• Start with a crisp definition
• Use standard exam headings and subheadings
• Give classifications in tables or flowcharts where useful
• Include etiopathogenesis, clinical features, investigations, complications, and management in sequence
• Mention important diagnostic criteria, drug doses, and emergency steps when relevant
• Add differentiating points, viva pearls, and common examiner-favourite facts
• Write in a format suitable for 5-mark, 10-mark, or long-answer questions
• Include mnemonics only when they genuinely help recall
• Keep terminology aligned with standard undergraduate medicine texts and current guidance where applicable

1. Definition and universal diagnostic criteria
2. Etiology, risk factors, and pathogenesis
3. STEMI versus NSTEMI
4. Clinical features and examination
5. ECG localization and evolution
6. Cardiac biomarkers and other investigations
7. Immediate treatment and reperfusion strategy
8. Complications with time course and management
9. Secondary prevention and discharge advice

• Start with a crisp definition
• Use standard exam headings and subheadings
• Give classifications in tables or flowcharts where useful
• Include etiopathogenesis, clinical features, investigations, complications, and management in sequence
• Mention important diagnostic criteria, drug doses, and emergency steps when relevant
• Add differentiating points, viva pearls, and common examiner-favourite facts
• Write in a format suitable for 5-mark, 10-mark, or long-answer questions
• Include mnemonics only when they genuinely help recall
• Keep terminology aligned with standard undergraduate medicine texts and current guidance where applicable

1. Definition and universal diagnostic criteria
2. Etiology, risk factors, and pathogenesis
3. STEMI versus NSTEMI
4. Clinical features and examination
5. ECG localization and evolution
6. Cardiac biomarkers and other investigations
7. Immediate treatment and reperfusion strategy
8. Complications with time course and management
9. Secondary prevention and discharge advice

Definition

• Ischemic symptoms
• New ischemic ECG changes
• Development of pathological Q waves
• New regional wall-motion abnormality or loss of viable myocardium on imaging
• Coronary thrombus on angiography/autopsy

Classification

1. According to ECG

2. Universal definition of MI

Etiology and Risk Factors

Usual mechanism

1. Platelet adhesion and activation
2. Platelet aggregation
3. Activation of coagulation cascade
4. Formation of occlusive coronary thrombus
5. Myocardial ischemia and necrosis

Non-modifiable risk factors

• Increasing age
• Male sex, or postmenopausal woman
• Family history of premature CAD
• Genetic predisposition

Modifiable risk factors

• Smoking
• Diabetes mellitus
• Hypertension
• Dyslipidemia
• Obesity and sedentary lifestyle
• Unhealthy diet
• Psychosocial stress
• Cocaine/amphetamine use

Less common causes

• Coronary vasospasm, for example cocaine-induced
• Coronary embolism
• Spontaneous coronary artery dissection
• Coronary arteritis/vasculitis
• Severe anemia, shock, hypoxemia, sepsis, tachyarrhythmia: Type 2 MI

Pathogenesis

Sequence

• ATP depletion begins within seconds.
• Loss of contractility occurs within about 1 minute.
• Irreversible myocyte injury begins after approximately 20-30 minutes of severe ischemia.
• Necrosis progresses from subendocardium to subepicardium over several hours: the wavefront phenomenon.
• Early reperfusion salvages ischemic but viable myocardium: “Time is muscle.”

Coronary artery commonly involved

Clinical Features

Symptoms

Typical presentation

• Severe central/retrosternal constricting or crushing chest pain
• Lasts >20 minutes
• May radiate to left shoulder, left arm, neck, jaw, epigastrium, interscapular area
• Not completely relieved by rest or sublingual nitrate
• Sweating, anxiety, restlessness, sense of impending doom
• Dyspnea
• Palpitations
• Nausea and vomiting, especially in inferior-wall MI
• Syncope, especially with arrhythmia or cardiogenic shock

Atypical or silent MI

• Elderly patients
• Women
• Diabetes mellitus
• Chronic kidney disease

• Dyspnea
• Syncope
• Acute pulmonary edema
• Unexplained weakness
• Epigastric discomfort
• Confusion
• Sudden collapse

Signs

• Pallor, sweating, cold clammy extremities
• Tachycardia or bradycardia
• Hypotension
• Raised JVP in right ventricular infarction
• S4 gallop: reduced LV compliance
• S3 gallop: LV failure
• Basal crepitations/pulmonary edema
• New pansystolic murmur:
  • Acute MR due to papillary muscle rupture
  • VSD due to interventricular septal rupture
• Pericardial rub in acute pericarditis

Diagnosis

1. ECG - obtain within 10 minutes of first medical contact

STEMI criteria

• Generally ≥1 mm in all leads other than V2-V3
• In V2-V3, higher cutoffs apply:
  • Men ≥40 years: ≥2 mm
  • Men <40 years: ≥2.5 mm
  • Women: ≥1.5 mm

ECG localization

Evolution of ECG changes

1. Hyperacute tall T waves
2. ST elevation
3. Development of pathological Q waves
4. T-wave inversion
5. ST segment returns to baseline over days
6. Q waves may persist permanently

