Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA.
JACC Cardiovasc Imaging. 2011 Jul;4(7):754-61. doi: 10.1016/j.jcmg.2011.04.011.
Our goal was to evaluate the associations of central arterial stiffness, measured by aortic pulse wave velocity (aPWV), with subclinical target organ damage in the coronary, peripheral arterial, cerebral, and renal arterial beds.
Arterial stiffness is associated with adverse cardiovascular outcomes. We hypothesized that aPWV is associated with subclinical measures of atherosclerosis-coronary artery calcification (CAC) and ankle-brachial index (ABI) and arteriolosclerosis-brain white matter hyperintensity (WMH) and urine albumin-creatinine ratio (UACR).
Participants (n = 812; mean age 58 years; 58% women, 71% hypertensive) belonged to hypertensive sibships and had no history of myocardial infarction or stroke. aPWV was measured by applanation tonometry, CAC by electron beam computed tomography, ABI using a standard protocol, WMH volume by brain magnetic resonance, and UACR by standard methods. WMH was log-transformed, whereas CAC and UACR were log-transformed after adding 1 to reduce skewness. The associations of aPWV with CAC, ABI, WMH, and UACR were assessed by multivariable linear regression using generalized estimating equations to account for the presence of sibships. Covariates included in the models were age, sex, body mass index, history of smoking, hypertension and diabetes, total and high-density lipoprotein cholesterol, estimated glomerular filtration rate, use of aspirin and statins, and pulse pressure.
The mean ± SD aPWV was 9.8 ± 2.8 m/s. After adjustment for age, sex, conventional cardiovascular risk factors, and pulse pressure, higher aPWV (1 m/s increase) was significantly associated with higher log (CAC + 1) (β ± SE = 0.14 ± 0.04; p = 0.0003), lower ABI (β ± SE = -0.005 ± 0.002; p = 0.02), and greater log (WMH) (β ± SE = 0.03 ± 0.009; p = 0.002), but not with log (UACR + 1) (p = 0.66).
Higher aPWV was independently associated with greater burden of subclinical disease in coronary, lower extremity, and cerebral arterial beds, highlighting target organ damage as a potential mechanism underlying the association of arterial stiffness with adverse cardiovascular outcomes.
本研究旨在评估主动脉脉搏波速度（aPWV）所反映的中心动脉僵硬与冠状动脉、外周动脉、脑和肾动脉等靶器官亚临床损害之间的相关性。
动脉僵硬与不良心血管结局相关。我们假设 aPWV 与亚临床动脉粥样硬化（冠状动脉钙化 [CAC] 和踝臂指数 [ABI]）和小动脉疾病（脑白质高信号 [WMH] 和尿白蛋白/肌酐比 [UACR]）相关。
参与者（n=812；平均年龄 58 岁，58%为女性，71%为高血压患者）来自高血压同胞家庭，无心肌梗死或卒中病史。通过平板张力测量法测量 aPWV，通过电子束计算机断层扫描测量 CAC，使用标准方案测量 ABI，通过脑磁共振测量 WMH 容积，通过标准方法测量 UACR。为了减少偏度，对 WMH 进行对数转换，对 CAC 和 UACR 进行加 1 后的对数转换。使用广义估计方程（考虑到同胞家庭的存在），通过多变量线性回归评估 aPWV 与 CAC、ABI、WMH 和 UACR 的相关性。模型中包含的协变量包括年龄、性别、体重指数、吸烟史、高血压和糖尿病、总胆固醇和高密度脂蛋白胆固醇、估计肾小球滤过率、阿司匹林和他汀类药物的使用以及脉压。
平均±标准差 aPWV 为 9.8±2.8 m/s。在校正年龄、性别、传统心血管危险因素和脉压后，较高的 aPWV（每增加 1 m/s）与较高的 log（CAC+1）（β±SE=0.14±0.04；p=0.0003）、较低的 ABI（β±SE=-0.005±0.002；p=0.02）和更大的 log（WMH）（β±SE=0.03±0.009；p=0.002）显著相关，但与 log（UACR+1）无关（p=0.66）。
较高的 aPWV 与冠状动脉、下肢和脑动脉等靶器官亚临床疾病负担增加独立相关，突出了靶器官损害是动脉僵硬与不良心血管结局相关的潜在机制之一。
