[OP.5B.04] SMOKING POTENTIATES THE RISK OF CARDIOVASCULAR DISEASE ASSOCIATED WITH TACHYCARDIA. (September 2017)

• Record Type: Journal Article
• Authors: Palatini, P.; Saladini, F.; Fania, C.; Mos, L.; Mazzer, A.; Casiglia, E.
• Is Part Of: Journal of hypertension. Volume 35(2017)Supplement 2
• Publication Date: 2017-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000523094.33698.15
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: Several studies have shown that resting heart rate (RHR) is a predictor of adverse outcome in hypertension. Smoking causes repeated sharp rises in RHR during the daytime hours which could favour this association. We did a prospective study to investigate whether smoking influences the risk of cardiovascular events (CVE) associated with elevated RHR in stage 1 hypertension. Design and method: The study was conducted in a cohort of 1204 18-to-45-year-old participants screened for stage 1 hypertension (21% smokers) from the HARVEST and followed for a median of 12.5 years (interquartile range, 5.5–17.4). RHR was calculated as the mean of 6 readings over 2 visits. Ambulatory heart rate was obtained in duplicate. Participants were stratified into 4 groups according to smoking (no/yes) and the presence or absence of tachycardia (RHR>80 bpm). In Cox regressions, data were adjusted for age, gender, BMI, parental CVE, lifestyle factors, baseline office and 24 h BP, total cholesterol, serum creatinine, and changes in BP and body weight from baseline to last available visit. Results: Tachycardia was present in 26.5% of participants. RHR did not differ according to smoking. However, the difference between age-and-sex-adjusted daytime heart rate and RHR was higher in smokers than non-smokers (2.6 ± 0.6 bpm versus 0.5 ± 0.3 bpm, p = 0.0023). During the follow-up 74 participants (6.1%) developed a CVE. RHR was an independent predictor of CVE (p = 0.0043) with a 63% increase in risk (95%CI, 17%-128%) for each 10-bpm increment in RHR. Inclusion of physical activity slightly attenuated the RHR-CVE association (p = 0.0082). In sensitivity analysis, the association held true among smokers (p = 0.0033) but not non-smokers (p = 0.12). Compared with non-smokers with normal RHR, the risk of CVE was 2.26 (1.06–4.85) in non-smokers with tachycardia, was 2.62 (1.44–4.78) in smokers with normal RHR, and was 5.65 (2.43–13.11) in smokers with tachycardia. In addition, for each 10-bpm increment in RHR during the follow-up there was a 35% (5%-72%) increase in risk of CVE. Conclusions: High RHR is an independent predictor of CVE in young subjects with stage 1 hypertension. Smoking causes an increase in daytime heart rate and magnifies the association between RHR and adverse outcome.