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Smoking-associated electrocardiographic abnormalities predict cardiovascular mortality
Affan Irfan1,2,3,4, Daniel W Riggs4,5, George A Koromia2
1Department of Cardiology, Mayo Clinic, Rochester, MN, USA.
Insights
Smoking significantly alters cardiac electrical activity, increasing the risk of arrhythmias and sudden cardiac death. This study links smoking to specific electrocardiogram (ECG) abnormalities, including shorter PR intervals and longer JT intervals, which predict mortality.
Area of Science:
- Cardiology
- Electrophysiology
- Public Health
Background:
- Smoking is a known risk factor for cardiac arrhythmia and sudden cardiac death, but underlying biological mechanisms require further elucidation.
- Electrocardiogram (ECG) parameters like QT interval, P wave, and PR segment duration are critical indicators of cardiac electrical activity and predict arrhythmia risk.
- Previous studies on smoking's impact on ECG abnormalities using the NHANES database were limited.
Purpose of the Study:
- To investigate the association between serum cotinine levels (a biomarker for smoking) and various ECG intervals in a nationally representative adult sample.
- To determine how smoking influences cardiac depolarization and repolarization parameters.
- To assess the predictive value of smoking-related ECG abnormalities for cardiovascular mortality.
Main Methods:
- Analysis of data from 5,653 adults in the National Health and Nutrition Examination Survey III (NHANES III).
- Utilized survey-weighted multinomial logistic regression to examine associations between tobacco use (serum cotinine > 15 ng/ml) and extreme ECG interval durations (short < 5th percentile, long > 95th percentile).
- Employed survey-weighted linear regression to assess the relationship between continuous cotinine levels and ECG parameters, adjusting for relevant covariates and medications.
Main Results:
- Smoking was significantly associated with a higher likelihood of short PR interval, short PR segment, short QRS duration, and long JT interval after adjusting for confounders.
- Serum cotinine levels showed an inverse association with PR segment duration and QTc interval.
- Over 22 years of follow-up, several ECG abnormalities (long JT, long QRS, long QTc, short QRS) predicted cardiovascular mortality specifically in smokers.
Conclusions:
- Smoking promotes rapid atrioventricular and ventricular depolarization and delayed ventricular repolarization, potentially increasing the risk of cardiac arrhythmias.
- Specific ECG changes associated with smoking, such as short PR and long JT intervals, are linked to increased cardiovascular mortality risk in smokers.
- These findings highlight the detrimental effects of smoking on cardiac electrical function and emphasize the need for smoking cessation to mitigate cardiovascular risk.
Abstract:
Background -Smoking is associated with arrhythmia and sudden cardiac death, but the biological mechanisms remain unclear. In electrocardiogram (ECG) recordings abnormal durations of ventricular repolarization (QT interval), atrial depolarization (P wave), and atrioventricular depolarization (PR interval and segment), predict cardiac arrhythmia and mortality. Previous analyses of the National Health and Nutrition Examination Survey (NHANES) database for associations between smoking and ECG abnormalities were incomplete. To elucidate how smoking affects cardiac excitation, we assessed in a nationally representative sample (NHANES III) the association between serum cotinine and P duration, PR interval, PR segment, rate-corrected QT (QTc), QRS duration, and JT interval. Methods and Results-We analyzed data from 5,653 adults using survey-weighted multinomial logistic regression to estimate associations between tobacco use (> 15 ng/ml serum cotinine) and short (< 5th percentile) or long (> 95th percentile) ECG intervals, relative to reference (5-95th percentile). After adjustment for demographics, risk factors, and conduction-altering medications, smoking was associated with a higher odds of short PR interval, PR segment, and QRS, and long JT. Broader effects of smoking on ECG were also assessed by survey-weighted linear regression of continuous cotinine and ECG, which revealed cotinine inversely associated with PR segment and QTc. Over a 22-year follow-up, many ECG abnormalities predicted cardiovascular mortality in smokers, including long JT, QRS, and QTc, and short QRS, whereas only short JT predicted mortality in nonsmokers. Conclusions -Smoking increases likelihood for rapid atrioventricular and ventricular depolarization and slow ventricular repolarization, which may promote cardiac arrhythmia and mortality.
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