Ibsen Hans, Wachtell Kristian, Olsen Michael H, Borch-Johnsen Knut, Lindholm Lars H, Mogensen Carl Erik, Dahlöf Björn, Devereux Richard B, de Faire Ulf, Fyhrquist Frej, Julius Stevo, Kjeldsen Sverre E, Lederballe-Pedersen Ole, Nieminen Markku S, Omvik Per, Oparil Suzanne, Wan Ying
Glostrup University Hospital, Denmark.
J Hypertens. 2004 Sep;22(9):1805-11. doi: 10.1097/00004872-200409000-00026.
To examine a possible relationship between baseline albuminuria and effect of losartan versus atenolol on cardiovascular (CV) events in hypertensive patients with left ventricular hypertrophy, the effect of losartan versus atenolol on albuminuria, and whether the benefits of losartan versus atenolol could be explained by influence of losartan on albuminuria.
Double-blind, randomized, controlled trial of 4.8 years.
Out-patient setting.
A total of 8206 with hypertension and left ventricular hypertrophy.
Losartan or atenolol, supplemented with diuretics and/or calcium antagonists to reach blood pressure < 140/90 mmHg
The urine albumin/creatinine ratio, and the primary composite endpoint (CEP) of CV death, myocardial infarction, and stroke.
The blood pressure was reduced similarly on losartan (30.2/16.6 mmHg) versus atenolol (29.1/16.8 mmHg). The risk of a primary CEP increased linearly from the lowest to the highest decile of baseline albuminuria. The benefits of losartan versus atenolol for the primary CEP and for stroke tended to be more pronounced among patients above the median value for baseline albuminuria (urine albumin/creatinine ratio, 1.28 mg/mmol). The decrease in albuminuria was significantly greater with losartan versus atenolol throughout the study (a decrease from baseline to year 2 of 33% losartan versus 25% atenolol). One-fifth of the difference in favor of losartan on the primary CEP was explained by the greater reduction in albuminuria on losartan.
Baseline albuminuria is a powerful risk factor for CV events. Baseline albuminuria did not identify the group of patients with greatest benefit on losartan versus atenolol in LIFE. Reduction in albuminuria explained one-fifth of the benefits of losartan versus atenolol.
探讨在伴有左心室肥厚的高血压患者中，基线蛋白尿与氯沙坦和阿替洛尔对心血管（CV）事件影响之间的可能关系、氯沙坦与阿替洛尔对蛋白尿的影响，以及氯沙坦相对于阿替洛尔的益处是否可通过氯沙坦对蛋白尿的影响来解释。
为期4.8年的双盲、随机、对照试验。
门诊。
共8206例高血压伴左心室肥厚患者。
氯沙坦或阿替洛尔，辅以利尿剂和/或钙拮抗剂，使血压降至<140/90 mmHg。
尿白蛋白/肌酐比值，以及CV死亡、心肌梗死和中风的主要复合终点（CEP）。
氯沙坦组（30.2/16.6 mmHg）与阿替洛尔组（29.1/16.8 mmHg）的血压下降幅度相似。原发性CEP的风险从基线蛋白尿的最低十分位数到最高十分位数呈线性增加。在基线蛋白尿中位数以上（尿白蛋白/肌酐比值，1.28 mg/mmol）的患者中，氯沙坦相对于阿替洛尔对原发性CEP和中风的益处往往更为明显。在整个研究过程中，氯沙坦组蛋白尿的下降幅度明显大于阿替洛尔组（从基线到第2年，氯沙坦组下降33%，阿替洛尔组下降25%）。氯沙坦在原发性CEP方面优于阿替洛尔的差异中有五分之一可通过氯沙坦组蛋白尿更大幅度的下降来解释。
基线蛋白尿是CV事件的一个强有力的危险因素。在LIFE研究中，基线蛋白尿并未识别出在氯沙坦与阿替洛尔治疗中获益最大的患者群体。蛋白尿的减少解释了氯沙坦相对于阿替洛尔益处的五分之一。
