% absolute and ∼20% relative
increases in the detection of type 1 MI and a
corresponding decrease in the diagnosis of
unstable angina
• Are associated with a 2-fold increase in the
detection of type 2 MI
• Levels of hs-cTn should be interpreted as
quantitative markers of cardiomyocyte
damage (i.e., the higher the level, the greater
the likelihood of MI):
• Elevations beyond 5-fold the upper reference
limit have high (>90%) PPV for acute type 1 MI
• Elevations up to 3-fold the upper reference
limit have only limited (50–60%) PPV for AMI
7. Conditions other than acute type 1 myocardial infarction associated
with cardiac troponin elevation
1. Tachyarrhythmias
2. Heart failure
3. Hypertensive emergencies
4. Critical illness (e.g., shock/sepsis/burns)
5. Myocarditis
6. Takotsubo syndrome
7. Aortic dissection
8. Pulmonary embolism
9. Renal dysfunction and associated cardiac disease
8. Acute myocardial infarction (AMI)
• Acute myocardial infarction (AMI) defines cardiomyocyte necrosis in a clinical
setting consistent with acute myocardial ischemia.
• A combination of criteria is required to meet the diagnosis of AMI.
• namely the detection of an increase and/or decrease of a cardiac biomarker,
preferably high-sensitivity cardiac troponins at least one of the following
1. Symptoms of myocardial ischemia
2. New ischemic ECG changes
3. Development of pathological Q waves on ECG
4. Imaging evidence of loss of viable myocardium or new regional wall motion
abnormality in a pattern consistent with an ischemic etiology
5. Intracoronary thrombus detected on angiography or autopsy
9. Acute myocardial infarction (AMI)
1. Type 1 myocardial infarction: characterized by atherosclerotic plaque rupture, ulceration,
fissure, or erosion with resulting intraluminal thrombus in one or more coronary arteries
leading to decreased myocardial blood flow and/or distal embolization and subsequent
myocardial necrosis.
2. Type 2 myocardial infarction: myocardial necrosis in which a condition other than coronary
plaque instability causes an imbalance between myocardial oxygen supply and demand.
Mechanisms include hypotension, hypertension, tachyarrhythmias, bradyarrhythmia's, anemia,
hypoxemia, but also by definition, coronary artery spasm, spontaneous coronary artery
dissection (SCAD), coronary embolism, and coronary microvascular dysfunction
3. Type 3 myocardial infarction: MI resulting in death when biomarkers are not available
4. Type 4 myocardial infarction: MI related to PCI
5. Type 5 myocardial infarction: MI related to coronary artery bypass grafting (CABG)
10. Diagnostic algorithm and triage in
acute coronary syndrome
The initial assessment is based on the integration
of low likelihood and/or high likelihood
features derived from the clinical setting
• symptoms, vital signs
• the 12-lead ECG: resting 12-lead ECG is the
first-line diagnostic tool in the assessment of
patients with suspected ACS. It is
recommended to perform it within 10 min of
the patient’s arrival in the emergency
• the cardiac troponin concentration determined
at presentation to the emergency department
and serially thereafter.
11. STEMI
• This is usually based on symptoms consistent with myocardial
ischemia (i.e., persistent chest pain) and signs [i.e., 12-lead
electrocardiogram (ECG)].
• In patients with a clinical suspicion of myocardial ischemia and ST-
segment elevation, reperfusion therapy needs to be initiated as soon
as possible.
• A complete normalization of the ST-segment elevation after
nitroglycerin administration, along with complete relief of symptoms,
is suggestive of coronary spasm
12. STEMI diagnosis
• ST-segment elevation (measured at the J-point) is considered suggestive of
ongoing coronary artery acute occlusion in the following cases:
1. at least two contiguous leads with ST-segment elevation ≥ 2.5 mm in men <
40 years, ≥2 mm in men ≥ 40 years
2. ≥ 1.5 mm in women in leads V2–V3 and/or ≥ 1 mm in the other leads [in the
absence of left ventricular (LV) hypertrophy or left bundle branch block LBBB)]
• inferior MI, it is recommended to record right precordial leads (V3R and V4R)
seeking ST-segment elevation, to identify concomitant right ventricular (RV)
infarction
• posterior MI:
• concomitant ST-segment elevation ≥ 0.5 mm recorded in leads V7–V9.
• ST-segment depression in leads V1–V3 suggests myocardial ischemia,
especially when the terminal T-wave is positive (ST-segment elevation
equivalent)
17. NSTE-ACS
• When using any algorithm:
1. Should only be used in conjunction
with all available clinical
information, including detailed
assessment of chest pain
characteristics and ECG
2. The ESC 0 h/1h and 0 h/2 h
algorithms apply to all patients
irrespective of chest pain onset.
3. Serial cardiac troponin testing
should be pursued if the clinical
suspicion remains high or
whenever the patient develops
recurrent chest pain
late increases in cardiac troponin have been
described in ∼1% of patients
19. Reference
1. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting
without persistent ST-segment elevation
2. Guidelines on Management of Acute Myocardial Infarction in Patients Presenting with ST-
Segment Elevation-2071
3. UpToDate
4. American Heart Association.
5. World health organization