Early impairment of coronary flow reserve and increase in minimum coronaryresistance in borderline hypertensive patients

Objective To evaluate relations between coronary flow velocity and myocardi al oxygen demand at rest, as well as coronary vasodilator capacity and flow reserve, in asymptomatic subjects with borderline hypertension as compared to normotensive controls and patients with sustained high blood pressure ( HBP) and without left ventricular hypertrophy (LVH). Subjects and methods Forty-two asymptomatic males were studied: 13 healthy normotensive volunteers; 12 subjects with borderline HBP and 17 asymptomati c subjects with sustained systemic hypertension. Coronary flow velocity in left anterior descending artery and coronary flow reserve were assessed by transesophageal echo-doppler at baseline and during intravenous adenosine i nfusion. Left ventricular mass, peak systolic wall stress (PSWS; Pa), and m idwall fractional shortening (MFS; %) were obtained from M-mode images of t he left ventricle in transthoracic long-axis view and in transesophageal tr ansgastric view. Results Coronary flow velocity at baseline was not significantly different in the three groups, despite significantly higher rate-pressure product (RP P) in the hypertensive groups as compared with controls. Only in control su bjects, was resting coronary flow velocity significantly correlated with RP P (y = 4279 + 200x, r = + 0.58, P < 0.05) and PSWS (y = 17.2 + 5.1x, r = 0.62, P < 0.05). Coronary reserve was 3.5 +/- 0.65 in controls and signific antly lower (P < 0.05) in borderline hypertensive (2.87 +/- 0.46) and in su stained hypertensive subjects (2.66 +/- 0.56). Minimum coronary resistance was significantly increased in both hypertensive groups (1.30 +/- 0.29 and 1.39 +/- 0.48 mmHg/s per cm) as compared to normotensive controls (0.93 +/- 0.20 mmHg/s per cm, P < 0.01). Conclusions In asymptomatic subjects with borderline hypertension and witho ut LVH, a significant reduction in coronary flow reserve is already detecta ble and appears almost entirely related to an impaired coronary vasodilator capacity rather than to an increased myocardial oxygen demand. J Hypertens 2000, 18:453-459 (C) Lippincott Williams & Wilkins.