Why the study?
Smoking is a major preventable risk factor for cardiovascular disease and is strongly associated with sudden cardiac death, prompting investigation into its relationship with heart rate recovery and ventricular repolarization recovery indices.
Does cigarette smoking impair heart rate recovery and ventricular repolarization parameters during exercise testing in healthy individuals without known cardiovascular disease?
Does cigarette smoking impair heart rate recovery and ventricular repolarization parameters during exercise testing in healthy individuals without known cardiovascular disease?
Cigarette smoking in healthy individuals is associated with impaired autonomic regulation and abnormal ventricular repolarization recovery during exercise testing, potentially explaining increased arrhythmia risk.
Smoking associated with impaired HRR and repolarization indices in healthy adults; hypothesis-generating for arrhythmia risk and needs prospective validation.
INTRODUCTION: Smoking is a major preventable risk factor for cardiovascular disease and is strongly associated with sudden cardiac death (SCD). This study investigated the relationship between the heart rate recovery index (HRR-I), T peak-end recovery index (Tp-eR-I), and QT interval recovery index (QTR-I) in smokers compared with non-smokers. METHODS: This cross-sectional study, conducted in Bilkent City Hospital, Ankara, Turkey, between May 2017 and June 2025, included 150 healthy smokers (120 males, 30 females) and 123 healthy non-smokers (97 males, 26 females). Smoking data are self-reported. All participants underwent symptom-limited treadmill exercise testing using the Bruce protocol. Heart rate (HR), QT, and Tp-e intervals were measured at baseline, peak exercise, and during recovery periods. HRR-I was calculated as the difference between peak HR and HR at the 1st, 2nd, and 3rd minutes of recovery. Tp-eR-I and QTR-I were calculated as the differences between baseline values and those obtained during peak, 1st, 2nd and 3rd minutes recovery times. RESULTS: Smokers exhibited significantly lower HRR-I values at the 1st [18.6 ± 7.1 vs 24.2 ± 6.9, p<0.001; 17.9 (95% CI: 12.9-22.9)], 2nd [27.4 ± 7.3 vs 33.1 ± 7.1, p<0.001; 10.7 (95% CI 7.3-14.1)], and 3rd minutes [33.8 ± 7.9 vs 39.5 ± 8.3, p<0.001; 13.4 (95% CI: 9.6-17.2)] of recovery compared with non-smokers. Tp-eR-I and QTR-I values were significantly higher in smokers [Tp-eR-I: 7.8 ± 2.6 vs 5.2 ± 2.1, p<0.001; 18 (95% CI: 12-24)] [QTR-I: 24.5 ± 6.3 vs 18.9 ± 5.8, p<0.001; 12 (95% CI: 6-18)]. Smoking intensity was positively associated with Tp-eR-I (r=0.41, p<0.001) and QTR-I (r=0.36, p<0.001), and negatively associated with HRR-I (r= -0.39, p<0.001). CONCLUSIONS: Cigarette smoking impairs autonomic regulation as reflected by reduced HRR-I and abnormal ventricular repolarization recovery, shown by increased Tp-eR-I and QTR-I. These findings suggest that smoking disrupts sympathetic-parasympathetic balance and myocardial repolarization, potentially explaining the higher incidence of arrhythmias and sudden cardiac death among smokers.
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Cosgun et al. (2026) studied this question.
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