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Published on: February 26, 2013
Lower heart rates and beta-blockers are associated with new-onset atrial fibrillation
Nicole Habel1, Jeanne du Fay de Lavallaz2, Margaret Infeld1
1University of Vermont Larner College of Medicine, Department of Medicine, Division of Cardiology, Burlington, VT, 05401, USA.
Insights
Lower heart rates (HRs) are linked to higher brain natriuretic peptide (BNP) levels and increased risk of atrial fibrillation (AF). Beta-blocker use also elevates AF risk, potentially by lowering resting HR.
Area of Science:
- Cardiology
- Clinical Electrophysiology
- Pharmacology
Background:
- Lower heart rates (HRs) can prolong diastole, increasing filling pressures and wall stress.
- This may lead to elevated brain natriuretic peptide (BNP) levels and incident atrial fibrillation (AF).
- Beta-blockers might increase AF risk by suppressing resting HRs.
Purpose of the Study:
- To investigate the relationship between HR, BNP, beta-blockers, and new-onset AF.
- To analyze these associations in the REVEAL-AF and SPRINT cohorts.
Main Methods:
- REVEAL-AF: 383 subjects without prior AF, mean CHA2DS2VASC score 4.4, followed up to 30 months with insertable cardiac monitors.
- SPRINT: 7595 patients without prior AF, mean CHA2DS2VASC score 2.3, followed up to 60 months.
Main Results:
- Below-median HRs (<75 bpm) were associated with 2.4-fold higher BNP levels and increased AF incidence (37% vs. 27%).
- In SPRINT, HR <75 bpm and beta-blocker use were linked to higher AF rates (1.9% vs. 0.7% and 2.5% vs. 0.6%, respectively).
- Beta-blocker use showed a hazard ratio of 3.72 for developing AF (p < 0.001).
Conclusions:
- Lower HRs correlate with higher BNP and incident AF, suggesting hemodynamic effects similar to diastolic dysfunction.
- Beta-blocker-induced suppression of resting HR may explain their association with increased AF risk.
Background:
Lower heart rates (HRs) prolong diastole, which increases filling pressures and wall stress. As a result, lower HRs may be associated with higher brain natriuretic peptide (BNP) levels and incident atrial fibrillation (AF). Beta-blockers may increase the risk for AF due to suppression of resting HRs.
Objective:
Examine the relationships of HR, BNP, beta-blockers and new-onset AF in the REVEAL-AF and SPRINT cohort of subjects at risk for developing AF.
Methods:
In REVEAL-AF, 383 subjects without a history of AF and a mean CHA2DS2VASC score of 4.4 ± 1.3 received an insertable cardiac monitor and were followed up to 30 months. In SPRINT, 7595 patients without prior history of AF and a mean CHA2DS2VASC score of 2.3 ± 1.2 were followed up to 60 months.
Results:
The median daytime HR in the REVEAL-AF cohort was 75bpm [IQR 68-83]. Subjects with below-median HRs had 2.4-fold higher BNP levels compared to subjects with above-median HRs (median BNP [IQR]: 62 pg/dl [37-112] vs. 26 pg/dl [13-53], p < 0.001). HRs <75bpm were associated with a higher incidence of AF: 37% vs. 27%, p < 0.05. This was validated in the SPRINT cohort after adjusting for AF risk factors. Both a HR < 75bpm and beta-blocker use were associated with a higher rate of AF: 1.9 vs 0.7% (p < 0.001) and 2.5% vs. 0.6% (p < 0.001), respectively. The hazard ratio for patients on beta-blockers to develop AF was 3.72 [CI 2.32, 5.96], p < 0.001.
Conclusions:
Lower HRs are associated with higher BNP levels and incident AF, mimicking the hemodynamic effects of diastolic dysfunction. Suppression of resting HR by beta-blockers could explain their association with incident AF.
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