Irfan Affan, Li Yabing, Bhatnagar Aruni, Soliman Elsayed Z
Department of Cardiology Services and Department of Clinical & Translational Sciences, Marshall University, Huntington, West Virginia.
Department of Physiology, University of Louisville, Louisville, Kentucky.
Ann Noninvasive Electrocardiol. 2019 Jan;24(1):e12586. doi: 10.1111/anec.12586. Epub 2018 Aug 27.
Although the harmful effect of tobacco exposure on cardiovascular disease (CVD) and its risk factors are well established, the constituents of cigarette-smoke and the pathophysiological mechanism involved are unknown. Recently, deep terminal negativity of P wave in V1 (DTNPV1) has emerged as a marker of left atrial abnormality that predicts atrial fibrillation, stroke, and death due to all-cause or CVD. Therefore, we examined the association between serum cotinine levels with abnormal DTNPV1 using the Third National Health and Nutrition Examination Survey.
This analysis included 4,507 participants (mean age 58 ± 13 years, 53% women, 49% non-Hispanic white) of NHANES III, without history of CVD or major electrocardiographic abnormalities and not on heart rate modifying medications. Multivariable logistic regression analysis was used to examine the association between serum cotinine and abnormal DTNPV1-defined from automatically processed electrocardiograms as values of the amplitude of the terminal negative phase of P wave in lead V1 exceeding 100 μV.
Abnormal DTNPV1 was detected in 2.3% (n = 105) of the participants. In a model adjusted for demographics and CVD risk factors, each 10 ng/ml serum cotinine was associated with 2% increased odds of abnormal DTNPV1 (odds ratio 1.02, 95% confidence interval 1.01-1.03, p-value < 0.001). This association was consistent in subgroups stratified by age, sex, race, smoking status, hypertension, diabetes, dyslipidemia, and chronic obstructive pulmonary disease.
Elevated serum cotinine levels are associated with an abnormal DTNPV1. This suggests that nicotine exposure can lead to left atrial abnormalities, a possible mechanism for increased risk of CVD.
尽管烟草暴露对心血管疾病(CVD)及其危险因素的有害影响已得到充分证实,但香烟烟雾的成分以及所涉及的病理生理机制尚不清楚。最近,V1导联P波深终末负向波(DTNPV1)已成为预测心房颤动、中风以及全因或CVD导致死亡的左心房异常的标志物。因此,我们利用第三次全国健康和营养检查调查研究了血清可替宁水平与异常DTNPV1之间的关联。
该分析纳入了4507名美国国家健康和营养检查调查III(NHANES III)的参与者(平均年龄58±13岁,53%为女性,49%为非西班牙裔白人),这些参与者无CVD病史或重大心电图异常,且未服用心率调节药物。采用多变量逻辑回归分析来研究血清可替宁与异常DTNPV1之间的关联,异常DTNPV1由自动处理的心电图定义为V1导联P波终末负向波振幅值超过100μV。
2.3%(n = 105)的参与者检测到异常DTNPV1。在根据人口统计学和CVD危险因素进行调整的模型中,血清可替宁每增加10 ng/ml,异常DTNPV1的发生几率增加2%(优势比1.02,95%置信区间1.01 - 1.03,p值<0.001)。在按年龄、性别、种族、吸烟状况、高血压、糖尿病、血脂异常和慢性阻塞性肺疾病分层的亚组中,这种关联是一致的。
血清可替宁水平升高与异常DTNPV1相关。这表明尼古丁暴露可导致左心房异常,这可能是CVD风险增加的一种机制。