Antihypertensive treatment in hypertensive patients with normal left ventricular mass is associated with left ventricular remodeling and improved diastolic function

Antihypertensive therapy in hypertensive patients with left ventricular (LV) hypertrophy causes hypertrophy regression and improved diastolic filling. Whether similar changes occur in hypertensive patients with diastolic dysfunction and no hypertrophy is unknown. We determined the effect of antihypertensive therapy on LV geometry and function in hypertensive patients without hypertrophy. In 18 mild to moderate hypertensive patients without significant hypertrophy, baseline echocardiograms and rest and exercise radionuclide angiograms were performed. Subjects were treated for 8 to 12 months with the calcium channel blocker felodipine and then restudied 2 weeks after treatment withdrawal. Blood pressure normalized with treatment (165 ± 22/ 98 ± 9 to 128 ± 12/80 ± 5 mm Hg, p < 0.001) and returned to pretreatment levels after therapy withdrawal. Rest ejection fraction and peak oxygen consumption and cardiac outputs were unchanged after treatment, but rest peak filling rate increased (2.63 ± 0.57 to 3.11 ± 0.95 end-diastolic volume/second, p 0.05). Ejection fraction increased with exercise only after treatment (64 ± 5% at rest to 71 ± 8% at peak exercise, p < 0.05). LV mass index was unchanged (97 ± 18 to 101 ± 23 g/m2), but relative wall thickness declined (0.41 ± 0.05 to 0.37 ± 0.05) and LV end-diastolic dimension increased (4.9 ± 0.4 to 5.2 ± 0.4, p = 0.01). Blood pressure control in hypertensive patients without hypertrophy leads to improved peak filling rates and remodeling with decreased relative wall thickness. Improved diastolic function can occur without alterations in LV mass.