Matthew Nayor1, Danielle M Enserro2, Vanessa Xanthakis3, Martin G Larson4, Emelia J Benjamin5, Jayashri Aragam6, Gary F Mitchell7, Ramachandran S Vasan8. 1. Framingham Heart Study, Framingham, Massachusetts; Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: mnayor@mgh.harvard.edu. 2. Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts. 3. Framingham Heart Study, Framingham, Massachusetts; Section of Preventive Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. 4. Framingham Heart Study, Framingham, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. 5. Framingham Heart Study, Framingham, Massachusetts; Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts; Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. 6. Cardiovascular Division, Veterans Administration Hospital, West Roxbury, Massachusetts; Harvard Medical School, Boston, Massachusetts. 7. Cardiovascular Engineering, Inc., Norwood, Massachusetts. 8. Framingham Heart Study, Framingham, Massachusetts; Section of Preventive Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Abstract
OBJECTIVES: This study sought to evaluate the course, correlates, and prognosis of longitudinal changes in left ventricular (LV) diastolic dysfunction (DD) in the community-based Framingham Heart Study. BACKGROUND: Relationships of clinical risk factors to longitudinal progression of DD are incompletely understood. METHODS: Diastolic function was assessed by echocardiography performed at consecutive examinations (visits 1 and 2, mean interval 5.6 years) in 1,740 participants (64 ± 8 years of age at visit 1, 59% women) with normal LV systolic function and no atrial fibrillation. RESULTS: Of 1,615 individuals with normal-to-mild DD at visit 1, 198 (12%) progressed to ≥ moderate DD at visit 2. Progression was more likely in women and with advancing age (p < 0.0001). Of 125 individuals with ≥ moderate DD at visit 1, 25 (20%) regressed to normal-to-mild DD by visit 2. Regression of DD was associated with younger age (p < 0.03). In stepwise regression models, age, female sex, baseline and changes in systolic blood pressure, diastolic blood pressure, body mass index, serum triglycerides, and diabetes were positively associated with worsening diastolic function (all p < 0.05). Noncardiac comorbidity tracked with progressive DD. Cardiovascular disease (CVD) or death events occurred in 44 of 1,509 participants free of CVD at visit 2, during 2.7 ± 0.6 years of post-visit 2 follow-up. Presence of ≥ moderate DD was associated with higher risk (age- and sex-adjusted hazard ratio for CVD or death: 2.14; 95% confidence interval: 1.06 to 4.32; p = 0.03). CONCLUSIONS: In a community-based cohort of middle-aged to older adults, cardiometabolic risk factors and noncardiac comorbidities were associated with DD progression. Moderate or worse DD was associated with higher risk of CVD or death.
OBJECTIVES: This study sought to evaluate the course, correlates, and prognosis of longitudinal changes in left ventricular (LV) diastolic dysfunction (DD) in the community-based Framingham Heart Study. BACKGROUND: Relationships of clinical risk factors to longitudinal progression of DD are incompletely understood. METHODS: Diastolic function was assessed by echocardiography performed at consecutive examinations (visits 1 and 2, mean interval 5.6 years) in 1,740 participants (64 ± 8 years of age at visit 1, 59% women) with normal LV systolic function and no atrial fibrillation. RESULTS: Of 1,615 individuals with normal-to-mild DD at visit 1, 198 (12%) progressed to ≥ moderate DD at visit 2. Progression was more likely in women and with advancing age (p < 0.0001). Of 125 individuals with ≥ moderate DD at visit 1, 25 (20%) regressed to normal-to-mild DD by visit 2. Regression of DD was associated with younger age (p < 0.03). In stepwise regression models, age, female sex, baseline and changes in systolic blood pressure, diastolic blood pressure, body mass index, serum triglycerides, and diabetes were positively associated with worsening diastolic function (all p < 0.05). Noncardiac comorbidity tracked with progressive DD. Cardiovascular disease (CVD) or death events occurred in 44 of 1,509 participants free of CVD at visit 2, during 2.7 ± 0.6 years of post-visit 2 follow-up. Presence of ≥ moderate DD was associated with higher risk (age- and sex-adjusted hazard ratio for CVD or death: 2.14; 95% confidence interval: 1.06 to 4.32; p = 0.03). CONCLUSIONS: In a community-based cohort of middle-aged to older adults, cardiometabolic risk factors and noncardiac comorbidities were associated with DD progression. Moderate or worse DD was associated with higher risk of CVD or death.
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