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

Objective 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. Design, setting and patients 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. Results At baseline, nine patients had left ventricular (LV) hypertrophy (LV mass index greater than or equal to 51 g/m(2.7)). 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%). Conclusions 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 (O-2 consumption) and hemodynamic (diastolic blood pressure) determinants. The increase of hyperemic coronary velocities appears due to the reduction of coronary resistance. (C) 2004 Lippincott Williams Wilkins.