Department of Cardiology, Erasmus Medical Center, Rotterdam, The Netherlands.
Am J Cardiol. 2011 Jul 15;108(2):265-71. doi: 10.1016/j.amjcard.2011.03.032. Epub 2011 May 10.
Recent trials have failed to show that statin therapy halts the progression of calcific aortic stenosis (AS). We hypothesized that statin therapy in younger patients with congenital AS would be more beneficial, because the valve is less calcified. In the present double-blind, placebo-controlled trial, 63 patients with congenital AS (age 18 to 45 years) were randomly assigned to receive either 10 mg of rosuvastatin daily (n = 30) or matched placebo (n = 33). The primary end point was the progression of peak aortic valve velocity. The secondary end points were temporal changes in the left ventricular mass, ascending aortic diameter, and N-terminal pro-brain natriuretic peptide (NT-proBNP). The median follow-up was 2.4 years (interquartile range 1.9 to 3.0). The mean increase in peak velocity was 0.05 ± 0.21 m/s annually in the rosuvastatin group and 0.09 ± 0.24 m/s annually in the placebo group (p = 0.435). The annualized change in the ascending aorta diameter (0.4 ± 1.7 mm with rosuvastatin vs 0.5 ± 1.6 mm with placebo; p = 0.826) and left ventricular mass (1.1 ± 15.8 g with rosuvastatin vs -3.7 ± 30.9 g with placebo; p = 0.476) were not significantly different between the 2 groups. Within the statin group, the NT-proBNP level was 50 pg/ml (range 19 to 98) at baseline and 21 pg/ml (interquartile range 12 to 65) at follow-up (p = 0.638). NT-proBNP increased from 40 pg/ml (interquartile range 20 to 92) to 56 pg/ml (range 26 to 130) within the placebo group (p = 0.008). In conclusion, lipid-lowering therapy with rosuvastatin 10 mg did not reduce the progression of congenital AS in asymptomatic young adult patients. Interestingly, statins halted the increase in NT-proBNP, suggesting a potential positive effect of statins on cardiac function in young patients with congenital AS.
最近的试验未能表明他汀类药物治疗可阻止钙化性主动脉瓣狭窄（AS）的进展。我们假设在患有先天性 AS 的年轻患者中进行他汀类药物治疗会更有益，因为瓣膜钙化程度较低。在这项双盲、安慰剂对照试验中，63 名患有先天性 AS（年龄 18 至 45 岁）的患者被随机分为接受每天 10 毫克瑞舒伐他汀治疗（n=30）或匹配的安慰剂（n=33）。主要终点是峰值主动脉瓣速度的进展。次要终点是左心室质量、升主动脉直径和 N 末端脑利钠肽前体（NT-proBNP）的时间变化。中位随访时间为 2.4 年（四分位距 1.9 至 3.0）。瑞舒伐他汀组的峰值速度平均每年增加 0.05±0.21 m/s，安慰剂组每年增加 0.09±0.24 m/s（p=0.435）。瑞舒伐他汀组升主动脉直径的年化变化（0.4±1.7 mm 与安慰剂组 0.5±1.6 mm；p=0.826）和左心室质量的年化变化（瑞舒伐他汀组 1.1±15.8 g 与安慰剂组-3.7±30.9 g；p=0.476）在两组之间无显著差异。在他汀组中，NT-proBNP 水平在基线时为 50 pg/ml（范围 19 至 98），随访时为 21 pg/ml（四分位距 12 至 65）（p=0.638）。安慰剂组中 NT-proBNP 从 40 pg/ml（四分位距 20 至 92）增加到 56 pg/ml（范围 26 至 130）（p=0.008）。总之，10 毫克瑞舒伐他汀的降脂治疗并未降低无症状年轻成年患者先天性 AS 的进展。有趣的是，他汀类药物阻止了 NT-proBNP 的增加，这表明他汀类药物对年轻先天性 AS 患者的心脏功能可能有积极影响。
