Affan Irfan1,2,3, Yabing Li4, Aruni Bhatnagar3, Elsayed Z Soliman4,5. 1. Department of Cardiology Services and Department of Clinical & Translational Sciences, Marshall University, Huntington, West Virginia. 2. Department of Physiology, University of Louisville, Louisville, Kentucky. 3. Diabetes and Obesity Center, University of Louisville, Louisville, Kentucky. 4. Epidemiological Cardiology Research Center (EPICARE), Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston Salem, North Carolina. 5. Department of Internal Medicine, Section on Cardiology, Wake Forest School of Medicine, Winston Salem, North Carolina.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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