What is MI
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Here is a thorough overview of Myocardial Infarction (MI) drawn from authoritative medical textbooks:
Myocardial Infarction (MI) - "Heart Attack"
Definition
Myocardial infarction (MI) is necrosis (death) of heart muscle resulting from ischemia - an inadequate supply of oxygenated blood to the myocardium. The 2018 joint U.S./European Cardiology 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 & Kumar Basic Pathology, p. 354
Causes & Pathogenesis
The vast majority (~90%) of MIs are caused by acute thrombosis within a coronary artery, triggered by rupture or erosion of an atherosclerotic plaque. The sequence of events:
- An atheromatous plaque is disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces, exposing subendothelial collagen and necrotic plaque contents.
- Platelets adhere, aggregate, and activate, releasing thromboxane A2, ADP, and serotonin - causing further platelet aggregation and vasospasm.
- Coagulation is activated via tissue factor, building a growing thrombus.
- Within minutes, the thrombus completely occludes the coronary artery.
In ~10% of MIs, no occlusive atherosclerosis is found. These cases involve:
-
Coronary artery vasospasm
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Embolization from mural thrombi (e.g., atrial fibrillation) or valve vegetations
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Small vessel disease: vasculitis, amyloid deposition, sickle cell stasis
-
Robbins & Kumar Basic Pathology, p. 354
Classification: Types of MI
| Type | Mechanism |
|---|---|
| Type 1 | Spontaneous ischemia from atherosclerotic plaque rupture/erosion + thrombus |
| Type 2 | Oxygen supply-demand imbalance WITHOUT plaque rupture (e.g., severe tachycardia, anemia, hypotension) |
By ECG Pattern (Clinical Subtypes)
| Subtype | ECG Finding | Extent |
|---|---|---|
| STEMI | ST-segment elevation in ≥2 contiguous leads | Transmural (full-thickness) |
| NSTEMI | No ST elevation; elevated troponin | Subendocardial |
| Unstable Angina (UA) | ECG changes but NO troponin rise | No necrosis (ischemia only) |
- STEMI criteria: new ST elevation ≥0.1 mV at J-point in ≥2 contiguous leads (≥0.2 mV in V2-V3 in men ≥40 yrs)
- Frameworks for Internal Medicine; Robbins Pathology
Myocardial Response to Ischemia
Within seconds: aerobic metabolism ceases → ATP drops → lactic acid accumulates.
Within minutes: loss of contractility.
At 20-40 minutes: irreversible cell death (coagulative necrosis) begins.
-
The subendocardium is most vulnerable - it has the highest oxygen demand and its blood vessels are compressed by systolic contraction.
-
Necrosis starts in the subendocardium and expands outward in a "wavefront" pattern.
-
A full transmural infarct achieves maximum extent in 3-6 hours without intervention.
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Cardiac muscle needs ~1.3 mL O2/100g/min to survive; normal delivery is ~8 mL O2/100g/min. Even 15-30% of normal flow can prevent death.
-
Guyton and Hall Textbook of Medical Physiology, p. 271
Locations of MI (by Vessel)
| Artery Occluded | Area Infarcted | % of MIs |
|---|---|---|
| LAD (proximal) | Anterior LV wall, anterior 2/3 of septum, apex | 40-50% |
| RCA (proximal) | Right ventricle, posterior LV | 30-40% |
| LCX (proximal) | Lateral left ventricle | 15-20% |
- Robbins & Kumar Basic Pathology, p. 355
Patterns of Infarction
- Transmural infarction: Full-thickness necrosis; caused by epicardial vessel occlusion with thrombosis. Produces Q waves on ECG (STEMI).
- Subendocardial infarction: Restricted to the inner <1/2 of ventricular wall; corresponds to NSTEMI. More common when there is diffuse severe atherosclerosis without complete occlusion.
Causes of Death After MI
- Decreased cardiac output and cardiogenic shock (systolic stretch - ischemic muscle bulges outward instead of contracting)
- Pulmonary edema from damming of blood in pulmonary vessels
- Ventricular fibrillation - the most common cause of death (80-90% of cardiac deaths post-MI)
- Cardiac rupture (less common)
- Guyton and Hall Textbook of Medical Physiology, p. 271
Epidemiology (2025 ACC/AHA Data)
- ~805,000 MIs per year in the U.S. (605,000 first-time; 200,000 recurrent)
- Economic burden: ~$84.9 billion annually
- ~10% of MIs occur before age 40; ~45% before age 65
- Men are at greater risk, but the gap narrows with age (women are relatively protected pre-menopause)
- Mortality has declined thanks to early reperfusion and evidence-based prevention
Key Biomarker: Troponin
The earliest detectable sign of myocyte necrosis is disruption of the sarcolemmal membrane, allowing intracellular proteins - especially cardiac troponin I and T - to leak into the bloodstream. This is the basis of the troponin blood test used to diagnose MI.
Summary
MI = blocked coronary artery → ischemia → myocardial cell death. The key points are:
- Most are caused by plaque rupture + thrombus
- Time is muscle - intervention within 3-6 hours limits infarct size
- Classified as STEMI (transmural, needs immediate reperfusion) vs. NSTEMI (subendocardial)
- Diagnosed by troponin rise + ECG changes + symptoms
- The #1 cause of death post-MI is ventricular fibrillation
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