Response to Letter Regarding Article, “Atrial Fibrillation Begets Heart Failure and Vice Versa: Temporal Associations and Differences in Preserved Versus Reduced Ejection Fraction”
2016; Lippincott Williams & Wilkins; Volume: 133; Issue: 23 Linguagem: Inglês
10.1161/circulationaha.116.022835
ISSN1524-4539
AutoresRajalakshmi Santhanakrishnan, Na Wang, Martin G. Larson, Jared W. Magnani, David D. McManus, Steven A. Lubitz, Patrick T. Ellinor, Susan Cheng, Ramachandran S. Vasan, Douglas S. Lee, Thomas J. Wang, Daniel Levy, Emelia J. Benjamin, Jennifer E. Ho,
Tópico(s)Cardiac electrophysiology and arrhythmias
ResumoHomeCirculationVol. 133, No. 23Response to Letter Regarding Article, "Atrial Fibrillation Begets Heart Failure and Vice Versa: Temporal Associations and Differences in Preserved Versus Reduced Ejection Fraction" Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Letter Regarding Article, "Atrial Fibrillation Begets Heart Failure and Vice Versa: Temporal Associations and Differences in Preserved Versus Reduced Ejection Fraction" Rajalakshmi Santhanakrishnan, MBBS Na Wang, MA Martin G. Larson, SD Jared W. Magnani, MD, MSc David D. McManus, MD Steven A. Lubitz, MD, MPH and Patrick T. Ellinor, MD, PhD Susan Cheng, MD Ramachandran S. Vasan, MD Douglas S. Lee, MD Thomas J. Wang, MD Daniel Levy, MD Emelia J. Benjamin, MD, ScM Jennifer E. Ho, MD Rajalakshmi SanthanakrishnanRajalakshmi Santhanakrishnan Cardiovascular Medicine Section Department of Medicine Boston University School of Medicine Boston, MA Na WangNa Wang Data Coordinating Center Boston University School of Public Health Boston, MA Martin G. LarsonMartin G. Larson Department of Mathematics and Statistics Boston University Boston, MA Jared W. MagnaniJared W. Magnani Cardiovascular Medicine Section Department of Medicine Boston University School of Medicine Boston, MA David D. McManusDavid D. McManus Cardiology Division Department of Medicine University of Massachusetts Medical School Boston, MA Steven A. LubitzSteven A. Lubitz Cardiology Division Massachusetts General Hospital Harvard Medical School Boston, MA and Patrick T. EllinorPatrick T. Ellinor Cardiology Division Massachusetts General Hospital Harvard Medical School Boston, MA Susan ChengSusan Cheng National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham, MA Ramachandran S. VasanRamachandran S. Vasan Section of Preventive Medicine and Epidemiology Boston University School of Medicine Boston, MA Douglas S. LeeDouglas S. Lee Institute for Clinical Evaluative Sciences and Toronto General Hospital University of Toronto Ontario, Canada Thomas J. WangThomas J. Wang Division of Cardiovascular Medicine Department of Medicine Vanderbilt University Nashville, TN Daniel LevyDaniel Levy National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham, MA Emelia J. BenjaminEmelia J. Benjamin Department of Epidemiology Boston University School of Public Health Boston, MA Jennifer E. HoJennifer E. Ho Cardiovascular Research Center Massachusetts General Hospital Boston, MA Originally published7 Jun 2016https://doi.org/10.1161/CIRCULATIONAHA.116.022835Circulation. 2016;133:e692–e693We appreciate the insights presented by Providencia and Lambiase in a letter referring to our article, "Atrial Fibrillation Begets Heart Failure and Vice Versa."1 We share the view that the close association of atrial fibrillation (AF) and heart failure (HF) may represent clinical manifestations of the same underlying "whole-heart" cardiomyopathy, driven by common mechanisms such as fibrosis and inflammation.2 The authors raise the question of whether temporality in AF and HF development may support a global cardiomyopathy.We focused our article on HF subtypes, which did not allow for examination of subgroups with concurrent versus preexisting or future AF because of limited power within each HF subtype. However, the effect of concurrent AF/HF (versus diagnoses separated in time) was previously examined for overall HF among Framingham Heart Study participants.3 In subjects with AF, HF as a comorbid condition was associated with higher mortality, with similar effect sizes for prior HF (hazard ratio, 2.2; 95% confidence interval, 1.6–3.0 in men) and HF diagnosed concurrently on the same day as AF (hazard ratio, 2.4; 95% confidence interval, 1.6–3.5 in men). Conversely, in those with known HF, AF (whether preexisting or concurrent) was not associated with increased mortality. Similarly, in a study from Olmsted County that examined participants with HF with preserved ejection fraction, the presence of concurrent AF (diagnosed within 30 days of HF) showed a trend toward poor survival but was not significant in an age- and sex-adjusted model in comparison with sinus rhythm patients (P=0.11).4 This study did not directly compare mortality