Müllerleile U, Garbrecht M, Hanrath P, Langenstein B A, Bieber K, Bleifeld W, Hossfeld D K
Klin Wochenschr. 1984 Nov 2;62(21):1032-7. doi: 10.1007/BF01711726.
An increased cytoplasmatic calcium level seems to play an important role in the pathogenesis of Adriamycin (ADM)-induced cardiomyopathy. Experiments have shown that calcium channel blockers such as verapamil may prevent this type of cardiomyopathy in animals, but data are contradictory. In a clinical pilot trial, the left ventricular function of 22 patients undergoing ADM-chemotherapy in combination with verapamil was examined. M-mode echocardiograms were performed parallel to every chemotherapy course. Left ventricular function was determined by fractional shortening rate (FS) and peak fibre shortening velocity (V ef max.). Three 40-mg doses of verapamil were given p.o./day continuously. Data of these patients were compared with a control group of 61 patients treated and checked equally without additional verapamil therapy. In the course of therapy parameters of left ventricular function remained almost constant in the verapamil group but decreased significantly in the control group. In the verapamil group FS changed by -0.05 FS %/100 mg ADM/m2, V ef max. by +0.015 circ./s/100 mg ADM/m2 compared with -2.31 FS % and -0.33 circ./s in the control group (P 0.01 and 0.001, respectively). In the verapamil group no congestive heart failure occurred and no patient showed FS below 30%, whereas in the control group in 23% (14) of the cases ADM therapy had to be stopped because FS fell below 30%. One congestive heart failure was observed. These clinical results suggest that verapamil may be a useful drug for preventing ADM-induced cardiomyopathy but further investigations are necessary.