Atorvastatin and cardiac hypertrophy and function in hypertrophic cardiomyopathy: a pilot study.
Atorvastatin and cardiac hypertrophy and function in hypertrophic cardiomyopathy: a pilot study.
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阿托伐他汀与肥厚型心肌病中的心脏肥大和功能：一项初步研究。
DOI：
10.1111/j.1365-2362.2010.02349.x
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发表时间：
2010
影响因子：
5.5
通讯作者：
Marian,AliJ
中科院分区：
文献类型：
--
作者：
Nagueh,SherifF;Lombardi,Raffaella;Tan,Yanli;Wang,Jianwen;Willerson,JamesT;Marian,AliJ
EURJ Clin Invest 2010；40(11)：976-983摘要背景肥厚性心肌病(HCM)是一种心肌肥厚的遗传范例。心肌肥厚是肥厚性心肌病猝死风险和发病率的主要决定因素。他汀类药物可逆转肥厚心肌动物模型的肥大。我们用阿托伐他汀进行了一项可行性研究，以收集设计随机疗效研究的先决条件数据。结果我们在18个 月内筛查了32例肥厚性心肌病患者。21名患者符合研究标准并同意参与。参加活动的人和没有参加活动的人的人口统计学和超声心动图表型没有显著差异。我们用递增剂量的阿托伐他汀(20、40和80 mg day−1)治疗参与者2 年。分别于治疗前和治疗后3、6、12、24个月进行心电图、超声心动图检查，并检测血脂、肝酶、肌酸激酶和B型利钠肽水平。治疗前和治疗后3、6、12、24 。15、12和11例患者分别完成了6、12和24个月的 治疗。6名患者因感觉缺乏益处而停用阿托伐他汀。我们对4名患者停用阿托伐他汀，原因是肝酶、肌酸激酶或背痛有轻微升高。那些完成或没有完成研究的人的特征没有显著差异。血浆低密度脂蛋白-胆固醇平均水平降低55%。然而，心脏肥厚和功能的超声心动图指数仍然没有改变。结论这些发现说明了在设计有效性研究以测试阿托伐他汀对人肥厚性心肌病的潜在益处时将遇到的挑战。
Eur J Clin Invest 2010; 40 (11): 976–983AbstractBackgroundHypertrophic cardiomyopathy (HCM) is a genetic paradigm of cardiac hypertrophy. Cardiac hypertrophy is a major determinant of risk of sudden death and morbidity in HCM. Treatment with statins reverses hypertrophy in animal models of HCM. Thus, statins may afford therapeutic benefits in HCM.MethodsWe performed a feasibility study with atorvastatin to gather the pre‐requisite data for designing randomized efficacy studies.ResultsWe screened 32 patients with HCM in 18 months. Twenty‐one patients met the study criteria and consented to participate. The demographics and echocardiographic phenotype of those who did and those who did not participate were not significantly different. We treated the participants with escalating doses of atorvastatin (20, 40 and 80 mg day−1) for 2 years. We performed ECG and echocardiography and measured plasma lipids, liver enzymes, creatine kinase and B‐type natriuretic peptide levels before and after 3, 6, 12 and 24 months of therapy. Fifteen, 12 and 11 patients completed 6, 12 and 24 months of therapy respectively. Six patients discontinued atorvastatin because of perceived lack of benefit. We stopped atorvastatin in 4 patients because of modest elevations in liver enzymes, creatine kinase or back pain. The characteristics of those who did or did not complete the study were not significantly different. The mean plasma low‐density lipoprotein‐cholesterol level was reduced by 55%. However, echocardiographic indices of cardiac hypertrophy and function remained unchanged.ConclusionsThe findings illustrated the challenges that will be encountered in designing efficacy studies to test the potential beneficial effects of atorvastatin in human HCM.