Association of Bradycardia With Incident CVD and Mortality
What is the effect of resting bradycardia on mortality in patients without cardiovascular disease (CVD)?
Individuals n = 6,733, ages 45-84 years, and without known CVD at baseline [2000-2002]) who participated in the MESA study were subjects of this retrospective analysis. Resting heart rate (HR) was determined on a standard 12-lead electrocardiogram. Patients with atrial arrhythmias or evidence of a pacemaker were excluded. Bradycardia was defined as HR <50 bpm. Study participants were followed for cardiovascular events and mortality every 9-12 months. The analysis was performed in 2014.
The mean age was 62 years and 47% of the cohort was male. The mean HR among participants (n = 5,831) not taking a HR-modifying drug (beta-blockers, nondihydropyridine calcium channel blockers, digitalis, or antiarrhythmic medications) was 63 ± 10 bpm; and 5% of these individuals had a HR <50 bpm. The mean HR among those taking a HR-modifying agent (n = 902) was 60 ± 10 bpm, with 11% having bradycardia. Among the former, the adjusted mortality risk was not different in individuals with bradycardia (hazard ratio, 0.71; 95% confidence interval [CI], 0.41-1.1; p = 0.12), whereas it was higher in patients with HR >80 bpm (hazard ratio, 1.5; 95% CI, 1.1-2.1; p = 0.01). In individuals taking HR-modifying drugs, the mortality rates were higher both for those with HR <50 bpm (hazard ratio, 2.4; 95% CI, 1.4-4.2; p = 0.002) and HR >80 bpm (hazard ratio, 3.6; 95% CI, 1.6-7.6; p = 0.001).
Bradycardia was not associated with an increase in mortality in individuals without CVD. It may be associated with adverse events in patients taking HR-altering medications.
These findings should be reassuring for individuals with bradycardia who are free of CVD. Bradycardia can be found in a variety of contexts, including heightened vagal tone as in fit individuals, genetic basis, treatment with HR-modifying agents, structural remodeling of the atria (including the sinus node complex), and others. Given the diverse mechanisms of bradycardia, outcomes should be expected to be different as well. The main limitation of the study is the inclusion of individuals in whom CVD was thought to be absent and yet were taking HR-modifying agents.
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