1. Definition and universal diagnostic criteria
2. Causes, risk factors, and precipitating triggers
3. Classification: STEMI, NSTEMI, and infarct territory
4. Pathogenesis and coronary plaque rupture
5. Clinical features and physical signs
6. Investigations, including cardiac biomarkers and imaging
7. Serial ECG evolution from day 0 to day 7
8. Early and late complications
9. Immediate management, reperfusion, and secondary prevention

1. Definition and universal diagnostic criteria
2. Causes, risk factors, and precipitating triggers
3. Classification: STEMI, NSTEMI, and infarct territory
4. Pathogenesis and coronary plaque rupture
5. Clinical features and physical signs
6. Investigations, including cardiac biomarkers and imaging
7. Serial ECG evolution from day 0 to day 7
8. Early and late complications
9. Immediate management, reperfusion, and secondary prevention

1. Basics: definition, causes, risk factors, classification, pathogenesis
2. Clinical features and investigations
3. Serial ECG changes from day 0 to day 7
4. Complications
5. Management of STEMI and NSTEMI

1. Basics of Myocardial Infarction

Definition

• A rise and/or fall in cardiac troponin, with at least one value above the 99th-percentile upper reference limit, and
• Evidence of acute myocardial ischemia, such as ischemic symptoms, new ischemic ECG changes, pathological Q waves, imaging evidence of new loss of viable myocardium/regional wall-motion abnormality, or demonstration of coronary thrombus.

Causes

A. Most common cause: Type 1 MI

Vulnerable atherosclerotic plaque rupture or erosion → platelet activation and aggregation → thrombus formation ± coronary vasospasm → abrupt reduction/cessation of coronary blood flow → ischemia → irreversible myocardial necrosis.

B. Other causes of MI

1. Coronary vasospasm
   • Prinzmetal vasospasm
   • Cocaine or amphetamine use
   • Severe adrenergic stress
2. Coronary embolism
   • Atrial fibrillation with embolus
   • Infective endocarditis vegetation
   • Prosthetic valve thrombus
   • Paradoxical embolus
3. Spontaneous coronary artery dissection (SCAD)
   • More frequent in younger women, pregnancy/postpartum states, or fibromuscular dysplasia.
4. Coronary arteritis/vasculitis
   • Kawasaki disease
   • Polyarteritis nodosa
   • Takayasu arteritis
   • SLE-associated vasculopathy
5. Coronary trauma or iatrogenic obstruction
   • Coronary intervention, surgery, or catheter-related complications.
6. Type 2 MI: oxygen supply-demand mismatch
   • Severe anemia
   • Hypoxemia/respiratory failure
   • Hypotension or shock
   • Sepsis
   • Tachyarrhythmia or severe bradyarrhythmia
   • Hypertensive crisis
   • Severe aortic stenosis or hypertrophic cardiomyopathy.

Risk Factors

Non-modifiable

• Increasing age
• Male sex
• Family history of premature coronary artery disease
• Genetic predisposition, including familial hypercholesterolemia
• Postmenopausal state in women

Modifiable major risk factors

• Dyslipidemia, especially raised LDL cholesterol
• Hypertension
• Cigarette smoking/tobacco exposure
• Diabetes mellitus
• Obesity, especially central obesity
• Physical inactivity
• Unhealthy diet
• Chronic inflammatory states
• Chronic kidney disease
• Psychosocial stress
• Excess alcohol use
• Cocaine and amphetamine use

Precipitating Factors

• Heavy or unusual physical exertion
• Acute emotional stress, anger, anxiety, grief
• Early morning sympathetic surge
• Heavy meal
• Exposure to cold weather
• Sexual activity
• Acute infection, fever, or sepsis
• Acute blood loss or severe anemia
• Hypoxia
• Severe hypertension
• Tachyarrhythmia
• Cocaine, amphetamines, or sympathomimetic drugs
• Surgery or major trauma

• A risk factor predisposes to coronary artery disease over years.
• A precipitating factor triggers an acute event over minutes to hours.

Classification of Myocardial Infarction

A. Universal Definition: etiological classification

B. ECG-based clinical classification

1. ST-elevation myocardial infarction (STEMI)
   • Usually due to acute, persistent, complete coronary occlusion.
   • Typically produces transmural ischemia/infarction.
   • Requires immediate reperfusion therapy.
2. Non-ST-elevation myocardial infarction (NSTEMI)
   • Usually due to partial, intermittent, or transient coronary occlusion.
   • Often produces subendocardial infarction.
   • ECG may show ST depression, T-wave inversion, or occasionally be initially normal.

