Bazzano Lydia A, He Jiang, Muntner Paul, Vupputuri Suma, Whelton Paul K
Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana 70112, USA.
Ann Intern Med. 2003 Jun 3;138(11):891-7. doi: 10.7326/0003-4819-138-11-200306030-00010.
Few studies have examined the relationship between cigarette smoking and novel risk factors for cardiovascular disease in a general population or have included a biochemical marker of current smoking.
To examine the relationship between cigarette smoking and serum C-reactive protein, fibrinogen, and homocysteine levels.
Cross-sectional study.
The U.S. general population.
4187 current smokers, 4791 former smokers, and 8375 never-smokers 18 years of age or older who participated in the Third National Health and Nutrition Examination Survey conducted between 1988 and 1994.
Serum C-reactive protein levels were categorized as detectable (2.2 to 9.9 mg/L) or clinically elevated (> or =10 mg/L), and fibrinogen and homocysteine levels were defined as elevated if in the 85th percentile or greater (11.1 micromol/L and 12.7 mmol/L, respectively).
After adjustment for traditional cardiovascular disease risk factors, cigarette smoking was related to elevated levels of C-reactive protein, fibrinogen, and homocysteine. Compared with never smoking cigarettes, self-reported current cigarette smoking was associated with a C-reactive protein level in the detectable (odds ratio, 1.66 [95% CI, 1.40 to 1.97]; P < 0.001) or clinically elevated (odds ratio, 1.98 [CI, 1.57 to 2.51]; P < 0.001) ranges, with elevated levels of fibrinogen (odds ratio, 2.15 [CI, 1.65 to 2.80]; P < 0.001) and homocysteine (odds ratio, 2.10 [CI, 1.62 to 2.74]; P < 0.001). There were positive and significant dose-response relationships between measures of cigarette smoking (cigarettes per day, pack-years, and serum cotinine levels) and elevated levels of novel risk factors.
These findings suggest that inflammation and hyperhomocysteinemia may be important mechanisms by which smoking promotes atherosclerotic disease.
很少有研究在普通人群中探讨吸烟与心血管疾病新风险因素之间的关系，或者纳入当前吸烟的生化标志物。
研究吸烟与血清C反应蛋白、纤维蛋白原和同型半胱氨酸水平之间的关系。
横断面研究。
美国普通人群。
4187名当前吸烟者、4791名既往吸烟者和8375名18岁及以上从不吸烟者，他们参与了1988年至1994年进行的第三次全国健康和营养检查调查。
血清C反应蛋白水平分为可检测（2.2至9.9mg/L）或临床升高（≥10mg/L），纤维蛋白原和同型半胱氨酸水平如果处于第85百分位数或更高（分别为11.1μmol/L和12.7mmol/L）则定义为升高。
在对传统心血管疾病风险因素进行校正后，吸烟与C反应蛋白、纤维蛋白原和同型半胱氨酸水平升高有关。与从不吸烟相比，自我报告的当前吸烟与可检测范围内的C反应蛋白水平（比值比，1.66[95%CI，1.40至1.97]；P<0.001）或临床升高水平（比值比，1.98[CI，1.57至2.51]；P<0.001）、纤维蛋白原水平升高（比值比，2.15[CI，1.65至2.80]；P<0.001）和同型半胱氨酸水平升高（比值比，2.10[CI，1.62至2.74]；P<0.001）相关。吸烟量指标（每天吸烟支数）、吸烟包年数和血清可替宁水平）与新风险因素水平升高之间存在正相关且显著的剂量反应关系。
这些发现表明，炎症和高同型半胱氨酸血症可能是吸烟促进动脉粥样硬化疾病的重要机制。
