ANALYSIS OF THE MECHANISMS UNDERLYING THE CHANGES IN LEFT-VENTRICULAR FILLING DYNAMICS DURING ORAL NISOLDIPINE THERAPY IN PATIENTS WITH ANTERIOR MYOCARDIAL-INFARCTION

The aim of this study was to clarify the mechanisms responsible for the increase in early filling rate observed during oral nisoldipine therapy in patients with ischaemic left ventricular (LV) dysfunction. For that purpose, the global and regional L Vfunction was analysed before and after 2 months ofdouble-blindmonotherapy with nisoldipine (10 mg twice daily) or a placebo, in 17 patients with a previous anterior myocardial infarction. The baseline LV ejection fraction ranged from 34-51% and no patient had heart failure. Compared to the placebo, nisoldipine significantly lowered LV systolic pressure and end-diastolic pressure ( -3 mmHg vs + 6 with the placebo; P < 0.01) and the L V pressure at the time of mitral opening ( -.20 ± 3.4 mmHg vs + 3.5 ± 3.0; P < 0.01). Despite this reduction in driving pressure, the global L V early peak filling rate improved with nisoldipine only and this improvement was related to a selective increase in expansion rate of the anterior areas, from 1010±360to 1339 ±496 mm2.s-1 (P<0.001). The time to regional peak filling rate (-8%; P<0.01), the asynchrony of diastolic wall motion and the regional ejection fraction (33 ± 10 to 38 ± 12%; P < 0.001) also improved in the anterior areas with nisoldipine but not with the placebo. In contrast, in the inferior, control zones, the regional ejection fraction and filling rate remained unchanged, both when compared to baseline and to the placebo. In conclusion, prolonged nisoldipine therapy had no significant effect on the normal myocardium but improved systolic and diastolic function in hypokinetic areas. The functional improvement in such areas might be related to improved perfusion, to a greater sensitivity to afterload reduction or to an effect of nisoldipine on myocardial calcium handling. © 1992 The European Society of Cardiology.