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This study aimed determining the chronic effects of nifedipine (N) on left ventricular filling in 25 patients (mean age 55) with mild to moderate arterial hypertension. M-mode, B-mode and pulsed Doppler measurements were performed at baseline, after 30 min from administration of sublingual N (10 mg) and after 6 months of therapy with slow release N (max dose: 60 mg die). Acute and chronic N reduced significantly both systolic (p less than 0.001) and diastolic pressure (p less than 0.001). At the end of the treatment with slow release N, and septal wall thicknesses had a slight but significant decrease (p less than 0.01). Diastolic and systolic dimension were not modified. Left ventricular mass index decreased significantly from 141 +/- 34 to 130 +/- 31 g/m2 (p less than 0.05). The Doppler-derived diastolic filling indexes (peak E, ratio peak E/A,E deceleration) were abnormal at baseline, and had a significant increase after sublingual and chronic therapy. Changes in left ventricular mass index and diastolic filling indexes were not correlated. A significant correlation was found between peak E changes after acute and chronic N administration (r = 0.732 and p less than 0.001). The results of this study demonstrate that both acute and chronic administration of N modify transmitral flow velocity pattern, suggesting that, in hypertensive patients, left ventricular filling abnormalities are partly dynamic and reversible. Our findings also demonstrate that acute N effects may predict the chronic results.

This study was undertaken to determine the acute effects of nifedipine on left ventricular filling, examined by Doppler echocardiography in patients with arterial hypertension and normal left ventricular systolic function. Twenty-seven patients with mild to moderate systemic hypertension, and 18 normotensive subjects were studied. Pulsed Doppler, M-mode and B-mode measurements were performed before and 30 min after sublingual nifedipine administration (10 mg). Peak E, peak A, area A, area E, ratio area A/area E, E deceleration and E acceleration time were measured. Before administering nifedipine, some of these diastolic filling parameters were significantly different in the hypertensive patients as compared with normal subjects. After nifedipine, in patients with arterial hypertension, peak E and area E increased significantly (p less than 0.01), while ratio peak A/E and ratio area A/area E showed a significant decrease (p less than 0.001). No significant changes were observed in normal subjects. The result of this study demonstrates that the acute administration of nifedipine modifies transmitral flow velocity pattern in hypertensive patients, suggesting that the left ventricular filling abnormalities are in part dynamic and reversible.