G. Bigalli

Coronary Vasodilator Capacity and Epicardial Vessel Remodeling in Physiological and Hypertensive Hypertrophy

The aim of this study was to compare resting coronary flow velocity, determinants of myocardial oxygen demand, and coronary vasodilator capacity in subjects with physiological, exercise-induced, and hypertensive left ventricular hypertrophy. Sixteen healthy sedentary men, 16 endurance athletes, and 16 hypertensive subjects (mean±SEM for left ventricular mass index: 94.9±5.5, 184.6±8.4, 154.4±9.5 g/m2, respectively) were studied by transesophageal and transthoracic Doppler echocardiography. Coronary flow velocity in left anterior descending artery and cross-sectional area of left main artery were assessed at rest and during dipyridamole-induced vasodilation. Myocardial oxygen demand was estimated through rate-pressure product, left ventricular wall stress, and inotropic function. Coronary flow reserve and minimum coronary resistance were comparable to those of sedentary men in athletes (mean±SEM: 3.23±0.16 versus 3.60±0.18 and 0.96±0.06 versus 1.04±0.04 mm Hg · s · cm−1), while in hypertensive subjects they were decreased and increased, respectively (mean±SEM: 2.31±0.08 and 1.21±0.10 mm Hg · s · cm−1;P <0.05 for both). Resting flow velocity was directly related to rate-pressure product in sedentary men and athletes and also to wall stress in athletes, while these correlations were absent in hypertensives. Dilation of left main artery after dipyridamole was significantly higher in athletes than in sedentary men and hypertensive subjects (mean±SEM for area change: 32.9±3.7% versus 12.8±2.5% and 6.4±3.3%;P <0.05 and 0.01). These data indicate that vasodilator capacity of coronary microcirculation is not impaired in athletes with physiological hypertrophy, in contrast to hypertensive patients. The relationship between resting flow velocity and determinants of oxygen demand is preserved in physiological hypertrophy but missing in hypertensive hypertrophy. Furthermore, the vasodilator capacity of coronary macrocirculation is also enhanced in exercise-trained subjects.

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

Objective To 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 methods Forty-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. Results Coronary 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). Conclusions In 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.