Olsen Michael H, Wachtell Kristian, Bella Jonathan N, Palmieri Vittorio, Gerdts Eva, Smith Gunnar, Nieminen Markku S, Dahlöf Björn, Ibsen Hans, Devereux Richard B
Department of Internal Medicine, Glostrup University Hospital, Glostrup, Denmark.
Am J Hypertens. 2005 Nov;18(11):1430-6. doi: 10.1016/j.amjhyper.2005.05.030.
Aortic valve (AV) sclerosis and urine albumin/creatinine ratio (UACR) are both markers of atherosclerosis. We aimed to investigate whether they predicted cardiovascular (CV) events independently in patients with hypertension and electrocardiographic left ventricular (LV) hypertrophy.
After 2 weeks of placebo treatment, clinical, laboratory, and echocardiographic variables were assessed in 960 hypertensive patients from the LIFE Echo substudy who had electrocardiographic LV hypertrophy. Morning urine albumin and creatinine were measured calculating UACR. The presence of AV sclerosis was defined as valve thickening or calcification. Fifteen patients with mild AV stenosis were excluded. The patients were followed for 60 +/- 4 months and the composite endpoint (CEP) of CV death, nonfatal stroke, or nonfatal myocardial infarction was recorded.
A value of UACR above the median value of 1.406 was associated with higher incidence of CEP and CV death in patients with AV sclerosis (CEP: 18.8% v 9.0% P < 0.05, CV death: 7.1% v 0.7% P < 0.01) and in patients without AV sclerosis (CEP: 14.0% v 4.9% P < 0.001, CV death: 5.1% v 1.1% P < 0.01). In Cox regression analysis, AV sclerosis predicted CEP (hazard ratio [HR] = 1.52, P < .05), but not CV death (HR = 1.30 [0.62 to 2.70], NS) independently of logUACR (HR = 1.70 and HR = 3.25, both P < .001). After adjusting for the Framingham Risk Score, CV disease, diabetes, smoking, and treatment allocation, AV sclerosis predicted CEP (HR = 1.5, P < .05) but not CV death (HR = 1.4, NS) independently of logUACR (HR = 1.2, P = .09 and HR = 1.94, P < .05).
In hypertensive patients with electrocardiographic LV hypertrophy, AV sclerosis predicted CEP but not CV death independently of UACR after adjusting for CV risk factors and treatment allocation, indicating that AV sclerosis and UACR might be markers of different aspects of the atherosclerotic process.
主动脉瓣(AV)硬化和尿白蛋白/肌酐比值(UACR)均为动脉粥样硬化的标志物。我们旨在研究在高血压和心电图左心室(LV)肥厚患者中,它们是否能独立预测心血管(CV)事件。
经过2周的安慰剂治疗后,对来自LIFE Echo子研究的960例有心电图LV肥厚的高血压患者进行临床、实验室和超声心动图变量评估。测量晨尿白蛋白和肌酐以计算UACR。AV硬化的存在定义为瓣膜增厚或钙化。排除15例轻度AV狭窄患者。对患者进行60±4个月的随访,并记录CV死亡、非致死性卒中或非致死性心肌梗死的复合终点(CEP)。
UACR值高于中位数1.406与AV硬化患者(CEP:18.8%对9.0%,P<0.05;CV死亡:7.1%对0.7%,P<0.01)和无AV硬化患者(CEP:14.0%对4.9%,P<0.001;CV死亡:5.1%对1.1%,P<0.01)中CEP和CV死亡的较高发生率相关。在Cox回归分析中,独立于logUACR(HR = 1.70和HR = 3.25,均P<0.001),AV硬化可预测CEP(风险比[HR]=1.52,P<0.05),但不能预测CV死亡(HR = 1.30[0.62至2.70],无统计学意义)。在调整Framingham风险评分、CV疾病、糖尿病、吸烟和治疗分配后,独立于logUACR(HR = 1.2,P = 0.09和HR = 1.94,P<0.05),AV硬化可预测CEP(HR = 1.5,P<0.05),但不能预测CV死亡(HR = 1.4,无统计学意义)。
在有心电图LV肥厚的高血压患者中,调整CV危险因素和治疗分配后,AV硬化独立于UACR可预测CEP,但不能预测CV死亡,这表明AV硬化和UACR可能是动脉粥样硬化过程不同方面的标志物。