Article Text
Abstract
Objective A higher premature ventricular complex (PVC) frequency is associated with incident congestive heart failure (CHF) and death. While certain PVC characteristics may contribute to that risk, the current literature stems from patients in medical settings and is therefore prone to referral bias. This study aims to identify PVC characteristics associated with incident CHF in a community-based setting.
Methods The Cardiovascular Health Study is a cohort of community-dwelling individuals who underwent prospective evaluation and follow-up. We analysed 24-hour Holter data to assess PVC characteristics and used multivariable logistic and Cox proportional hazards models to identify predictors of a left ventricular ejection fraction (LVEF) decline and incident CHF, respectively.
Results Of 871 analysed participants, 316 participants exhibited at least 10 PVCs during the 24-hour recording. For participants with PVCs, the average age was 72±5 years, 41% were women and 93% were white. Over a median follow-up of 11 years, 34% developed CHF. After adjusting for demographics, cardiovascular comorbidities, antiarrhythmic drug use and PVC frequency, a greater heterogeneity of the PVC coupling interval was associated with an increased risk of LVEF decline and incident CHF. Of note, neither PVC duration nor coupling interval duration exhibited a statistically significant relationship with either outcome.
Conclusions In this first community-based study to identify Holter-based features of PVCs that are associated with LVEF reduction and incident CHF, the fact that coupling interval heterogeneity was an independent risk factor suggests that the mechanism of PVC generation may influence the risk of heart failure.
- ventricular premature complexes
- cardiomyopathies
- heart failure
- arrhythmias
- cardiac
- echocardiography
Data availability statement
Data may be obtained from a third party and are not publicly available.
Statistics from Altmetric.com
Data availability statement
Data may be obtained from a third party and are not publicly available.
Footnotes
Presented at Part of the data and the abstract included in this manuscript were electronically presented at the Heart Rhythm Society Scientific Sessions in San Diego, May 2020.
Contributors WBL and GMM conceived of the analysis plan. ES, CF, DSS, BMP, NS, SH, PKS and JG assisted with data collection and material support. WBL performed primary Holter data analysis with assistance of XH and RH. TAD, EV and GN performed the statistical analyses. WBL and GMM prepared the manuscript. All authors contributed to reviewing or revising the manuscript and approved the final version.
Funding In addition to a Resident Clinical and Translational Research Funding (RRF) and a Cardiology Innovation Award from the University of California, San Francisco, this research was supported by contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, 75N92021D00006, and grants U01HL080295 and U01HL130114 from the National Heart, Lung, and Blood Institute (NHLBI), with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided by R01AG023629 from the National Institute on Ageing (NIA). A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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