among participants with concurrent versus prevalent AF. Interestingly, individuals with previous AF had larger left atrial volumes than those with concurrent AF (55 versus 47 mL/m2, respectively, P<0.05).Taken together, these existing studies do not support a worse prognosis among individuals who develop concurrent HF and AF in comparison with those who develop HF and AF separated in time. However, we do know that AF and HF conjointly portend a poor prognosis. We agree with the authors that much remains to be discovered with respect to defining underlying pathophysiologic mechanisms, with the ultimate goal of targeted therapies, whether these therapies be aimed at rhythm control or myocardial processes. We also find intriguing the concept of distinct atrial and ventricular myopathic processes as raised by Providencia and Lambiase, and agree that advanced imaging techniques may be useful in interrogating these processes in future work.Rajalakshmi Santhanakrishnan, MBBSCardiovascular Medicine SectionDepartment of MedicineBoston University School of MedicineBoston, MANa Wang, MAData Coordinating Center Boston University School of Public Health, Boston, MAMartin G. Larson, SDDepartment of Mathematics and StatisticsBoston UniversityBoston, MAJared W. Magnani, MD, MScCardiovascular Medicine SectionDepartment of MedicineBoston University School of MedicineBoston, MADavid D. McManus, MDCardiology DivisionDepartment of MedicineUniversity of Massachusetts Medical SchoolBoston, MASteven A. Lubitz MD, MPHPatrick T. Ellinor MD, PhDCardiology DivisionMassachusetts General HospitalHarvard Medical SchoolBoston, MASusan Cheng, MDNational Heart, Lung, and Blood Institute's and Boston University's Framingham Heart StudyFramingham, MARamachandran S. Vasan, MDSection of Preventive Medicine and EpidemiologyBoston University School of MedicineBoston, MADouglas S. Lee, MDInstitute for Clinical Evaluative Sciences and Toronto General HospitalUniversity of TorontoOntario, CanadaThomas J. Wang, MDDivision of Cardiovascular MedicineDepartment of MedicineVanderbilt UniversityNashville, TNDaniel Levy, MDNational Heart, Lung, and Blood Institute's and Boston University's Framingham Heart StudyFramingham, MAEmelia J. Benjamin, MD, ScMDepartment of EpidemiologyBoston UniversitySchool of Public HealthBoston, MAJennifer E. Ho, MDCardiovascular Research Center Massachusetts General HospitalBoston, MASources of FundingDr Ho is supported by NIH K23-HL116780.DisclosuresNone.References1. Santhanakrishnan R, Wang N, Larson MG, Magnani JW, McManus DD, Lubitz SA, Ellinor PT, Cheng S, Vasan RS, Lee DS, Wang TJ, Levy D, Benjamin EJ, Ho JE. Atrial fibrillation begets heart failure and vice versa: temporal associations and differences in preserved versus reduced ejection fraction.Circulation. 2016; 133:484–492. doi: 10.1161/CIRCULATIONAHA.115.018614.LinkGoogle Scholar2. Everett TH, Olgin JE. Atrial fibrosis and the mechanisms of atrial fibrillation.Heart Rhythm. 2007; 4(3 suppl):S24–S27. doi: 10.1016/j.hrthm.2006.12.040.CrossrefMedlineGoogle Scholar3. Wang TJ, Evans JC, Benjamin EJ, Levy D, LeRoy EC, Vasan RS. Natural history of asymptomatic left ventricular systolic dysfunction in the community.Circulation. 2003; 108:977–982. doi: 10.1161/01.CIR.0000085166.44904.79.LinkGoogle Scholar4. Zakeri R, Chamberlain AM, Roger VL, Redfield MM. Temporal relationship and prognostic significance of atrial fibrillation in heart failure patients with preserved ejection fraction: a community-based study.Circulation. 2013; 128:1085–1093. doi: 10.1161/CIRCULATIONAHA.113.001475.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Sugumar H, Nanayakkara S, Vizi D, Wright L, Chieng D, Leet A, Mariani J, Voskoboinik A, Prabhu S, Taylor A, Kalman J, Kistler P, Kaye D and Ling L (2021) A prospective STudy using invAsive haemodynamic measurements foLLowing catheter ablation for AF and early HFpEF : STALL AF‐HFpEF , European Journal of Heart Failure, 10.1002/ejhf.2122, 23:5, (785-796), Online publication date: 1-May-2021. 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Kim M, Yu H, Kim T, Uhm J, Joung B, Lee M and Pak H (2021) One-Year Change in the H2FPEF Score After Catheter Ablation of Atrial Fibrillation in Patients With a Normal Left Ventricular Systolic Function, Frontiers in Cardiovascular Medicine, 10.3389/fcvm.2021.699364, 8 Denham N, Pearman C, Caldwell J, Madders G, Eisner D, Trafford A and Dibb K (2018) Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure, Frontiers in Physiology, 10.3389/fphys.2018.01380, 9 June 7, 2016Vol 133, Issue 23 Advertisement Article InformationMetrics © 2016 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.116.022835PMID: 27267541 Originally publishedJune 7, 2016 PDF download Advertisement
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