Myocardial infarction

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Myocardial Infarction (MI)

Definition

MI ("heart attack") is necrosis of cardiac muscle resulting from prolonged ischemia. The 2018 joint ESC/ACC/AHA task force defines it as "the presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischemia." - Robbins Basic Pathology, p. 357

Approximately 800,000 Americans experience MI annually - nearly one every 40 seconds - causing ~400,000 deaths/year. About 10% occur before age 40 and 45% before age 65.

Pathogenesis

Typical Mechanism (90% of cases)

The classic sequence of events in plaque disruption-mediated MI:

An atheromatous plaque is eroded or suddenly disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces - exposing subendothelial collagen and necrotic plaque contents to blood
Platelets adhere, aggregate, and activate, releasing thromboxane A2, ADP, and serotonin - causing further platelet aggregation and vasospasm
Coagulation is activated by exposed tissue factor, building the thrombus
Within minutes, the enlarging thrombus can completely occlude the coronary artery lumen

When angiography is performed within 4 hours of MI onset, coronary thrombosis is demonstrated in nearly 90% of cases. At 12-24 hours (without intervention), only 60% show thrombosis - some occlusions clear spontaneously via thrombus lysis or spasm relaxation. This is the therapeutic rationale for early thrombolysis/angioplasty.

Robbins & Cotran Pathologic Basis of Disease, p. 511

Atypical Causes (~10%)

Vasospasm (with or without atherosclerosis) - cocaine, ephedrine
Embolism from left atrial mural thrombus (in AF), infective endocarditis vegetations, prosthetic material, or paradoxical embolism via patent foramen ovale
Severe fixed coronary stenosis with a period of increased demand (tachycardia, hypertension) - causes subendocardial infarction
Small vessel disease: vasculitis, amyloid deposition, sickle cell disease

Coronary Artery Territories and Infarct Sites

Artery	Frequency	Territory Infarcted
LAD	40-50%	Anterior LV wall near apex; anterior ventricular septum; apex circumferentially
RCA	30-40%	Inferior/posterior LV wall; posterior septum; inferior/posterior RV free wall (in some)
LCx	15-20%	Lateral LV wall (except apex)

Of RCA occlusions, 15-30% extend into the right ventricular wall. Isolated RV infarction occurs in only 1-3% of cases.
Robbins & Cotran, p. 512

Morphologic Evolution (Timeline)

The gross and microscopic changes evolve in a predictable sequence:

Time Frame	Gross Features	Light Microscopy	Key Points
0-30 min	None	None	Reversible injury; EM shows myofibril relaxation, glycogen loss, mitochondrial swelling
30 min - 4 hr	None	Usually none; wavy fibers at border	Irreversible: sarcolemmal disruption, mitochondrial amorphous densities
4-12 hr	Occasional dark mottling	Coagulative necrosis begins; edema; hemorrhage	-
12-24 hr	Dark mottling	Coagulative necrosis ongoing; nuclear pyknosis; hypereosinophilic myocytes; contraction band necrosis; early neutrophil infiltrate	Gross ID possible as reddish-blue area from congestion
3-7 days	Soft, yellow-tan; hyperemic rim	Neutrophil infiltration peaks, then disappears; macrophage infiltration begins	Rimmed by highly vascularized granulation tissue
1-3 weeks	Yellow-tan, soft, depressed	Granulation tissue replaces necrotic area	Progressive fibrosis
>6 weeks	Gray-white scar	Dense fibrous scar	Stable; no regeneration of cardiomyocytes

Staining trick: Triphenyl tetrazolium chloride (TTC) - viable myocardium stains brick-red (lactate dehydrogenase intact); infarcted zone stays pale/unstained (LDH leaks out). Useful for infarcts >3 hours old.

Robbins Basic Pathology, p. 357; Robbins & Cotran, p. 512

ECG Changes - Electrophysiology

Three major membrane abnormalities cause ECG changes in acute MI (Ganong's Physiology):

Defect in Infarcted Cells	Current Flow	ECG Change (leads over infarct)
Rapid repolarization (accelerated K+ channel opening)	Out of infarct	ST segment elevation
Decreased resting membrane potential (loss of intracellular K+)	Into infarct	TQ depression (recorded as ST elevation)
Delayed depolarization	Out of infarct	ST segment elevation

Hallmark of acute MI: ST segment elevation in leads overlying the infarcted area; ST depression in leads on the opposite side
After days to weeks: ST changes subside; dead muscle becomes electrically silent
Q waves may appear (reflects electrically silent dead tissue during systole)
Non-Q-wave infarcts tend to be less severe but have a higher rate of subsequent reinfarction
Ganong's Review of Medical Physiology, 26th ed., p. 534

Clinical Features

Chest pain: severe, crushing/pressure-like, substernal, may radiate to left arm, jaw, or back; typically >20 minutes and not relieved by nitrates
Diaphoresis, nausea, vomiting
Dyspnea (from LV dysfunction)
Sense of impending doom
Silent MI: common in diabetics and elderly (no chest pain)

Biomarkers:

