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(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

Michael R. Ward, MBBS, PhD; Niall A. Herity, MD

Department of Cardiovascular Medicine, Stanford University Medical Center, Stanford, Calif

	Introduction

 
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 . . . [Full Text of this Article]