C. Pathological classification

1. Transmural infarction
   • Necrosis involves the full thickness of ventricular wall.
   • Generally follows complete and persistent epicardial coronary occlusion.
   • Often associated with STEMI and pathological Q waves.
2. Subendocardial infarction
   • Necrosis limited to the inner one-third to one-half of ventricular wall.
   • May result from partial coronary obstruction or global hypoperfusion.
   • Usually associated with NSTEMI.

Pathogenesis of Type 1 MI

Stepwise mechanism

1. Atherosclerosis develops
   • Endothelial dysfunction permits LDL entry into the intima.
   • LDL oxidation promotes inflammation.
   • Macrophages ingest lipid and become foam cells.
   • Atherosclerotic plaque forms, with lipid core and fibrous cap.
2. A vulnerable plaque develops
   • Large lipid-rich necrotic core
   • Thin fibrous cap
   • High macrophage/inflammatory-cell content
   • Low smooth-muscle-cell and collagen content
3. Plaque disruption occurs
   • Rupture, erosion, fissuring, ulceration, or intraplaque hemorrhage.
   • Mechanical stress, raised blood pressure, platelet reactivity, and inflammation promote disruption.
4. Thrombosis forms
   • Exposure of collagen, tissue factor, and thrombogenic lipid material causes platelet adhesion, activation, and aggregation.
   • Coagulation cascade produces fibrin-rich thrombus.
   • Vasoconstrictors from platelets can worsen coronary spasm.
5. Coronary blood flow falls abruptly
   • Complete occlusion commonly results in STEMI and transmural necrosis.
   • Partial/transient occlusion commonly causes NSTEMI and subendocardial necrosis.
6. Myocardial ischemia becomes irreversible
   • ATP declines and anaerobic metabolism causes lactate accumulation.
   • Contractility decreases within seconds to minutes.
   • Irreversible myocyte injury begins after approximately 20-30 minutes of severe ischemia.
   • Necrosis progresses from the subendocardium outward, becoming transmural over several hours if flow is not restored.

Short exam flowchart

Key one-line answer

Myocardial infarction usually occurs when rupture or erosion of a vulnerable coronary atherosclerotic plaque causes platelet-rich thrombus formation, acute coronary occlusion, prolonged ischemia, and irreversible myocardial necrosis.

Clinical Features of Acute Myocardial Infarction

1. Chest pain or discomfort

• Site: Retrosternal, precordial, or left-sided chest.
• Character: Heavy, crushing, constricting, squeezing, tightness, pressure, burning, or “weight on the chest.”
• Radiation: Left shoulder and medial aspect of left arm, both arms, neck, throat, jaw, epigastrium, interscapular area, or occasionally right arm.
• Duration: Usually more than 20-30 minutes, often hours.
• Onset: May occur at rest, during sleep, or with minimal exertion. It commonly builds up over several minutes.
• Response to rest/nitrates: Typically not fully relieved by rest or sublingual nitroglycerin, unlike stable angina.

2. Associated symptoms

• Dyspnea due to LV dysfunction, pulmonary congestion, or anxiety
• Sweating: cold, clammy diaphoresis
• Nausea and vomiting, especially with inferior-wall MI due to vagal stimulation
• Palpitations due to arrhythmia
• Weakness, fatigue, dizziness, or light-headedness
• Syncope or presyncope, particularly with arrhythmia, severe bradycardia, or cardiogenic shock
• Anxiety, agitation, or a sense of impending death
• Epigastric discomfort, indigestion, or abdominal discomfort, particularly in inferior MI

Atypical and Silent Presentation

• Older adults
• Women
• People with diabetes mellitus, due to autonomic neuropathy
• Chronic kidney disease
• Dementia or frailty
• Postoperative or critically ill patients

• Sudden unexplained dyspnea
• Isolated nausea/vomiting or epigastric pain
• Weakness, unusual fatigue, or collapse
• Syncope
• Confusion or acute delirium in elderly patients
• Palpitations
• Silent MI detected only by ECG, troponin, or imaging

Physical Signs of MI

1. General appearance

• Patient may look ill, anxious, pale, and sweaty
• Often lies still because movement aggravates the discomfort
• Cool, clammy extremities due to sympathetic activation and poor peripheral perfusion
• Restlessness may be prominent in severe pain or shock

2. Pulse and blood pressure

Pulse

• Sinus tachycardia is common from pain, anxiety, sympathetic discharge, fever, or heart failure.
• Bradycardia may occur in inferior-wall MI due to increased vagal tone or AV nodal ischemia.
• Irregular pulse suggests arrhythmias such as atrial fibrillation, ventricular ectopics, ventricular tachycardia, or conduction block.

