Abstract

It has been estimated that 20% of patients who undergo coronary angiography for the evaluation of chest pain have angiographically normal coronary vessels with no other car• diac cause for their discomfort. Although the natural history of this patient group is favorable (1-3), the mechanisms responsible for the pain frequently remain mysterious. In the 1960s the explanations commonly given for this syn• drome were a noncardiac cause of the pain (for example, esophageal spasm) and an inadequate number of angio• graphic projections to exclude coronary obstructive lesions or coronary spasm. In addition, a psychogenic cause was suspected in many such patients. It is now generally agreed that these mechanisms are not responsible for causing chest pain in the majority of patients with angina and normal coronary vessels. Measuring the coronary reserve. In the past 5 to 10 years it has become increasingly evident that there are many disease states associated with decreased coronary reserve and angiographically normal coronary vessels. Ideally, coronary reserve should be assessed by measuring the min• imal coronary vascular resistance in each of the transmural layers of the left ventricular myocardium served by major coronary vessels (4). Because this cannot be accomplished in humans with available methods, a composite index of coronary reserve is usually obtained by measuring the dif• ference between resting and maximal coronary flow over all layers. In normal humans, the ratio between resting and maximal coronary flow is between 4 and 6 (5). Role of cardiac hypertrophy. Almost all causes of pathologic cardiac hypertrophy are associated with substan-

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