Olsen Michael H, Wachtell Kristian, Ibsen Hans, Lindholm Lars H, Dahlöf Björn, Devereux Richard B, Kjeldsen Sverre E, Oikarinen Lasse, Okin Peter M
Glostrup University Hospital, Denmark.
J Hypertens. 2006 Apr;24(4):775-81. doi: 10.1097/01.hjh.0000217862.50735.dc.
In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, reduced urine albumin/creatinine ratio (UACR) as well as regression of left ventricular hypertrophy have been associated with lower incidence of cardiovascular events. We wanted to investigate whether these prognostic improvements were independent.
In 6679 hypertensive patients included in the LIFE study, we measured UACR, left ventricular hypertrophy by electrocardiography, serum cholesterol, plasma glucose and blood pressure after 2 weeks of placebo treatment and again after 1 year of anti-hypertensive treatment with either an atenolol- or a losartan-based regimen. During this first year of treatment, 77 patients encountered a non-fatal stroke or myocardial infarction and were excluded to avoid bias. During the next 3-4 years, 610 composite endpoints [cardiovascular death (n = 228), fatal or non-fatal myocardial infarction or stroke] were recorded.
In Cox regression analyses, the composite endpoint was after adjustment for treatment allocation predicted by baseline logUACR [hazard ratio (HR) = 1.16 per 10-fold increase, P < 0.05], 1-year logUACR (HR = 1.29 per 10-fold increase), baseline Sokolow-Lyon voltage (HR = 1.01 per mm, both P < 0.001) and 1-year Cornell product (HR = 1.01 per 100 mm x ms, P < 0.01). Cardiovascular death was predicted by 1-year logUACR (HR = 1.59, P < 0.001), baseline Sokolow-Lyon voltage (HR = 1.01, P = 0.06) and 1-year Cornell product (HR = 1.02, P < 0.001). Both were predicted independent of age, Framingham risk score, current smoking, history of cardiovascular disease and diabetes. Gender, serum cholesterol, plasma glucose and blood pressure did not enter the models.
Baseline UACR and Sokolow-Lyon voltage, as well as in-treatment UACR and Cornell product, added to the risk prediction independent of traditional risk factors, indicating that albuminuria and left ventricular hypertrophy reflect different aspects of cardiovascular damage and are modifiable cardiovascular risk factors.
在氯沙坦降低高血压终点事件（LIFE）研究中，尿白蛋白/肌酐比值（UACR）降低以及左心室肥厚消退与心血管事件发生率降低相关。我们想研究这些预后改善是否独立。
在LIFE研究纳入的6679例高血压患者中，我们在安慰剂治疗2周后以及使用阿替洛尔或氯沙坦为基础的治疗方案进行1年抗高血压治疗后，测量了UACR、通过心电图测量左心室肥厚、血清胆固醇、血糖和血压。在治疗的第一年，77例患者发生非致命性中风或心肌梗死并被排除以避免偏倚。在接下来的3 - 4年中，记录了610个复合终点事件[心血管死亡（n = 228）、致命或非致命性心肌梗死或中风]。
在Cox回归分析中，调整治疗分配后，复合终点事件由基线对数UACR预测[风险比（HR）=每增加10倍为1.16，P < 0.05]、1年对数UACR（HR =每增加10倍为1.29）、基线索科洛夫 - 里昂电压（HR =每毫米为1.01，均P < 0.001）和1年康奈尔乘积（HR =每100毫米×毫秒为1.01，P < 0.01）。心血管死亡由1年对数UACR预测（HR = 1.59，P < 0.001）、基线索科洛夫 - 里昂电压（HR = 1.01，P = 0.06）和1年康奈尔乘积（HR = 1.02，P < 0.001）。两者均独立于年龄、弗雷明汉风险评分、当前吸烟、心血管疾病史和糖尿病进行预测。性别、血清胆固醇、血糖和血压未纳入模型。
基线UACR和索科洛夫 - 里昂电压，以及治疗中的UACR和康奈尔乘积，独立于传统风险因素增加了风险预测，表明蛋白尿和左心室肥厚反映了心血管损伤的不同方面，并且是可改变的心血管风险因素。
