Nebivolol improves coronary flow reserve in hypertensive patients without coronary heart disease

To examine the effects of nebivolol, a beta-blocker with nitroxide-mediated vasodilating properties, on coronary flow reserve (CFR) in patients with uncomplicated arterial hypertension.

Fourteen newly diagnosed, never-treated, World Health Organization grade I-II hypertensive patients (male/female, 10/4; mean age, 47 years), free of coronary heart disease, underwent standard Doppler echocardiography and determination of CFR in the distal left anterior descending artery by low-dose dipyridamole (0.56 mg/kg intravenously in 4 min) at baseline and after 4 weeks of treatment with 5 mg nebivolol once daily.

At baseline, nine patients had left ventricular (LV) hypertrophy (LV mass index > or = 51 g/m). After 4 weeks of therapy, the blood pressure was decreased from 148 +/- 8.1/101.4 +/- 4.6 mmHg to 140.7 +/- 7.0/91.1 +/- 7.4 mmHg and end-systolic stress was also significantly reduced. Heart rate was reduced (P <0.01), whereas LV end-diastolic diameter and stroke volume tended to increase (P=0.07 and P=0.09, respectively). No changes were detected in the LV mass index, relative wall thickness, fractional shortening and LV diastolic properties. Both resting and dipyridamole rate-pressure products were lower after nebivolol but dipyridamole-induced changes were not influenced by the therapy. In contrast, nebivolol therapy did not alter coronary velocities at rest, but caused a greater increase in coronary velocities after dipyridamole (P <0.03), leading to a greater CFR (2.12 +/- 0.33 versus 1.89 +/- 0.31, P <0.0001). Nebivolol induced an absolute increase of 8% in the CFR in nine of 14 patients (64.3%).

In hypertensive patients free of coronary artery disease, 4-week nebivolol therapy induces a significant increase of the CFR. Nebivolol preserves coronary flow at rest despite the reduction of metabolic (O2 consumption) and hemodynamic (diastolic blood pressure) determinants. The increase of hyperemic coronary velocities appears due to the reduction of coronary resistance.