BACKGROUND: Atrial fibrillation (AF) is widely perceived to originate from the left atrium (LA). Whether increases in right ventricular (RV) afterload in older adults play an etiological role in AF genesis independent of LA and left ventricular (LV) remodeling is unknown.
RESEARCH QUESTION: Is higher RV afterload associated with greater AF risk independent of LA and LV remodeling?
STUDY DESIGN AND METHODS: In this observational prospective study, we included 2,246 community-dwelling older adults (mean age, 75 years) without known cardiovascular disease, with LV ejection fraction > 50%, LA volume index < 34 mL/m 2, and E/e' ratio < 14 and a measurable functional tricuspid regurgitation jet velocity. From 2D-echocardiograms, we estimated pulmonary artery systolic pressure (PASP) and pulmonary vascular resistance (PVR). We ascertained incident AF (through 2018) from hospital discharge codes and death certificates. We estimated hazard ratios (HR) by Cox regression.
RESULTS: During follow-up (median, 6.3 years; interquartile interval, 5.5-6.9 years), 215 participants developed AF. AF risk was significantly higher in the third (vs first) tertile of PASP (HR, 1.65; 95% CI, 1.08-2.54) and PVR (HR, 1.38; 95% CI, 1.00-2.08) independent of LA and LV structure and function, heart rate, BMI, prevalent sleep apnea, systemic BP, antihypertensive medications, and lung, kidney, and thyroid function. These associations persisted after further exclusion of participants with tricuspid regurgitation jet velocity > 2.8 m/s and lateral and septal mitral annular velocity above age- and sex-specific reference limits.
INTERPRETATION: In older adults, higher RV afterload is associated with greater AF risk independent of LA and LV remodeling. Future research should focus on confirming this novel association and elucidate underlying mechanisms.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Oct 2022|
Bibliographical noteFunding Information:
Funding/support: The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health , Department of Health and Human Services , under Contract nos. ( HHSN268201700001I , HHSN268201700002I , HHSN268201700003I , HHSN268201700005I , and HHSN268201700004I ).
Author contributions: All authors contributed substantially to this research. R. R. Parikh takes responsibility for (is the guarantor of) the content of the manuscript, including the data and analysis. R. R. Parikh and L. Y. Chen contributed to concept, study design, drafting manuscript, and data analysis. Remaining authors, F. L Norby, W. Wang, T. Thenappan, K. W Prins, J. R. Van't Hof, P. L. Lutsey, S. D. Solomon, and A. M. Shah contributed to study design, reviewed the interpretations of the outcomes of the data analysis, and provided recommendations for improvements, made critical revisions to the manuscript about the research, and finalized the manuscript about the research. Funding/support: The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under Contract nos. (HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700005I, and HHSN268201700004I). Financial/nonfinancial disclosures: The authors have reported to CHEST the following: T. T. reports receiving honoraria from Gilead and Actelion outside the submitted work. K. W. P. reports receiving honoraria from Actelion and research support from United Therapeutics outside the submitted work. A. M. S. reports receiving research support from National Institutes of Health/National Heart, Lung, and Blood Institute, and from Novartis through the Brigham and Women's Hospital and consulting fees from Bellerophon and Philips Ultrasound outside the submitted work. S. D. S. reported grants from Alnylam, Amgen, AstraZeneca, Bellerophon, Bayer, BMS, Celladon, Cytokinetics, Eidos, Gilead, GSK, Ionis, Lone Star Heart, Mesoblast, MyoKardia, Neurotronik, National Institutes of Health/National Heart, Lung, and Blood Institute, Novartis, Respicardia, Sanofi Pasteur, Theracos, and personal fees from Akros, Alnylam, Amgen, Arena, AstraZeneca, Bayer, BMS, Cardior, Cardurion, Corvia, Cytokinetics, Daiichi-Sankyo, Gilead, GSK, Ironwood, Merck, Myokardia, Novartis, Roche, Takeda, Theracos, Quantum Genetics, Cardurion, AoBiome, Janssen, Cardiac Dimensions, Sanofi Pasteur, Tenaya, Dinaqor, Tremeau, CellProThera, and Moderna outside the submitted work. L. Y. C. is supported by grants R01 HL126637, R01 HL141288, RF1 NS127266, R01 HL158022, and K24 HL155813 from the National Heart, Lung, and Blood Institute of the National Institutes of Health. None declared (R. P. W. W. F. L. N. J. R. V. P. L. L.). Role of sponsor: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript. Other contributions: The authors thank the staff and participants of the ARIC study for their important contributions. Additional information: The e-Appendix and e-Tables are available online under “Supplementary Data.”
- Antihypertensive Agents
- Atrial Fibrillation/complications
- Cyclophosphamide/analogs & derivatives
- Prospective Studies
- Tricuspid Valve Insufficiency
- Ventricular Remodeling
PubMed: MeSH publication types
- Observational Study
- Journal Article
- Research Support, N.I.H., Extramural