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

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ObjectiveTo evaluate relations between coronary flow velocity and myocardial 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 methodsForty-two asymptomatic males were studied: 13 healthy normotensive volunteers; 12 subjects with borderline HBP and 17 asymptomatic subjects with sustained systemic hypertension. Coronary flow velocity in left anterior descending artery and coronary flow reserve were assessed by transesophageal echodoppler at baseline and during intravenous adenosine infusion. Left ventricular mass, peak systolic wall stress (PSWS; Pa), and midwall fractional shortening (MFS; %) were obtained from M-mode images of the left ventricle in transthoracic long-axis view and in transesophageal transgastric view.ResultsCoronary flow velocity at baseline was not significantly different in the three groups, despite significantly higher rate-pressure product (RPP) in the hypertensive groups as compared with controls. Only in control subjects, was resting coronary flow velocity significantly correlated with RPP (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 significantly lower (P < 0.05) in borderline hypertensive (2.87 ± 0.46) and in sustained 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).ConclusionsIn asymptomatic subjects with borderline hypertension and without LVH, a significant reduction in coronary flow reserve is already detectable and appears almost entirely related to an impaired coronary vasodilator capacity rather than to an increased myocardial oxygen demand.

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