M-2 treatment reduced the incidence of post-infarction cardiomyopathy development to 33.3% compared to 66.7% with captopril and 100% in controls in a rat model of myocardial infarction.
Does M-2 prevent cardiomyopathy development and improve hemodynamics compared to captopril in rats post-myocardial infarction?
In a rat model of post-infarction heart failure, the furnidipine metabolite M-2 was superior to captopril in preventing cardiomyopathy development and stimulating angiogenesis.
Absolute Event Rate: 33.33% vs 66.67%
During the last 25 years angiotensin-converting enzyme inhibitors spectacularly conquered the field of cardiovascular diseases therapy. Nevertheless, lack of new studies concerning side effects associated with their chronic administration seems to be rather confusing. In our previous research, we proved that the main furnidipines' metabolite (M-2) possess multiple cardioprotective actions. Currently, we compared effects of post-infarction long-term oral treatment with M-2 and captopril on hemodynamic parameters and "ischemic cardiomyopathy" development in rats. Myocardial infarction was evoked by permanent left anterior descending coronary artery occlusion for 35 days. Surviving rats were treated with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) from 6th- 35th day. At 35th day rats' hearts were tested on working heart setup, where following parameters were measured: heart rate, preload pressure, aortic systolic and diastolic pressures, aortic maximum rise and fall, aortic and coronary flow, myocardial oxygen consumption and oximetry in perfusate. Subsequently, heart tissue specimens were assessed during morphological estimation. Captopril caused significant heart rate increase and markedly diminished preload pressure in comparison to M-2. Both drugs evoked essential aortic pressure increase. Aortic flow was significantly decreased after M-2, whereas captopril increased this parameter in comparison to M-2. Both agents caused marked coronary flow increase. Morphologic examination in captopril revealed cardiomyopathic process in 70% of hearts, whereas in M-2 this value reached 30%. Neovascularization of post-infarcted myocardium was visible only after M-2 therapy. Concluding, M-2 presented itself as more attractive agent in long-term post-infarction treatment by preventing cardiomyopathy development, angiogenesis stimulation and preserving cardiac performance.
Mitręga et al. (Wed,) conducted a other in Myocardial infarction (n=43). M-2 (furnidipine metabolite) vs. Captopril (2 x 25 mg/kg daily) and Control (0.9% NaCl) was evaluated on Incidence of cardiomyopathy development. M-2 treatment reduced the incidence of post-infarction cardiomyopathy development to 33.3% compared to 66.7% with captopril and 100% in controls in a rat model of myocardial infarction.