119. Acute coronary syndromes (unstable angina pectoris, Prinzmetal angina) - etiology, pathogenesis, clinical manifestations.

Acute coronary syndromes (unstable angina pectoris, Prinzmetal angina) – etiology, pathogenesis, and clinical manifestations.

ACS refers to a spectrum of acute myocardial ischemic states, typically caused by sudden reduction in coronary blood flow, including:

Unstable angina pectoris.

Non- ST- segment elevation myocardial infarction (NSTEMI).

ST- segment elevation myocardial infarction (STEMI).

Etiology

Common general cause (for ACS)

Atherosclerotic plaque rupture or erosion, leading to thrombosis and acute reduction of coronary blood flow.

I. Unstable angina pectoris

Specific etiology

Rupture or erosion of an atherosclerotic plaque → platelet aggregation → subocclusive thrombus.

Severe fixed coronary artery stenosis with superimposed vasoconstriction or microthrombi.

Pathogenesis

1. Plaque disruption exposes subendothelial collagen and necrotic lipid core.
2. Platelet adhesion and aggregation → local thrombus formation.
3. Thrombus causes transient or incomplete occlusion → episodic ischemia at rest or with minimal exertion.
4. No significant myocyte necrosis (no release of cardiac biomarkers).

Clinical manifestations

Crescendo angina: increased frequency, duration, or severity of chest pain.

Occurs at rest or with minimal exertion, often lasts >20 minutes.

Not completely relieved by nitroglycerin or rest.

Possible new- onset severe angina.

Associated symptoms: dyspnea, sweating, nausea.

II. Prinzmetal angina (variant angina )

Specific etiology

Focal coronary artery spasm, usually in a segment with or without mild atherosclerosis.

Trigger factors: cold exposure, stress, certain drugs (e.g., cocaine), hyperventilation.

Pathogenesis

1. Transient coronary artery spasm → temporary, significant reduction in blood flow.
2. Occurs independently of exertion.
3. No plaque rupture or thrombus (mainly functional vasospasm).

Clinical manifestations

Rest angina, typically at night or early morning.

Transient ST-segment elevation during attacks (resolves with nitroglycerin or calcium channel blockers).

Pain similar to classic angina but not provoked by effort.

Usually no permanent myocardial damage if promptly relieved.

Summary table