Al Rifai Mahmoud, DeFilippis Andrew P, McEvoy John W, Hall Michael E, Acien Ana Navas, Jones Miranda R, Keith Rachel, Magid Hoda S, Rodriguez Carlos J, Barr Graham R, Benjamin Emelia J, Robertson Rose Marie, Bhatnagar Aruni, Blaha Michael J
Department of Medicine, University of Kansas School of Medicine, Wichita, KS, USA; Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, MD, USA.
Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, MD, USA; Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, KY, USA; Division of Cardiology, University of Louisville School of Medicine, Louisville, KY, USA.
Atherosclerosis. 2017 Mar;258:119-130. doi: 10.1016/j.atherosclerosis.2017.01.021. Epub 2017 Jan 19.
Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure.
We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration.
Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP.
Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.
现代烟草监管科学需要了解哪些心血管损伤生物标志物对吸烟暴露最为敏感。
我们对动脉粥样硬化多民族研究中的自我报告现吸烟者进行了研究。吸烟强度由每日吸烟支数和尿可替宁水平定义。使用炎症标志物[高敏C反应蛋白（hsCRP）、白细胞介素6和2（IL - 2和IL - 6）、肿瘤坏死因子α（TNF - α）]、血栓形成标志物（纤维蛋白原、D - 二聚体、同型半胱氨酸）、心肌损伤标志物（肌钙蛋白T；TnT）、内皮损伤标志物（白蛋白：肌酐比值）以及血管功能标志物[主动脉和颈动脉扩张性、血流介导的扩张（FMD）]评估亚临床心血管损伤。使用针对心血管危险因素和吸烟持续时间进行多变量调整的线性回归模型，将生物标志物建模为绝对变化和百分比变化。
在843名现吸烟者中，平均年龄为58（9）岁，53%为男性，39%为非裔美国人，每日平均吸烟支数为13（10）支，中位吸烟持续时间为39（15）年。吸烟支数与较高的hsCRP、IL - 6和纤维蛋白原显著相关（β系数分别为：0.013、0.011、0.60），而对数转换后的可替宁与相同的生物标志物相关（β系数分别为：0.12、0.04、5.3），并与主动脉扩张性呈负相关（β系数： - 0.13）。仅在部分调整模型中，吸烟强度与同型半胱氨酸、D - 二聚体以及白蛋白：肌酐比值之间存在有限的关联，而在任何模型中与IL - 2、TNF - α、颈动脉扩张性、FMD或TnT均无关联。在百分比变化分析中，与hsCRP的关系最为显著。
吸烟强度与心血管疾病的早期生物标志物相关，特别是全身炎症标志物。其中，hsCRP可能最为敏感。
