Angina pectoris, chronic ischemic heart disease

1. Concept

Ischemic heart disease (IHD) = imbalance between coronary supply and myocardial O₂ demand. ~90% from reduced supply (coronary atherosclerosis), ~10% from increased demand (hypertrophy/HTN). Four syndromes: angina pectoris, AMI, chronic IHD, sudden cardiac death.

2. Angina pectoris

Transient (seconds–10 min), reversible ischemia causing chest pain — no necrosis.

Type	Trigger	Mechanism	ECG / relief
Stable (typical)	Exertion / ↑demand	Fixed AS plaque >75%	ST depression; relieved by rest/nitroglycerin
Unstable (crescendo)	At rest, ↑frequency/intensity	Plaque disruption • thrombosis (microinfarcts)	Pre-infarction warning
Prinzmetal (variant)	At rest	Coronary vasospasm (± plaque)	ST elevation; relieved by vasodilators

• Stable = ST depression (subendocardial); Prinzmetal = ST elevation (transmural, spasm). Nitroglycerin = venodilation → ↓preload → ↓cardiac work.

3. Chronic ischemic heart disease (CIHD)

• Progressive heart failure from cumulative ischemic myocardial damage (slow, allows preventive measures).
• Causes: post-MI scarring, hypertension (hypertrophy → ↑demand), diffuse coronary atherosclerosis → patchy necrosis/fibrosis.
• Morphology: enlarged heart, LV dilation + hypertrophy, patchy myocardial fibrosis (white scars), moderate-severe coronary AS, fibrous endocardial thickening.
• Consequences: progressive pump failure (decompensation), arrhythmias (fibrosis disrupts conduction).

💡 High-yield: Angina = reversible ischemia, no necrosis. Stable (exertion, fixed >75% plaque, ST depression, relieved by rest/nitro) → Unstable (rest, plaque rupture, pre-infarction) → Prinzmetal (vasospasm, ST elevation). CIHD = chronic progressive HF from ischemia → patchy fibrosis, LV dilation/hypertrophy, arrhythmias.