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Angina is a frequent and disabling complication of atherosclerotic cardiovascular disease. The pathophysiology of angina is complex and it is now appreciated that symptomatic response to vasoconstrictors in the coronary microvasculature, without myocardial ischemia, may be the predominant mechanism of angina. The vasoconstrictors responsible for vasospasm and ischemia are still not established; but evidence is growing that these might be subtle changes in coronary vascular tone, primarily the result of enhanced release of excitatory neurotransmitters and/or modulation of receptors, which may also be operative in the subendocardial microcirculation. Vasospasm is likely to respond to specific treatment that includes calcium channel blockers. The benefits of percutaneous transluminal coronary angioplasty (PTCA) are uncertain. Studies show that the procedure is effective in preventing future episodes of angina, but the extent to which this represents a true regression of the vasospasm or rather a dilatation of the stenotic lesions, is difficult to determine, especially in the presence of myocardial ischemia. PTCA does not alter the course of chronic stable ischemic heart disease and, in selected patients, it is associated with short-term reversal of vasospastic angina. However, the procedure can cause transient restenosis and angioplasty should be performed only in the correct subset of patients, after a trial period of optimal medical therapy. Successful PTC
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