Angina Pectoris

Overview

Angina = IHD syndrome from transient reversible myocardial ischaemia. Paroxysmal substernal/precordial pain, worse with ↑demand, relieved by rest. Radiates to left arm/neck/jaw/right arm. Men >5th decade. With acute MI + sudden cardiac death = acute coronary syndrome triad.

Three patterns (distinct mechanisms, not just severity grades)

1. Stable (typical) angina — commonest. Pain on exertion/emotion, relieved by rest. Pathogenesis: fixed stenosing coronary atherosclerosis — can’t meet ↑demand though adequate at rest. ECG: ST DEPRESSION (subendocardial ischaemia — last territory perfused, first to suffer). NO enzyme rise (reversible, no irreversible injury).

2. Prinzmetal’s variant angina — pain AT REST, unrelated to activity (opposite trigger pattern). Pathogenesis: not fully known — (i) sudden coronary vasospasm (on top of atherosclerosis) or (ii) mast cell humoral vasoconstrictors in adventitia. TRANSMURAL ischaemia → ECG: ST ELEVATION (opposite direction from stable angina). Responds well to vasodilators (nitroglycerin) — supports vasospasm mechanism.

3. Unstable (crescendo) angina — “pre-infarction angina”/“acute coronary insufficiency.” Most serious pattern. More frequent, longer, often at rest pain — WORSENING over time. Signals impending MI. Pathogenesis (multifactorial): stenosing atherosclerosis + complicated plaques (thrombosis, haemorrhage, rupture, ulceration) + platelet thrombi + vasospasm. Often in a branch vessel → collaterals prevent full infarction despite severity.

Unstable angina vs acute MI: distinguished by ECG — MI = ST ELEVATION; unstable angina = non-ST elevation. (Careful: Prinzmetal’s also shows ST elevation despite not being MI — elevation there is from transient spasm-induced transmural ischaemia, not fixed ongoing occlusion; context+reversibility separates them, not ECG alone.)

Comparison table

Clinical relevance

Enzyme-negative status (all 3 patterns) = the fact separating angina from MI mechanistically — reversible ischaemia never crosses into irreversible injury, however severe/frequent the pain. ST depression (stable, subendocardial) vs ST elevation (Prinzmetal’s, transmural) = high-yield pair, learn together — each makes sense only in contrast to the other. “Pre-infarction angina” label for unstable angina isn’t vague — reflects testable pathogenesis (plaque complication+thrombosis) mechanistically identical to early acute MI, differing only in whether occlusion becomes complete/sustained. Prinzmetal’s response to nitroglycerin = treatment response supporting proposed mechanism, not just symptom relief.

Overview

Angina pectoris is the clinical syndrome of ischaemic heart disease arising from transient, reversible myocardial ischaemia — paroxysmal substernal/precordial chest pain, aggravated by increased cardiac demand and relieved by decreased cardiac workload. Pain often radiates to the left arm, neck, jaw, or right arm; more common in men past the 5th decade. It sits alongside acute MI and chronic ischaemic heart disease as one of the possible outcomes of coronary artery disease, spanning a spectrum from an asymptomatic state to sudden cardiac death depending on the suddenness, duration, degree, location, and extent of the ischaemic insult. Together with acute MI and sudden cardiac death, unstable angina forms the acute coronary syndrome triad.

Pathophysiology — Three Overlapping Clinical Patterns

Angina has three patterns, each with a genuinely distinct underlying mechanism rather than being graded severities of one process.

1. Stable (Typical) Angina

The most common pattern. Pain follows physical exertion or emotional excitement and is relieved by rest.

Pathogenesis: chronic stenosing coronary atherosclerosis narrows the vessel enough that it cannot increase perfusion when cardiac workload rises — the fixed anatomic lesion is adequate at rest but cannot meet increased demand. During an attack, the ECG shows ST-segment depression, reflecting poor perfusion of the subendocardial region of the left ventricle (the last territory to be perfused and first to suffer under a fixed stenosis). Critically, there is no elevation of cardiac enzymes, because the ischaemia is transient and reversible — no irreversible myocardial injury has occurred. This enzyme-negative, ECG-reversible pattern is what mechanistically distinguishes angina from infarction at the cellular level: demand-ischaemia against a fixed lesion, not vessel occlusion.

2. Prinzmetal’s Variant Angina

Pain occurs at rest, with no relationship to physical activity — the opposite triggering pattern from stable angina, which is the first clue that a different mechanism is at work.

Pathogenesis: not fully established, but two proposed mechanisms: (i) sudden vasospasm of a coronary trunk, itself induced by underlying coronary atherosclerosis, or (ii) release of humoral vasoconstrictors from mast cells resident in the coronary adventitia. Unlike stable angina’s subendocardial ischaemia, Prinzmetal’s angina produces transmural ischaemia, reflected on ECG as ST-segment elevation (the opposite ECG direction from stable angina — worth holding these two patterns’ ECG changes in direct mental contrast). These patients respond well to vasodilators such as nitroglycerin, a therapeutic response that itself supports the vasospastic mechanism.

3. Unstable (Crescendo) Angina

Also called “pre-infarction angina” or “acute coronary insufficiency” — the most serious pattern, and the one that sits functionally on the boundary of acute MI. Characterised by more frequent pain episodes, of longer duration, occurring more often at rest — a pattern that, unlike stable angina, is actively worsening over time (hence “crescendo”). It signals impending acute myocardial infarction.

Pathogenesis is multifactorial, combining several processes acting together rather than any single mechanism: stenosing coronary atherosclerosis as the base lesion, complicated coronary plaques (superimposed thrombosis, haemorrhage, rupture, ulceration), platelet thrombi forming over the atherosclerotic plaque, and coronary vasospasm. The lesion more often sits in a branch of a major coronary trunk, so collateral circulation frequently prevents full-thickness infarction despite the severity of the underlying plaque disease — this is why unstable angina, though the most dangerous angina pattern, is not itself infarction.

Distinguishing unstable angina from acute MI: both can present with similar clinical severity, so the distinction rests on ST-segment behaviour on ECG — acute MI shows ST-segment elevation, while unstable angina characteristically shows a non-ST-elevation pattern. (Note the terminology overlap to keep straight: Prinzmetal’s angina also shows ST elevation despite not being infarction — the elevation in Prinzmetal’s reflects transient transmural spasm-induced ischaemia, not the fixed, ongoing occlusion of true MI; clinical context and reversibility, not the ECG finding alone, separates the two.)

Summary Comparison

Clinical Relevance

• The enzyme-negative status shared by all three angina patterns is the single fact that mechanistically separates angina, as a category, from myocardial infarction — reversible ischaemia never crosses into the irreversible cell injury that releases cardiac enzymes, regardless of how severe or frequent the pain becomes.
• The mirrored ECG findings — ST depression in stable angina (subendocardial ischaemia under a fixed lesion) versus ST elevation in Prinzmetal’s angina (transmural ischaemia from vasospasm) — is a compact, high-yield pair worth learning together rather than separately, since each only makes sense in contrast to the other.
• Unstable angina’s designation as “pre-infarction angina” is not a vague severity label — it reflects a specific, testable pathogenesis (plaque complication plus superimposed thrombosis) that is mechanistically identical to the early stage of acute MI, differing only in whether the coronary lesion progresses to complete, sustained occlusion.
• Prinzmetal’s angina’s response to nitroglycerin is a clean example of a treatment response supporting a proposed mechanism — the drug’s vasodilator action relieving pain is itself evidence for coronary vasospasm as the underlying process, not just a symptomatic fix.

• Three angina patterns compared: trigger, mechanism, ischaemia depth, and ECG change side by side