Troponin I/T: gold standard; rises within 3-4 hours, peaks at 24-48 hours, elevated for up to 10-14 days
CK-MB: rises within 4-6 hours, normalizes within 48-72 hours - useful for detecting reinfarction
Myoglobin: earliest to rise (1-2 hours) but non-specific

Types of MI

STEMI (ST-elevation MI): full-thickness (transmural) occlusion - requires emergent reperfusion
NSTEMI (Non-ST-elevation MI): partial occlusion or spontaneous reperfusion - managed with early invasive strategy
Type 1 MI: plaque rupture/erosion with thrombus
Type 2 MI: supply-demand mismatch (e.g., severe anemia, tachyarrhythmia, coronary spasm) without primary plaque rupture

Complications

Nearly three-quarters of patients experience one or more complications after acute MI. Overall in-hospital death rate is <7% (STEMI ~9%, NSTEMI ~6%), but out-of-hospital STEMI mortality is ~33% - most die from arrhythmia within 1 hour.

Fig. 12.17 - Robbins & Cotran: Complications of MI

Complication	Details
Contractile dysfunction	LV failure proportional to volume of damage; cardiogenic shock in ~10% of transmural MIs (requires ≥40% LV damage)
Papillary muscle dysfunction	Postinfarct mitral regurgitation; papillary muscle rupture is rare but catastrophic
RV infarction	With RCA occlusion; leads to right heart failure and systemic hypotension
Free wall rupture	1-3% of MIs; usually fatal hemopericardium and cardiac tamponade (days 3-7, when necrosis is maximal)
Ventricular septal rupture	Creates VSD with left-to-right shunt
Papillary muscle rupture	Severe acute mitral regurgitation; acute pulmonary edema
Mural thrombus	Forms over akinetic endocardium; risk of systemic embolism
Ventricular aneurysm	Late complication; paradoxical bulging during systole; predisposes to arrhythmias, mural thrombus, and HF
Arrhythmias	Most common early cause of death; VF accounts for most out-of-hospital deaths; reentry circuits from disrupted gap junctions
Fibrinous pericarditis	Dressler syndrome (autoimmune) - occurs weeks post-MI
Heart block	AV node dysfunction; ranges from 1st degree to complete block

Robbins & Cotran Pathologic Basis of Disease, pp. 513-518

Treatment (Acute Management)

STEMI - Reperfusion is the Priority ("Time is Muscle")

Primary PCI (percutaneous coronary intervention): preferred if available within 90 minutes of first medical contact - balloon inflation within 120 minutes of symptom onset
Thrombolytics (e.g., alteplase, tenecteplase): if PCI not available within 120 minutes; must be given within 12 hours of symptom onset; contraindicated in prior stroke, active bleeding, recent surgery

Pharmacological Treatment (Both STEMI and NSTEMI)

Drug Class	Agent	Purpose
Dual antiplatelet	Aspirin + P2Y12 inhibitor (ticagrelor, clopidogrel, prasugrel)	Prevent further thrombus; ticagrelor/prasugrel preferred over clopidogrel
Anticoagulation	Heparin (UFH or LMWH), or bivalirudin	Prevent thrombus extension
Beta-blocker	Metoprolol, carvedilol	Reduce heart rate/demand; reduce arrhythmia risk; reduce infarct size
ACE inhibitor/ARB	Ramipril, lisinopril	Reduce LV remodeling; mortality benefit especially with reduced EF
Statin	Atorvastatin 80 mg	Plaque stabilization; secondary prevention
Nitrates	GTN/nitroglycerin	Symptom relief; reduce preload; NOT for hypotension or RV infarction
Morphine	IV morphine	Pain relief (use cautiously - may delay P2Y12 absorption)
Oxygen	Only if SpO2 <90%	Avoid routine oxygen - may increase infarct size in normoxic patients

NSTEMI - Antithrombotic and Risk Stratification

High-risk NSTEMI: early invasive strategy (coronary angiography within 24 hours)
Low-risk: conservative/ischemia-guided strategy

Secondary Prevention

Lifelong aspirin + statin
Beta-blocker for at least 1 year (longer if reduced EF)
ACE inhibitor/ARB indefinitely if EF <40% or HF
Aldosterone antagonist (eplerenone) if EF <40% + HF or diabetes
Cardiac rehabilitation
Lifestyle modification: smoking cessation, diet, exercise, weight loss

Key Pathophysiology Summary

Plaque rupture/erosion
        ↓
Platelet adhesion → aggregation → TXA2, ADP, serotonin release
        ↓
Tissue factor exposure → coagulation cascade
        ↓
Coronary occlusion → ischemia → ATP depletion
        ↓
     < 20 min: reversible injury
     > 20 min: irreversible necrosis
        ↓
Coagulative necrosis → inflammatory infiltration → scar formation

Sources: Robbins & Cotran Pathologic Basis of Disease (10th ed.); Robbins Basic Pathology (11th ed.); Ganong's Review of Medical Physiology (26th ed.); Braunwald's Heart Disease (12th ed.)

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