(Circulation. 1999;100:e84-e85.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Percutaneous Transluminal Coronary Angioplasty Reverses Vasoconstriction of Stenotic Coronary Arteries in Hypertensive Patients
Department of Cardiovascular Medicine, Stanford University Medical Center, Stanford, Calif
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To the Editor:
We read with interest the study by Frielingsdorf et al1 in which exercise-induced dilation (measured by biplane angiography) of "normal" coronary arteries was impaired in hypertensive compared with normotensive patients. The vasodilator response in normal arteries during exercise is dependent on flow-sensitive release of nitric oxide from the endothelium.2 However, attributing an impaired dilator response in hypertensives to deficient release of endothelium-derived vasodilators ("endothelial dysfunction") dismisses the alternative potential importance of variability in exercise-induced flow.
Demonstration of impaired flow-dependent dilation requires measurement of flow; however, few studies in this field measure and adjust for it. It is well known that microvascular disease reduces the hyperemic response to exercise. Indeed, coronary flow reserve has been shown to be significantly impaired in hypertensives, even in the absence of left ventricular hypertrophy, probably as a result of perivascular fibrosis, microvascular remodeling, and reduced diastolic perfusion time due to impaired ventricular relaxation.3 4 Thus, in hypertensive patients, reduced vasodilation during the coronary hyperemic response to exercise is likely to be due, at least in part, to a blunted increase in flow. Similarly, vasoconstrictor responses with exercise may be an appropriate response, because flow through stenotic segments may actually be reduced with exercise owing to partial perfusion of the distal bed by collaterals, or steal, which results from a greater relative drop in vascular resistance in neighboring vascular beds. In addition, circulating catecholamine levels5 and cardiac uptake of catecholamines6 are increased in hypertension and may attenuate both microvascular and macrovascular dilation.
Unfortunately, exactly how much dilation is expected for each increment in flow is unknown. It is therefore uncertain to what degree an attenuated vasodilator response is due to macrovascular and microvascular endothelial dysfunction, respectively. It would be interesting to know whether macrovascular endothelial dysfunction represents a shift of the curve to the right, a blunting of the slope of the flow/dilation curve, or a reduction in the maximal dilation response. Although these considerations are particularly pertinent to the coronary circulation in hypertensives, they may also affect interpretation of studies that measure flow-mediated dilation after forearm ischemia. Perhaps a more thorough exploration of these methodological issues would lead to consensus on exactly what values constitute abnormal macrovascular endothelial function.
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1. Frielingsdorf J, Kaufmann P, Suter T, Hug R, Hess OM. Percutaneous transluminal coronary angioplasty reverses vasoconstriction of stenotic coronary arteries in hypertensive patients. Circulation. 1998;98:1192–1197.
2.
Maxwell AJ, Schauble E, Bernstein D, Cooke JP. Limb
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5.
de Champlain J, Farley L, Cousineau D, van Ameringen
MR. Circulating catecholamine levels in human and
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