Past exam of the medicine course of the University of Oxford / 1865 / Second examination / Pathology / 7 / Solution

Angina pectoris is most usefully explained by transient inadequacy of the myocardial oxygen supply relative to demand. It is a clinical syndrome, rather than the name of one visible anatomical lesion. The characteristic constricting chest discomfort may radiate to the arm, neck or jaw and be provoked by effort; the question concerns its causes, not a claim that every chest pain is angina pectoris.^[ref]

The common structural basis is coronary atherosclerosis. Narrowing limits the increase of coronary blood flow that should accompany exercise. An affected heart may receive sufficient oxygen at rest and insufficient oxygen when its rate, force of contraction and wall stress rise. Plaque disruption with thrombosis can abruptly worsen supply; persistent severe ischemia can then cause myocardial infarction. Pain from transient ischemia does not by itself prove myocardial necrosis.

Other mechanisms include coronary artery spasm, impaired regulation of small coronary vessels, or increased demand in left ventricular hypertrophy, severe aortic stenosis, or tachycardia. Reduced delivery through severe anaemia, low arterial oxygen or low perfusion pressure may provoke symptoms even without a new obstructing plaque. Structural narrowing, vasomotor change, blood oxygen-carrying capacity and cardiac work therefore have to be considered together.^[ref]

For an 1865 interpretation, coronary “ossification” or degeneration, diseased cardiac or aortic structures and neural or spasmodic explanations belonged to the historical discussion. These did not establish a single universal cause. A report published in January 1865 described a pathological case associated angina pectoris with diseased coronary arteries, but isolated cases cannot demonstrate that a particular valve or vessel lesion is necessary in every patient.^[ref] The modern supply-and-demand account explains why severe symptoms can coexist with relatively inconspicuous large coronary arteries, and why substantial coronary disease need not cause pain at every moment.

A pathological investigation inspects the coronary origins and course, their lumen and wall, the myocardium, the aortic valve and ventricular thickness. Clinical investigation adds evidence of reversible myocardial ischaemia and distinguishes it from infarction or non-cardiac pain. Modern electrocardiography and appropriate imaging address functions that a nineteenth-century post-mortem inspection alone could not measure. A normal-looking vessel on gross inspection cannot exclude coronary microvascular disease or a transient coronary artery spasm.