Key result
Among smokers, smoking-associated electrocardiographic abnormalities such as an abnormally long JT interval significantly predicted an increased risk of cardiovascular mortality (HR 2.31) over a 22-year follow-up.
Why the study?
Smoking is linked to arrhythmia and sudden cardiac death through unclear mechanisms, and previous NHANES analyses of smoking and ECG abnormalities were incomplete.
Does smoking (serum cotinine > 15 ng/ml) increase the risk of ECG abnormalities and cardiovascular mortality in adults?
Cohort (n=5,653)
Yes
Does smoking (serum cotinine > 15 ng/ml) increase the risk of ECG abnormalities and cardiovascular mortality in adults?
Hazard Ratio: 2.31 (95% CI 1.13–4.71)
Smoking is associated with specific ECG abnormalities, including shortened PR and QRS and prolonged JT intervals, which predict long-term cardiovascular mortality in smokers.
ECG abnormalities may flag high-risk smokers for closer monitoring; extends prognostic associations but leaves open interventional trials.
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.
No takes yet. Share an insight, caveat, or question.
Irfan et al. (2024) conducted a cohort in General population (n=5,653). Smoking (serum cotinine > 15 ng/ml) vs. Nonsmokers (serum cotinine ≤ 15 ng/ml) was evaluated on Cardiovascular mortality in smokers with abnormally long JT interval (>95th percentile) (HR 2.31, 95% CI 1.13-4.71). Among smokers, smoking-associated electrocardiographic abnormalities such as an abnormally long JT interval significantly predicted an increased risk of cardiovascular mortality (HR 2.31) over a 22-year follow-up.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: