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"myocardial infarction"[MeSH Terms] AND "management"[MeSH Terms]

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Myocardial Infarction (MI)

Definition

MI, commonly called a "heart attack," is the death of cardiac muscle tissue due to prolonged ischemia. In the United States, approximately 800,000 MIs occur each year - nearly one every 40 seconds - causing around 400,000 deaths annually. The major underlying cause is atherosclerosis.

Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 511

Pathogenesis

The most common sequence of events:

Plaque disruption - An atheromatous plaque is eroded or suddenly ruptured by endothelial injury, intraplaque hemorrhage, or mechanical forces, exposing subendothelial collagen and necrotic plaque contents to blood.
Platelet activation - Platelets adhere, aggregate, and release thromboxane A2, ADP, and serotonin, causing further platelet aggregation and vasospasm.
Coagulation cascade - Activation via tissue factor adds to the growing thrombus.
Occlusion - Within minutes, the thrombus can completely occlude the coronary artery lumen.

When angiography is performed within 4 hours of MI onset, thrombotic occlusion is demonstrated in ~90% of cases.

In approximately 10% of cases, MI occurs without typical coronary atherothrombosis. Other causes include:

Vasospasm (with or without atherosclerosis; drugs like cocaine or ephedrine)
Embolism (from left atrial thrombus in AF, infective endocarditis vegetations, or prosthetic material)
Uncommon causes: vasculitis, sickle cell disease, amyloid deposition, vascular dissection, severe myocardial hypertrophy, systemic hypotension, or inadequate myocardial protection during cardiac surgery
Robbins, Cotran & Kumar Pathologic Basis of Disease, pp. 511-512

Cellular Sequence of Injury

Time After Occlusion	Event
Seconds	Cessation of aerobic metabolism, lactic acid accumulation
~1 minute	Loss of myocardial contractility
Minutes	Ultrastructural changes (myofibrillar relaxation, glycogen depletion, cell/mitochondrial swelling) - still reversible
20-30 min (at <10% flow)	Irreversible myocyte necrosis begins
6-12 hours	Necrosis becomes complete

The first detectable sign of necrosis is disruption of the sarcolemmal membrane, allowing intracellular proteins (e.g. troponin) to leak into the bloodstream - the basis for cardiac biomarker testing.

Necrosis starts in the subendocardial zone (most vulnerable because it receives blood last from epicardial vessels and experiences the highest intramural compression), then spreads outward as a wavefront toward the epicardium.

Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 512
Guyton and Hall Textbook of Medical Physiology, p. 271

Types of MI by Extent

Type	Mechanism
Transmural infarction	Full-thickness necrosis from complete epicardial vessel occlusion; associated with atherosclerosis + acute plaque change + superimposed thrombus
Subendocardial (non-transmural) infarction	Plaque disruption with spontaneous or therapeutic lysis before full-thickness necrosis; or global hypotension superimposed on chronic stenoses (circumferential pattern)
Multifocal microinfarction	Pathology involving only smaller intramural vessels (microembolization, vasculitis, catecholamine-induced vasospasm)

Morphological Evolution

Time	Gross Appearance	Microscopic Appearance
0-12 hours	None visible (may see "coagulative" pallor late)	Wavy fibers, coagulative necrosis, edema
1-3 days	Pale/yellow-tan area	Dense neutrophil infiltration
7-10 days	Yellow-tan center, hyperemic border	Macrophage phagocytosis of necrotic cells
2-4 weeks	Gelatinous/fibrotic	Granulation tissue (loose collagen, capillaries)
2+ months	White scar	Dense collagenous scar; residual myocytes show compensatory hypertrophy

Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 513-515

ECG Changes

Three major ECG abnormalities occur in acute MI (per Ganong's Review of Medical Physiology):

Defect in Infarcted Cells	Current Flow	ECG Change (leads over infarct)
Rapid repolarization	Out of infarct	ST segment elevation
Decreased resting membrane potential	Into infarct	TQ depression (appears as ST elevation)
Delayed depolarization	Out of infarct	ST segment elevation

The hallmark of acute MI is ST segment elevation in leads overlying the infarcted area (STEMI). Leads on the opposite side show ST depression (reciprocal changes).

After days to weeks:

ST changes resolve
Q waves may appear (representing electrically silent scar)
Non-Q-wave infarcts also occur (less severe, but higher risk of reinfarction)

Causes of Death After MI

Decreased cardiac output / cardiogenic shock - due to "systolic stretch" where ischemic muscle bulges outward during contraction instead of contributing to ejection
Pulmonary edema - from blood damming in the pulmonary vasculature
Ventricular fibrillation - the most feared early complication
Cardiac rupture - occurs at the junction of infarcted and viable myocardium (days 3-7)

Guyton and Hall Textbook of Medical Physiology, p. 271

Reperfusion and Treatment Principle

The therapeutic goal is to restore perfusion as quickly as possible - "time is myocardium." Methods include:

Thrombolysis (tissue plasminogen activator)
Percutaneous coronary intervention (PCI) / angioplasty
Coronary artery bypass grafting (CABG)

However, late reperfusion can cause reperfusion injury, potentially contributing to up to 50% of the final infarct size, through:

Mitochondrial dysfunction and apoptosis
Myocyte hypercontracture (from calcium overload)
Free radical generation (O2-, H2O2, peroxynitrite, OH-)
Leukocyte aggregation causing the "no-reflow" phenomenon
Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 515

Risk Factors

Age (risk rises progressively; 45% of MIs occur before age 65)
Male sex (females are relatively protected until menopause)
Atherosclerotic risk factors: hypertension, dyslipidemia, diabetes, smoking
Post-menopausal estrogen decline (associated with worsening coronary artery disease)
Note: post-menopausal hormone replacement therapy has NOT been shown protective and may even be detrimental (pro-thrombotic effect)

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