Myocardial Infarction (MI)

Definition

MI, commonly called a "heart attack," is necrosis (death) of heart muscle resulting from prolonged ischemia. The 2018 joint task force of U.S. and European cardiology groups defines it as "the presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischemia."

Roughly 800,000 people in the United States experience an MI each year (nearly one every 40 seconds), causing almost 400,000 deaths annually.

Robbins, Cotran & Kumar Pathologic Basis of Disease

Causes and Risk Factors

The major underlying cause is atherosclerosis (coronary artery disease)
~10% of MIs occur before age 40; ~45% before age 65
Men are at greater risk than women, though the gap narrows after menopause (decline in estrogen leads to worsening coronary artery disease)
In ~10% of cases, MI occurs without classic atherothrombosis, due to:
- Coronary vasospasm (e.g., cocaine, ephedrine use)
- Embolism (from left atrial thrombus in atrial fibrillation, endocarditis vegetations, prosthetic valves)
- Microvessel pathology (vasculitis, amyloid, sickle cell disease)

Pathogenesis - How MI Develops

The typical sequence:

An atheromatous plaque is disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces, exposing subendothelial collagen
Platelets adhere, aggregate, and activate - releasing thromboxane A2, ADP, and serotonin, causing further aggregation and vasospasm
Coagulation is activated via tissue factor exposure, enlarging the thrombus
Within minutes, the thrombus completely occludes the coronary artery lumen

Angiography within 4 hours of MI onset demonstrates coronary thrombosis in ~90% of cases. Early thrombolysis and/or angioplasty can be highly effective in limiting the extent of necrosis.

Types of MI (by Location/Extent)

Distribution of myocardial ischemic necrosis based on coronary artery occlusion - showing transmural vs non-transmural infarcts

Type	Cause	Pattern
Transmural (STEMI)	Complete occlusion of epicardial vessel	Full-thickness wall necrosis in distribution of one coronary artery
Subendocardial (NSTEMI)	Partial/transient occlusion, or global hypotension	Inner layer necrosis; may be regional or circumferential
Microinfarction	Small intramural vessel occlusion (embolism, vasculitis)	Multifocal scattered infarcts

Coronary artery territory:

Left Anterior Descending (LAD): anterior wall + anterior interventricular septum (most common)
Right Coronary Artery (RCA): posterior wall, posterior septum, inferior-posterior left ventricle
Left Circumflex (LCX): lateral wall of left ventricle

ECG Changes

Three major electrical changes occur (per Ganong's Review of Medical Physiology):

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

Acute MI hallmark: ST elevation in leads overlying the infarct; ST depression in opposite leads
After days/weeks: ST changes resolve; Q waves may appear (indicating dead myocardium)

Clinical Features

Chest pain: Prolonged (>30 min), crushing/squeezing/stabbing, typically radiating to arm, jaw, or back
Diaphoresis (profuse sweating)
Nausea and vomiting (especially posterior-inferior MI with vagal stimulation)
Dyspnea (due to impaired contractility and pulmonary congestion)
Up to 25% are silent (especially in diabetics due to neuropathy)

Diagnosis

Cardiac Biomarkers (most important):

Troponin T and I (cTnT, cTnI) are the most specific and sensitive markers
- Begin rising ~3-6 hours after MI onset
- Peak at ~24-48 hours
- Remain elevated for up to ~10-14 days (cTnI) or ~14-21 days (cTnT)
CK-MB: rises earlier, used for reinfarction detection

ECG and Imaging (echocardiography, coronary angiography) complete the workup.

Causes of Death After MI

Per Guyton & Hall Textbook of Medical Physiology:

Decreased cardiac output (cardiogenic shock, systolic stretch/paradoxical expansion of infarcted zone)
Pulmonary edema (blood damming in pulmonary vessels)
Ventricular fibrillation (most common early cause of death)
Cardiac rupture (rare, occurs 3-7 days after MI)

Reperfusion and Its Effects

Restoring blood flow (via thrombolysis, angioplasty/PCI, or CABG) is the cornerstone of treatment. However, reperfusion injury can occur:

Mitochondrial dysfunction with apoptosis
Myocyte hypercontracture from calcium overload (contraction band necrosis on histology)
Free radical generation (superoxide, H2O2, hydroxyl radicals)
Leukocyte aggregation causing the "no-reflow" phenomenon

Two important post-ischemic phenomena:

Stunned myocardium: prolonged contractile dysfunction after short-term ischemia that eventually recovers
Hibernating myocardium: chronically reduced function in chronically ischemic muscle; can recover after revascularization

Universal Classification (5 Types)

Type	Mechanism
Type 1	Atherosclerotic plaque rupture/erosion with thrombus (classic)
Type 2	Supply-demand mismatch without plaque rupture (e.g., spasm, anemia, tachycardia)
Type 3	Sudden cardiac death before biomarkers can be measured
Type 4	PCI-related (during or after coronary intervention)
Type 5	CABG surgery-related

Sources: Robbins, Cotran & Kumar - Pathologic Basis of Disease | Robbins & Kumar Basic Pathology | Guyton & Hall Textbook of Medical Physiology | Ganong's Review of Medical Physiology

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