Solomon Scott D, Janardhanan Rajesh, Verma Anil, Bourgoun Mikhail, Daley William L, Purkayastha Das, Lacourcière Yves, Hippler Stephen E, Fields Harold, Naqvi Tasneem Z, Mulvagh Sharon L, Arnold J Malcolm O, Thomas James D, Zile Michael R, Aurigemma Gerard P
Cardiovascular Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
Lancet. 2007 Jun 23;369(9579):2079-87. doi: 10.1016/S0140-6736(07)60980-5.
Diastolic dysfunction might represent an important pathophysiological intermediate between hypertension and heart failure. Our aim was to determine whether inhibitors of the renin-angiotensin-aldosterone system, which can reduce ventricular hypertrophy and myocardial fibrosis, can improve diastolic function to a greater extent than can other antihypertensive agents.
Patients with hypertension and evidence of diastolic dysfunction were randomly assigned to receive either the angiotensin receptor blocker valsartan (titrated to 320 mg once daily) or matched placebo. Patients in both groups also received concomitant antihypertensive agents that did not inhibit the renin-angiotensin system to reach targets of under 135 mm Hg systolic blood pressure and under 80 mm Hg diastolic blood pressure. The primary endpoint was change in diastolic relaxation velocity between baseline and 38 weeks as determined by tissue doppler imaging. Analyses were done by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00170924.
186 patients were randomly assigned to receive valsartan; 198 were randomly assigned to receive placebo. 43 patients were lost to follow-up or discontinued the assigned intervention. Over 38 weeks, there was a 12.8 (SD 17.2)/7.1 (9.9) mm Hg reduction in blood pressure in the valsartan group and a 9.7 (17.0)/5.5 (10.2) mm Hg reduction in the placebo group. The difference in blood pressure reduction between the two groups was not significant. Diastolic relaxation velocity increased by 0.60 (SD 1.4) cm/s from baseline in the valsartan group (p<0.0001) and 0.44 (1.4) cm/s from baseline in the placebo group (p<0.0001) by week 38. However, there was no significant difference in the change in diastolic relaxation velocity between the groups (p=0.29).
Lowering blood pressure improves diastolic function irrespective of the type of antihypertensive agent used.
舒张功能障碍可能是高血压和心力衰竭之间重要的病理生理中间环节。我们的目的是确定可减轻心室肥厚和心肌纤维化的肾素 - 血管紧张素 - 醛固酮系统抑制剂，是否比其他抗高血压药物能更大程度地改善舒张功能。
有高血压且存在舒张功能障碍证据的患者被随机分配接受血管紧张素受体阻滞剂缬沙坦（滴定至每日一次320毫克）或匹配的安慰剂。两组患者还接受不抑制肾素 - 血管紧张素系统的联合抗高血压药物治疗，以使收缩压达到135毫米汞柱以下和舒张压达到80毫米汞柱以下的目标。主要终点是通过组织多普勒成像确定的基线至38周时舒张松弛速度的变化。分析采用意向性治疗。该试验已在ClinicalTrials.gov注册，编号为NCT00170924。
186例患者被随机分配接受缬沙坦；198例被随机分配接受安慰剂。43例患者失访或中断了指定的干预。在38周期间，缬沙坦组血压降低了12.8（标准差17.2）/7.1（9.9）毫米汞柱，安慰剂组血压降低了9.7（17.0）/5.5（10.2）毫米汞柱。两组间血压降低的差异无统计学意义。到第38周时，缬沙坦组舒张松弛速度较基线增加了0.60（标准差1.4）厘米/秒（p<0.0001），安慰剂组较基线增加了0.44（1.4）厘米/秒（p<0.0001）。然而，两组间舒张松弛速度变化的差异无统计学意义（p = 0.29）。
无论使用何种抗高血压药物，降低血压均可改善舒张功能。
