what is MI
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Here is a thorough overview of Myocardial Infarction (MI):
Myocardial Infarction (MI)
Definition
MI (heart attack) is necrosis of heart muscle resulting from ischemia - defined by the 2018 joint U.S./European Cardiology task force 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
- Guyton and Hall Textbook of Medical Physiology
Causes & Risk Factors
- Primary cause: Atherosclerosis of coronary arteries
- Most MIs are triggered by rupture or erosion of an atherosclerotic plaque, which acts as a nidus for thrombus formation
- ~10% of MIs occur without occlusive atherosclerosis - due to vasospasm, embolism (e.g., from atrial fibrillation), vasculitis, amyloid deposition, or sickle cell disease
- Risk increases with age, male sex (gap narrows post-menopause), hypertension, diabetes, smoking, hyperlipidemia
Pathogenesis (Step by Step)
- An atheromatous plaque is eroded or disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces - exposing subendothelial collagen and necrotic plaque contents
- Platelets adhere and aggregate, releasing thromboxane A2, ADP, and serotonin - causing further aggregation and vasospasm
- Coagulation is activated via tissue factor exposure, adding to the growing thrombus
- Within minutes, the thrombus may completely occlude the coronary lumen
Angiography within 4 hours of MI demonstrates coronary thrombosis in nearly 90% of cases.
Types of MI
| Type | Description |
|---|---|
| STEMI | ST-elevation MI - complete occlusion, transmural infarction, full-thickness muscle death |
| NSTEMI | Non-ST-elevation MI - partial/subtotal occlusion, subendocardial infarction |
| Subendocardial MI | Inner layer most vulnerable (highest O2 demand, most compressed vessels during systole) |
| Transmural MI | Full-thickness infarction of the ventricular wall |
What Happens to the Myocardium
- After occlusion, the infarcted area receives no functional blood flow
- Muscle becomes bluish-brown, vessels appear engorged, capillary walls become permeable causing edema
- Cardiac muscle requires ~1.3 mL O2 / 100g / min just to survive; if collateral flow provides 15-30% of normal, muscle survives - but in the central infarct zone with no collateral flow, cells die within hours
- Guyton and Hall Textbook of Medical Physiology
Consequences / Causes of Death
- Decreased cardiac output - systolic stretch of ischemic muscle reduces ventricular pumping
- Pulmonary edema - backup of blood into pulmonary circulation
- Ventricular fibrillation - most common cause of sudden death post-MI
- Cardiac rupture - rare but catastrophic complication
Diagnosis
- ECG: ST elevation (STEMI) or ST depression/T-wave changes (NSTEMI)
- Cardiac biomarkers: Troponin I/T (most sensitive & specific), CK-MB
- Imaging: Echocardiography (wall motion abnormalities), coronary angiography
Treatment Principles
- Reperfusion is the priority: thrombolysis or percutaneous coronary intervention (PCI/angioplasty)
- Early intervention limits the extent of necrosis
- Antiplatelet therapy (aspirin, P2Y12 inhibitors), anticoagulation, beta-blockers, ACE inhibitors
- Risk of death after STEMI in the developed world is approximately 10%
In summary: MI is ischemic death of heart muscle, most commonly from atherosclerotic plaque rupture triggering coronary thrombosis. Rapid diagnosis via ECG and troponins, and fast reperfusion therapy, are the cornerstones of management.
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