Mayank Sardana1, Gregory Nah2, Connie W Tsao3, Adedotun A Ogunsua1, Eric Vittinghoff2, Randell C Thomas2, Susan Cheng4, Aditya Vaze1, Jayashri R Aragam5, Gary F Mitchell6, Emelia J Benjamin7, Ramachandran S Vasan7, Gerard P Aurigemma1, Nelson B Schiller2, David D McManus1, Nisha I Parikh8. 1. Cardiology Division, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts. 2. Cardiology Division, Department of Medicine, University of California, San Francisco, San Francisco, California. 3. Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. 4. Boston University's and National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham; and Section of Preventive Medicine and Epidemiology and Cardiovascular Medicine, Department of Medicine, and Department of Epidemiology, Boston University Schools of Medicine and Public Health, Boston, Massachusetts; Cardiology Division, Department of Medicine, Brigham and Women's Hospital, Massachusetts. 5. Cardiology Division, Department of Medicine, Brigham and Women's Hospital, Massachusetts; Veterans Administration Medical Center, West Roxbury, and Harvard Medical School, Boston, Massachusetts. 6. Boston University's and National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham; and Section of Preventive Medicine and Epidemiology and Cardiovascular Medicine, Department of Medicine, and Department of Epidemiology, Boston University Schools of Medicine and Public Health, Boston, Massachusetts; Cardiovascular Engineering, Norwood, Massachusetts. 7. Boston University's and National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham; and Section of Preventive Medicine and Epidemiology and Cardiovascular Medicine, Department of Medicine, and Department of Epidemiology, Boston University Schools of Medicine and Public Health, Boston, Massachusetts. 8. Cardiology Division, Department of Medicine, University of California, San Francisco, San Francisco, California. Electronic address: nparikh@medicine.ucsf.edu.
Abstract
BACKGROUND: Left atrial (LA) remodeling is a predictor of cardiovascular disease (CVD). We performed measurement of the LA function index (LAFI), a composite measure of LA structure and function, in a community-based cohort and here report the distribution and cross-sectional correlates of LAFI. METHODS: In 1,719 Framingham Offspring Study participants (54% women, mean age 66 ± 9 years), we derived LAFI from the LA emptying fraction, left ventricular (LV) outflow tract velocity time integral, and indexed maximal LA volume. We used multivariable linear regression to assess the clinical and echocardiographic correlates of LAFI adjusting for age, sex, anthropometric measurements, and CVD risk factors. RESULTS: The average LAFI was 35.2 ± 12.1. Overall, LAFI declined with advancing age (β = -0.27, P < .001). LAFI was significantly higher (37.5 ± 11.6) in a subgroup of participants free of CVD and CVD risk factors compared with those with either of these conditions (34.5 ± 12.2). In multivariable models, LAFI was inversely related to antihypertensive use (β = -1.26, P = .038), prevalent atrial fibrillation (β = -4.46, P = .001), heart failure (β = -5.86, P = .008), and coronary artery disease (β = -2.01, P = .046). In models adjusting for echocardiographic variables, LAFI was directly related to LV ejection fraction (β = 14.84, P < .001) and inversely related to LV volume (β = -7.03, P < .001). CONCLUSIONS: LAFI was inversely associated with antihypertensive use and prevalent CVD and was related to established echocardiographic traits of LV remodeling. Our results offer normative ranges for LAFI in a white community-based sample and suggest that LAFI represents a marker of pathological atrial remodeling.
BACKGROUND: Left atrial (LA) remodeling is a predictor of cardiovascular disease (CVD). We performed measurement of the LA function index (LAFI), a composite measure of LA structure and function, in a community-based cohort and here report the distribution and cross-sectional correlates of LAFI. METHODS: In 1,719 Framingham Offspring Study participants (54% women, mean age 66 ± 9 years), we derived LAFI from the LA emptying fraction, left ventricular (LV) outflow tract velocity time integral, and indexed maximal LA volume. We used multivariable linear regression to assess the clinical and echocardiographic correlates of LAFI adjusting for age, sex, anthropometric measurements, and CVD risk factors. RESULTS: The average LAFI was 35.2 ± 12.1. Overall, LAFI declined with advancing age (β = -0.27, P < .001). LAFI was significantly higher (37.5 ± 11.6) in a subgroup of participants free of CVD and CVD risk factors compared with those with either of these conditions (34.5 ± 12.2). In multivariable models, LAFI was inversely related to antihypertensive use (β = -1.26, P = .038), prevalent atrial fibrillation (β = -4.46, P = .001), heart failure (β = -5.86, P = .008), and coronary artery disease (β = -2.01, P = .046). In models adjusting for echocardiographic variables, LAFI was directly related to LV ejection fraction (β = 14.84, P < .001) and inversely related to LV volume (β = -7.03, P < .001). CONCLUSIONS: LAFI was inversely associated with antihypertensive use and prevalent CVD and was related to established echocardiographic traits of LV remodeling. Our results offer normative ranges for LAFI in a white community-based sample and suggest that LAFI represents a marker of pathological atrial remodeling.
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