Department of Internal Medicine and Therapeutics, University of Pavia, Pavia, Italy.
Diabet Med. 2012 Jan;29(1):24-31. doi: 10.1111/j.1464-5491.2011.03383.x.
To compare the effects of losartan and amlodipine on myocardial structure and function in hypertensive patients with Type 2 diabetes and left ventricular hypertrophy.
After a 4-week placebo period, patients were randomized to losartan 50 mg (n = 90) or amlodipine 5 mg (n = 91) for 12 months, with a doubling of the dose in patients who did not respond after 4 weeks. Blood pressure was measured in the clinic every month, while conventional echocardiography and acoustic densitometry (integrated backscatter analysis) were performed at the end of the placebo period and after 12 months of treatment.
Both drugs reduced systolic/diastolic blood pressure to a comparable extent. Losartan significantly reduced left ventricular mass index (-19%, P < 0.001), interventricular septal thickness (-16.6%, P < 0.01) and left ventricular posterior wall thickness in diastole (-13.7%, P < 0.01). Amlodipine also decreased such measurements (-10%, P < 0.01 for left ventricular mass index, -9.3%, P < 0.05 for interventricular septal thickness in diastole and -10.1%, P < 0.05 for posterior wall thickness in diastole), but to a lesser extent than losartan. Both drugs significantly increased the ratio of peak filling velocity at early diastole to that at atrial contraction (E/A ratio) and decreased isovolumetric relaxation time: +13.7% and -8.5% with losartan,(both P < 0.01), and +7.9% and -4.9%, with amlopidine (both P < 0.05). Losartan, but not amlodipine, significantly reduced the relative integrated backscatter compared to baseline of the intraventricular septum (-10%, P < 0.01), and of the left ventricular posterior wall (-12%, P < 0.01), while increasing the cyclic variation of integrated backscatter of both the intraventricular septum (+35%, P < 0.001) and the left ventricular posterior wall (+32%, P < 0.001).
Losartan provided a greater attenuation of left ventricular hypertrophy than amlodipine, seemingly as a result of a greater reduction of myocardial fibrosis.
比较氯沙坦和氨氯地平对伴有 2 型糖尿病和左心室肥厚的高血压患者心肌结构和功能的影响。
经过 4 周的安慰剂期后，患者被随机分为氯沙坦 50mg 组（n=90）或氨氯地平 5mg 组（n=91），治疗 12 个月，4 周后无反应的患者加倍剂量。每月在诊所测量血压，而在安慰剂期结束和治疗 12 个月后进行常规超声心动图和背向散射密度（积分回波分析）。
两种药物均能使收缩压/舒张压降低到相当程度。氯沙坦显著降低左心室质量指数（-19%，P<0.001）、室间隔厚度（-16.6%，P<0.01）和舒张期左心室后壁厚度（-13.7%，P<0.01）。氨氯地平也降低了这些指标（左心室质量指数降低 10%，P<0.01；舒张期室间隔厚度降低 9.3%，P<0.05；舒张期后壁厚度降低 10.1%，P<0.05），但程度低于氯沙坦。两种药物均显著增加舒张早期充盈峰值速度与心房收缩速度的比值（E/A 比值），并降低等容舒张时间：氯沙坦分别增加 13.7%和-8.5%（均 P<0.01），氨氯地平分别增加 7.9%和-4.9%（均 P<0.05）。氯沙坦而非氨氯地平显著降低室间隔（-10%，P<0.01）和左心室后壁（-12%，P<0.01）的相对积分回波背向散射，同时增加室间隔（+35%，P<0.001）和左心室后壁（+32%，P<0.001）的积分回波循环变异。
氯沙坦对左心室肥厚的抑制作用大于氨氯地平，可能是由于心肌纤维化减少所致。
