Lifetime smoking exposure affects the association of C-reactive protein with cardiovascular disease risk factors and subclinical disease in healthy elderly subjects
Lifetime smoking exposure affects the association of C-reactive protein with cardiovascular disease risk factors and subclinical disease in healthy elderly subjects
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DOI：
10.1161/01.atv.17.10.2167
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发表时间：
1997-10-01
影响因子：
8.7
通讯作者：
Kuller, LH
中科院分区：
文献类型：
--
作者：
Tracy, RP;Psaty, BM;Kuller, LH
C反应蛋白（CRP）是一种炎症标志物，其血液水平与心血管疾病风险有关。为了确定老年人的横断面相关性，我们测量了400名年龄超过65岁且基线时无临床心血管疾病的男性和女性的CRP，作为心血管健康研究的一部分。只有2%的值大于10 mg/L，这是通常用于识别炎症的临界点。CRP水平似乎受到严格调控，因为CRP与以下因素之间存在强双变量相关性：炎症敏感蛋白，如纤维蛋白原（r=.52）;纤溶指标，如纤溶酶-抗纤溶酶复合物（r=.23）;吸烟包年（r=.30）;和体重指数（r=.24;所有P值均小于或等于.001）。与包年的关联是独立的时间长度，因为戒烟。CRP水平还与凝血因子VIIc、IXc和Xc、HDL胆固醇（阴性）和甘油三酯、糖尿病状态、利尿剂使用、ECG异常和运动水平相关。由于效应修正，开发了两个CRP的多元线性回归预测模型，分别用于从不吸烟者和曾经吸烟者。一个先验的生理模型被用来指导这些分析，这不允许使用其他炎症敏感的变量，如纤维蛋白原。在从不吸烟者中，独立的预测因子是体重指数（+）、糖尿病状态（+）、纤溶酶-抗纤溶酶复合物（+）和ECG异常（+）;该模型预测了15%的CRP人群方差。在曾经吸烟者中，预测因子是体重指数（+）、纤溶酶-抗纤溶酶复合物（+）、吸烟包年数（+）、高密度脂蛋白胆固醇（-）和踝臂血压指数（-）;该模型预测了42%的群体方差。我们的结论是，CRP水平在健康的老年人受到严格的监管，并反映终身暴露于吸烟以及肥胖水平，持续的纤溶水平，糖尿病状态，亚临床动脉粥样硬化血栓形成疾病的水平。此外，暴露于吸烟影响CRP与这些其他因素的关系。
Blood levels of C-reactive protein (CRP), a marker of inflammation, are related to cardiovascular disease risk. To determine cross-sectional correlates in the elderly, we measured CRP in 400 men and women older than 65 years and free of clinical cardiovascular disease at baseline as part of the Cardiovascular Health Study. Only 2% of the values were greater than 10 mg/L, the cut-point usually used to identify inflammation. CRP levels appeared tightly regulated, since there were strong bivariate correlations between CRP and the following: inflammation-sensitive proteins such as fibrinogen (r=.52); measures of fibrinolysis such as plasmin-antiplasmin complex (r=.23); pack-years of smoking (r=.30); and body mass index (r=.24; all P values less than or equal to.001). The association with pack-years was independent of the length of time since cessation of smoking. CRP levels were also associated with coagulation factors VIIc, IXc, and Xc; HDL cholesterol (negative) and triglyceride; diabetes status; diuretic use; ECG abnormalities; and level of exercise. Because of effect modification, two multiple linear regression prediction models were developed for CRP, one each for never smokers and ever smokers. An a priori physiologic model was used to guide these analyses, which disallowed the use of other inflammation-sensitive variables such as fibrinogen. In never smokers, the independent predictors were body mass index (+), diabetes status (+), plasmin-antiplasmin complex (+), and the presence of ECG abnormalities (+); this model predicted 15% of the CRP population variance. In ever smokers, the predictors were body mass index (+), plasmin-antiplasmin complex (+), pack-years of smoking (+), HDL cholesterol (-), and ankle-arm blood pressure index (-); this model predicted 42% of the population variance. We conclude that levels of CRP in the healthy elderly are tightly regulated and reflect lifetime exposure to smoking as well as level of obesity, ongoing level of fibrinolysis, diabetes status, and level of subclinical atherothrombotic disease. Moreover, exposure to smoking affects the relation of CRP to these other factors.