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      Atrial Fibrillation Begets Heart Failure and Vice Versa: Temporal Associations and Differences in Preserved Versus Reduced Ejection Fraction.

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          Abstract

          Atrial fibrillation (AF) and heart failure (HF) frequently coexist and together confer an adverse prognosis. The association of AF with HF subtypes has not been well described. We sought to examine differences in the temporal association of AF and HF with preserved versus reduced ejection fraction.

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          Most cited references42

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          Heart Disease and Stroke Statistics—2015 Update: A Report From the American Heart Association

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            A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation.

            Over the past decade, myocardial structure, cardiomyocyte function, and intramyocardial signaling were shown to be specifically altered in heart failure with preserved ejection fraction (HFPEF). A new paradigm for HFPEF development is therefore proposed, which identifies a systemic proinflammatory state induced by comorbidities as the cause of myocardial structural and functional alterations. The new paradigm presumes the following sequence of events in HFPEF: 1) a high prevalence of comorbidities such as overweight/obesity, diabetes mellitus, chronic obstructive pulmonary disease, and salt-sensitive hypertension induce a systemic proinflammatory state; 2) a systemic proinflammatory state causes coronary microvascular endothelial inflammation; 3) coronary microvascular endothelial inflammation reduces nitric oxide bioavailability, cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocytes; 4) low PKG activity favors hypertrophy development and increases resting tension because of hypophosphorylation of titin; and 5) both stiff cardiomyocytes and interstitial fibrosis contribute to high diastolic left ventricular (LV) stiffness and heart failure development. The new HFPEF paradigm shifts emphasis from LV afterload excess to coronary microvascular inflammation. This shift is supported by a favorable Laplace relationship in concentric LV hypertrophy and by all cardiac chambers showing similar remodeling and dysfunction. Myocardial remodeling in HFPEF differs from heart failure with reduced ejection fraction, in which remodeling is driven by loss of cardiomyocytes. The new HFPEF paradigm proposes comorbidities, plasma markers of inflammation, or vascular hyperemic responses to be included in diagnostic algorithms and aims at restoring myocardial PKG activity. Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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              Estimates of current and future incidence and prevalence of atrial fibrillation in the U.S. adult population.

              Estimates and projections of diagnosed incidence and prevalence of atrial fibrillation (AF) in the United States have been highly inconsistent across published studies. Although it is generally acknowledged that AF incidence and prevalence are increasing due to growing numbers of older people in the U.S. population, estimates of the rate of expected growth have varied widely. Reasons for these variations include differences in study design, covered time period, birth cohort, and temporal effects, as well as improvements in AF diagnosis due to increased use of diagnostic tools and health care awareness. The objective of this study was to estimate and project the incidence and prevalence of diagnosed AF in the United States out to 2030. A large health insurance claims database for the years 2001 to 2008, representing a geographically diverse 5% of the U.S. population, was used in this study. The trend and growth rate in AF incidence and prevalence was projected by a dynamic age-period cohort simulation progression model that included all diagnosed AF cases in future prevalence projections regardless of follow-up treatment, as well as those cases expected to be chronic in nature. Results from the model showed that AF incidence will double, from 1.2 million cases in 2010 to 2.6 million cases in 2030. Given this increase in incidence, AF prevalence is projected to increase from 5.2 million in 2010 to 12.1 million cases in 2030. The effect of uncertainty in model parameters was explored in deterministic and probabilistic sensitivity analyses. Variability in future trends in AF incidence and recurrence rates has the greatest impact on the projected estimates of chronic AF prevalence. It can be concluded that both incidence and prevalence of AF are likely to rise from 2010 to 2030, but there exists a wide range of uncertainty around the magnitude of future trends.
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                Author and article information

                Journal
                Circulation
                Circulation
                Ovid Technologies (Wolters Kluwer Health)
                1524-4539
                0009-7322
                Feb 02 2016
                : 133
                : 5
                Affiliations
                [1 ] From Cardiovascular Medicine Section, Department of Medicine (R.S., J.W.M., R.S.V., E.J.B.) and Section of Preventive Medicine and Epidemiology (R.S.V.), Boston University School of Medicine, MA; Data Coordinating Center (N.W.) and Department of Epidemiology (E.J.B.), Boston University School of Public Health, MA; Department of Mathematics and Statistics, Boston University, MA (M.G.L.); National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, MA (M.G.L., J.W.M., S.C., R.S.V., D.L., E.J.B., J.E.H.); Cardiology Division, Department of Medicine, University of Massachusetts Medical School, Boston (D.D.M., E.J.B.); Cardiology Division (S.A.L., P.T.E., J.E.H.) and Cardiovascular Research Center (S.A.L., P.T.E., J.E.H.), Massachusetts General Hospital, Harvard Medical School, Boston; Program in Medical Population Genetics, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge (S.A.L., P.T.E.); Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (S.C.); Institute for Clinical Evaluative Sciences and Toronto General Hospital, University of Toronto, ON, Canada (D.S.L.); Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University, Nashville, TN (T.J.W.); and Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, MD (D.L.).
                [2 ] From Cardiovascular Medicine Section, Department of Medicine (R.S., J.W.M., R.S.V., E.J.B.) and Section of Preventive Medicine and Epidemiology (R.S.V.), Boston University School of Medicine, MA; Data Coordinating Center (N.W.) and Department of Epidemiology (E.J.B.), Boston University School of Public Health, MA; Department of Mathematics and Statistics, Boston University, MA (M.G.L.); National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, MA (M.G.L., J.W.M., S.C., R.S.V., D.L., E.J.B., J.E.H.); Cardiology Division, Department of Medicine, University of Massachusetts Medical School, Boston (D.D.M., E.J.B.); Cardiology Division (S.A.L., P.T.E., J.E.H.) and Cardiovascular Research Center (S.A.L., P.T.E., J.E.H.), Massachusetts General Hospital, Harvard Medical School, Boston; Program in Medical Population Genetics, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge (S.A.L., P.T.E.); Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (S.C.); Institute for Clinical Evaluative Sciences and Toronto General Hospital, University of Toronto, ON, Canada (D.S.L.); Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University, Nashville, TN (T.J.W.); and Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, MD (D.L.). jho1@mgh.harvard.edu.
                Article
                CIRCULATIONAHA.115.018614 NIHMS747587
                10.1161/CIRCULATIONAHA.115.018614
                4738087
                26746177
                2a9ec2b8-3919-425c-aa00-b2c1918af08d
                History

                atrial fibrillation,epidemiology,heart failure,mortality,ventricular function, left

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