THE EFFECTS ON CARDIAC-ARRHYTHMIAS OF ANTIHYPERTENSIVE THERAPY CAUSING REGRESSION OF LEFT-VENTRICULAR HYPERTROPHY

To examine the effects of antihypertensive therapy causing regression of left ventricular hypertrophy on cardiac arrhythmias, 26 hypertensiv e subjects were treated with ramipril with felodipine if required, and followed for 6 months after blood pressure control. Compared with bas eline, left ventricular mass index (LVMI) was significantly reduced bo th at blood pressure control and after a further 6 months of treatment (baseline, blood pressure control, 6 months after blood pressure cont rol; LVMI 142 +/- 3.6, 131 +/- 3.4, 123 +/- 3.8 g/m(2), *P < .01 comp ared with baseline). There was a significant relationship between the decrease in systolic blood pressure and the decrease in LVMI after 6 m onths of blood pressure control compared with baseline (r = 0.41, P = .05). Compared with baseline, the average total number of ventricular ectopics decreased after blood pressure was controlled (88 +/- 59 and 21 +/- 12 respectively); however this reduction was not maintained aft er 6 months of further treatment, either before (78 +/- 50) or after d rug washout (86 +/- 40). Compared with baseline (639 +/- 590) supraven tricular ectopic total was not initially reduced after blood pressure control (650 +/- 604), but was reduced after a further 6 months of tre atment (294 +/- 261). This reduction was maintained after drug washout (267 +/- 254), although this did not reach statistical significance. Radionuclide scanning at baseline was not a predictor of patients with the highest risk of arrhythmia and there was no correlation between i mprovement or worsening of a defect with changes in ventricular ectopi c total. In conclusion, antihypertensive therapy with ramipril and fel odipine, although causing regression of left ventricular hypertrophy d id not lead to a sustained reduction in ventricular ectopic total. (C) 1997 American Journal of Hypertension, Ltd.