The vascular endothelium as a key to understanding coronary spasm and syndrome X

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Abstract
The coronary artery endothelium is now known to be a metabolically active tissue as well as a surface that regulates barrier function. Endothelial cells produce autocrine or paracrine hormones such as endothelium-derived relaxing factor. In addition, they enzymatically inactivate other circulating hormones such as norepinephrine, bradykinin, and serotonin. Endothelial cells contain an angiotensin-converting enzyme system for conversion of angiotensin I to its active form, angiotensin II, at the tissue level. Through these mechanisms, coronary endothelium plays a major role in the dynamic regulation of local vasomotor tone. When aberrations occur in this regulation, the endothelium may contribute to the pathogenesis of myocardial ischemia. Recently, the endothelium has been specifically implicated in variant angina and syndrome X. Endothelin seems to function as a calcium-channel agonist whose action can be blunted using calcium-channel antagonists. This substance can potentiate the vasoconstrictor effects of norepinephrine and serotonin in human coronary arteries. In patients with coronary spasm, endothelin levels are elevated: This suggests that endothelin may sensitize vascular smooth muscle to other vasoconstrictor stimuli, which could lead to coronary spasm. Recent studies suggest that one pathogenetic mechanism responsible for some cases of syndrome X may be a flow-limiting abnormality of the coronary microvasculature. In patients with hyperlipidemia and angiographically normal coronary arteries, an abnormal response consisting of epicardial constriction and increase in coronary resistance has been observed after acetylcholine administration. This paradoxical response could be important in the pathogenesis of syndrome X as well as in variant angina and other coronary artery disease syndromes.

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