Blood pressure

• May be normal initially.
• Hypertension can occur early because of pain and sympathetic stimulation.
• Hypotension suggests:
  • Large LV infarction with pump failure
  • Right ventricular infarction
  • Bradyarrhythmia/tachyarrhythmia
  • Mechanical complication
  • Cardiogenic shock

3. Precordial examination and heart sounds

• S4 gallop: Due to reduced LV compliance and ischemic ventricular stiffness. It may be heard early if the patient is in sinus rhythm.
• S3 gallop: Suggests LV failure, significant LV dysfunction, or a large infarction.
• Soft heart sounds: May occur in low-output states.
• New systolic murmur:
  • Apical pansystolic murmur radiating to axilla suggests acute mitral regurgitation, often from papillary muscle ischemia/dysfunction or rupture.
  • Harsh pansystolic murmur at lower left sternal border suggests ventricular septal rupture.
• Pericardial friction rub: May develop 1-3 days after transmural MI because of acute fibrinous pericarditis.

4. Respiratory signs

• Tachypnea
• Basal fine crepitations/rales
• Reduced oxygen saturation
• Wheeze, sometimes called cardiac asthma
• Pulmonary edema: diffuse crepitations, severe dyspnea, pink frothy sputum in advanced cases

5. Signs of cardiogenic shock

• Cold, mottled, clammy extremities
• Marked hypotension
• Tachycardia, unless bradyarrhythmia is the cause
• Weak, thready pulse
• Oliguria
• Altered sensorium, confusion, or drowsiness
• Peripheral cyanosis
• Elevated JVP may occur, particularly in right ventricular infarction or biventricular failure

6. Signs suggestive of right ventricular infarction

• Hypotension
• Raised JVP
• Clear lung fields, unless there is concurrent LV failure
• Kussmaul sign may be present

Exam-oriented Summary Table

One-line answer

Acute MI usually presents with severe prolonged retrosternal pressure radiating to the left arm, shoulder, neck, jaw, or epigastrium, associated with sweating, dyspnea, nausea, vomiting, anxiety, and palpitations; examination may show pallor, diaphoresis, tachycardia or bradycardia, S4/S3 gallop, basal crepitations, hypotension, murmurs of mechanical complications, or signs of cardiogenic shock.

Serial ECG Changes in Acute STEMI: Day 0 to Day 7

Sequence to remember

Hyperacute T wave → ST elevation → pathological Q wave → T-wave inversion → ST returns to baseline, Q wave may persist

1. Hyperacute T Waves

• Tall
• Broad-based
• Symmetrical
• Often seen in leads overlying the infarct area
• Not simply “peaked” as in hyperkalemia

2. ST-Segment Elevation

• ST elevation in two or more anatomically contiguous leads
• May become convex or merge with the T wave to form a “tombstone” appearance.
• Reflects acute myocardial injury.

Reciprocal ST depression

3. Pathological Q Waves

• Q wave duration ≥ 0.04 second, and/or
• Q-wave depth at least 25% of the following R wave in relevant leads.

4. T-Wave Inversion

• Symmetrical, often deep T-wave inversion
• Usually persists for days to weeks
• May gradually normalize over weeks or months

Important Exception: Persistent ST Elevation

• Persistent coronary occlusion or reinfarction
• Pericarditis
• Left ventricular aneurysm, especially after a large anterior MI

STEMI Versus NSTEMI

NSTEMI ECG

• ST-segment depression
• T-wave inversion
• Transient ST elevation that resolves
• A normal ECG initially

Short Exam Answer

In acute STEMI, the earliest ECG change is a tall, broad-based hyperacute T wave. This is followed within minutes to hours by ST-segment elevation in contiguous leads with reciprocal ST depression in opposite leads. Within hours to 1 day, R-wave loss and pathological Q waves develop. Over the next 1-3 days, ST elevation gradually regresses and T waves invert. By day 5-7, the ST segment usually returns to baseline, while deep T-wave inversion and pathological Q waves persist. Q waves may remain permanently, whereas T-wave inversion may resolve over weeks to months.