= Solution
\b[<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>.<Angina Causes and Risk Factors by NHLBI>[What causes angina; coronary disease, microvascular disease and spasm]{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>. \b[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.<Recent-onset Chest Pain of Suspected Cardiac Origin by NICE>[Recommendations 1.3.7 and factors intensifying ischaemia: anaemia, spasm, tachycardia and ventricular hypertrophy]{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.<Half-Yearly Report on Pathology and Principles and Practice of Medicine (1865)>[pp. 255–256, section XII: coronary openings narrowed and disease around the cardiac plexus]{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>.
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