Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy
Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy
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DOI：
10.1161/hc2801.094031
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发表时间：
2001-07-17
期刊：
影响因子：
37.8
通讯作者：
Marian, AJ
中科院分区：
文献类型：
--
作者：
Patel, R;Nagueh, SF;Marian, AJ
背景-肥厚型心肌病是一种遗传性疾病，其特征是心脏肥大、心肌细胞紊乱、间质纤维化和左心室功能障碍。我们提出肥大和纤维化是死亡率和发病率的主要决定因素，但可能是可逆的。方法和结果-我们将24只β-肌球蛋白重链-Q（403）兔子随机分为安慰剂组和辛伐他汀组（5 mg（.）kg（-1 .）d（-1））处理12周，包括12个非转基因对照。我们在治疗前后进行了二维和多普勒超声心动图以及组织多普勒成像。非转基因组、安慰剂组和辛伐他汀组的基线平均左室质量和室间隔厚度分别为3.9 ± 0.7、6.2 ± 2.0和7.5 ± 2.1 g（P
Background - Hypertrophic cardiomyopathy is a genetic disease characterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (LV) dysfunction. We have proposed that hypertrophy and fibrosis, the major determinants of mortality and morbidity, are potentially reversible. We tested this hypothesis in beta -myosin heavy chain-Q(403) transgenic rabbits.Methods and Results - We randomized 24 beta -myosin heavy chain-Q(403) rabbits to treatment with either a placebo or simvastatin (5 mg (.) kg(-1 .) d(-1)) for 12 weeks and included 12 nontransgenic controls. We performed 2D and Doppler echocardiography and tissue Doppler imaging before and after treatment. Demographic data were similar among the groups, Baseline mean LV mass and interventricular septal thickness in nontransgenic, placebo, and simvastatin groups were 3.9 +/-0.7, 6.2 +/-2.0, and 7.5 +/-2.1 g (P