2. Cardiac biomarkers

Important point

3. Other investigations

• Serial ECGs
• CBC: anemia, leukocytosis
• Blood glucose and HbA1c
• Renal function and electrolytes
• Lipid profile, preferably within 24 hours
• Coagulation profile
• Chest X-ray: pulmonary edema, exclude other causes
• Echocardiography:
  • Regional wall-motion abnormality
  • LV function/ejection fraction
  • Mechanical complications
  • LV thrombus
• Coronary angiography: defines culprit vessel and permits PCI

Management

Initial emergency management

Immediate steps

1. Admit to coronary care unit.
2. ABC approach.
3. Cardiac monitor and defibrillator readiness.
4. Two IV lines.
5. Obtain 12-lead ECG within 10 minutes.
6. Measure troponin, but do not delay reperfusion in clear STEMI.
7. Assess hemodynamic status and complications.

Immediate medications

Avoid/withhold nitrates if

• Systolic BP <90 mmHg
• Suspected right ventricular infarction
• Severe aortic stenosis
• Recent phosphodiesterase-5 inhibitor use:
  • Sildenafil/vardenafil within 24 h
  • Tadalafil within 48 h

Reperfusion Therapy in STEMI

Primary PCI - preferred reperfusion method

Indications

• STEMI within 12 hours of symptom onset
• Ongoing ischemia, shock, severe heart failure, or life-threatening arrhythmia even if presentation is late
• Contraindication to fibrinolysis

Advantages

• Higher rate of patency of infarct artery
• Lower risk of intracranial hemorrhage
• Can identify anatomy and treat culprit lesion
• Useful in cardiogenic shock and after failed thrombolysis

Fibrinolysis

• STEMI within 12 hours of onset, and
• Primary PCI cannot be performed within 120 minutes, and
• No contraindication exists.

Drugs

• Tenecteplase
• Alteplase
• Reteplase
• Streptokinase, where other agents are unavailable

Absolute contraindications to fibrinolysis

• Previous intracranial hemorrhage
• Known intracranial vascular lesion
• Known malignant intracranial tumor
• Ischemic stroke within previous 3 months
• Suspected aortic dissection
• Active bleeding/bleeding diathesis
• Significant closed head/facial trauma within 3 months
• Recent intracranial/intraspinal surgery

Signs of successful thrombolysis

• Relief of chest pain

• 50% reduction in ST elevation at 60-90 minutes

• Reperfusion arrhythmias, especially accelerated idioventricular rhythm
• Early peak of cardiac enzymes

Failed fibrinolysis

NSTEMI Management

• Aspirin + P2Y12 inhibitor
• Anticoagulation
• High-intensity statin
• Anti-ischemic treatment
• Risk stratification using GRACE score
• Early invasive coronary angiography in high-risk patients

Immediate invasive strategy

• Hemodynamic instability/cardiogenic shock
• Recurrent or refractory chest pain
• Life-threatening arrhythmia or cardiac arrest
• Acute heart failure due to ongoing ischemia
• Mechanical complication
• Recurrent dynamic ST/T changes

Early invasive strategy

Complications of AMI

1. Electrical complications

2. Pump failure

3. Mechanical complications

4. Inflammatory complications

• Early fibrinous pericarditis: 1-3 days; pleuritic chest pain and pericardial rub
• Dressler syndrome: weeks to months later; autoimmune fever, pericarditis, pleuropericardial effusion

5. Thromboembolic complications

• LV mural thrombus, particularly with large anterior MI
• Systemic embolism: stroke, limb ischemia, renal infarction

Secondary Prevention After MI

Drug therapy

• Aspirin indefinitely
• P2Y12 inhibitor usually for 12 months after ACS, adjusted for bleeding risk
• High-intensity statin
• Beta-blocker, especially with LV dysfunction, angina, arrhythmias
• ACE inhibitor/ARB, especially with LVEF ≤40%, diabetes, hypertension, CKD, or heart failure
• Mineralocorticoid receptor antagonist if LVEF ≤40% with heart failure or diabetes, provided renal function and potassium permit

Lifestyle and risk-factor control

• Complete smoking cessation
• Cardiac rehabilitation
• Regular graded exercise
• Weight reduction if overweight
• Diabetes and BP control
• Mediterranean-style heart-healthy diet
• Limit alcohol and avoid cocaine/amphetamines
• Influenza vaccination where appropriate
• Education regarding adherence and recurrent symptoms

One-Minute Proff Viva Summary

Acute MI is myocardial necrosis caused by acute ischemia, most commonly due to rupture or erosion of an atherosclerotic plaque followed by coronary thrombosis. Diagnosis requires a rise/fall of cardiac troponin with evidence of ischemia. STEMI requires urgent reperfusion, preferably primary PCI within 120 minutes of first medical contact; otherwise, fibrinolysis is used if no contraindication exists. Initial treatment includes aspirin, a P2Y12 inhibitor, anticoagulation, statin, nitrates where appropriate, oxygen only for hypoxemia, and management of pain and complications. Major complications are arrhythmias, LV failure, cardiogenic shock, papillary muscle rupture, VSD, free-wall rupture, pericarditis, mural thrombus, and ventricular aneurysm.