Acute coronary syndromes (myocardial infarction) – classification, etiology, pathogenesis, and clinical manifestations.
Myocardial infarction is necrosis of cardiac myocytes caused by prolonged severe ischemia, typically from abrupt reduction of coronary blood flow.
Classification
By ECG changes
By extent
Transmural infarction: full wall thickness.
Subendocardial infarction: inner third to half of wall.
By location (common examples)
Anterior wall (LAD occlusion).
Inferior wall (RCA occlusion).
Lateral wall (LCX occlusion).
Etiology
Primary cause (most common)
- Atherosclerotic plaque rupture or erosion → acute thrombosis → complete occlusion of coronary artery.
Predisposing factors
- Same as for atherosclerosis:
- Hypertension.
- Hyperlipidemia.
- Diabetes mellitus.
- Smoking.
- Obesity.
- Sedentary lifestyle.
Pathogenesis
- Plaque rupture/erosion exposes subendothelial collagen and necrotic lipid core.
- Platelet adhesion and aggregation, activation of the coagulation cascade.
- Thrombus formation leads to sudden, severe reduction or complete cessation of blood flow.
- Oxygen supply-demand imbalance causes myocardial ischemia.
- Irreversible myocyte necrosis begins within 20–30 minutes of complete occlusion.
- Progression from subendocardial zone outward ("wavefront phenomenon") if not reperfused.
Clinical manifestations
Pain
- Severe, prolonged chest pain (>20 minutes).
- Crushing, squeezing, or pressure- like.
- Retrosterna, may radiate to left arm, neck, jaw, or back.
- Not relieved by rest or nitroglycerin.
Autonomic symptoms
- Diaphoresis (profuse sweating).
- Cold, clammy skin (sympathetic activation).
- Nausea, vomiting.
Dyspnea
- Due to acute left ventricular dysfunction → pulmonary congestion.
Other signs
- Anxiety ("feeling of impending doom").
- Weakness, fatigue.
- Arrhythmias (palpitations, sudden cardiac arrest).
Silent infarction
- More common in elderly and diabetics due to autonomic neuropathy.