Author + information
- Received March 5, 2018
- Revision received April 26, 2018
- Accepted April 27, 2018
- Published online July 10, 2018.
- Sandeep Prabhu, MBBSa,b,c,d,∗,
- Ben T. Costello, MBBSa,b,∗,
- Andrew J. Taylor, MBBS, PhDa,b,e,
- Sarah J. Gutman, MBBSa,b,
- Aleksandr Voskoboinik, MBBSa,b,c,d,
- Alex J.A. McLellan, MBBS, PhDa,b,c,d,
- Kah Y. Peck, MBBSa,
- Hariharan Sugumar, MBBSa,b,c,d,
- Leah Iles, MBBS, PhDa,b,e,
- Bhupesh Pathik, MBBSc,d,
- Chrishan J. Nalliah, MBBSc,d,
- Geoff R. Wong, MBBSc,d,
- Sonia M. Azzopardi, CC Bc RNa,b,
- Geoffrey Lee, MBChB, PhDc,
- Justin Mariani, MBBS, PhDa,b,e,
- David M. Kaye, MBBS, PhDa,b,e,
- Liang-Han Ling, MBBS, PhDa,b,d,
- Jonathan M. Kalman, MBBS, PhDc,d and
- Peter M. Kistler, MBBS, PhDa,b,d,∗ ()
- aDepartment of Cardiology, Alfred Hospital, Victoria, Australia
- bBaker IDI Heart and Diabetes Institute, Victoria, Australia
- cCardiology Department, Royal Melbourne Hospital, Victoria, Australia
- dFaculty of Medicine, Dentistry, and Health Sciences, University of Melbourne, Victoria, Australia
- eMonash University, Melbourne, Australia
- ↵∗Address for correspondence:
Dr. Peter Kistler, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, Victoria, Australia 3004.
Objectives This study sought to determine if diffuse ventricular fibrosis improves in patients with atrial fibrillation (AF)-mediated cardiomyopathy following the restoration of sinus rhythm.
Background AF coexists in 30% of heart failure (HF) patients and may be an underrecognized reversible cause of left ventricular systolic dysfunction. Myocardial fibrosis is the hallmark of adverse cardiac remodeling in HF, yet its reversibility is unclear.
Methods Patients with persistent AF and an idiopathic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤45%) were randomized to catheter ablation (CA) or ongoing medical rate control as a pre-specified substudy of the CAMERA-MRI (Catheter Ablation versus Medical Rate Control in Atrial Fibrillation and Systolic Dysfunction—an MRI-Guided Multi-centre Randomised Controlled Trial) trial. All patients had cardiac magnetic resonance imaging scans (including myocardial T1 time), serum B-type natriuretic peptide, 6-min walk tests, and Short Form-36 questionnaires performed at baseline and 6 months. Sixteen patients with no history of AF or left ventricular systolic dysfunction were enrolled as normal controls for T1 time.
Results Thirty-six patients (18 in each treatment arm) were included in this substudy. Demographics, comorbidities, and myocardial T1 times were well matched at baseline. At 6 months, patients in the CA group had a significant reduction in myocardial T1 time from baseline compared with the medical rate control group (−124 ms; 95% confidence interval [CI]: −23 to −225 ms; p = 0.0176), although it remained higher than that of normal controls at 6 months (p = 0.0017). Improvements in myocardial T1 time with CA were associated with significant improvements in absolute LVEF (+12.5%; 95% CI: 5.9% to 19.0%; p = 0.0004), left ventricular end-systolic volume (p = 0.0019), and serum B-type natriuretic peptide (−216 ng/l; 95% CI: −23 to −225 ng/l; p = 0.0125).
Conclusions The improvement in LVEF and reverse ventricular remodeling following successful CA of AF-mediated cardiomyopathy is accompanied by a regression of diffuse fibrosis. This suggests timely treatment of arrhythmia-mediated cardiomyopathy may minimize irreversible ventricular remodeling.
↵∗ Drs. Prabhu and Costello contributed equally to this work and are joint first authors.
This was an investigator-initiated study. Abbott (Minneapolis, Minnesota) provided 17% of implantable loop recorders used in this study ex gratia; however, Abbott provided no funding and had no role in study design, data collection, data analysis, data interpretation, or writing of the report. This research was in part supported by fellowship stipends provided by the Baker Heart and Diabetes Institute, the National Health and Medical Research Council (NHMRC) of Australia, and the National Heart Foundation of Australia. Dr. Kistler has received funding from Abbott for consultancy and speaking engagements. Dr. Kalman has research and fellowship support from Abbott, Medtronic, Biosense Webster, Boston Scientific, and Abbott; and has received payment for advice to Biosense Webster. Dr. Mariani has received consultancy and speaking fees from Abbott, Medtronic, Biotronik, and Boehringer Ingelheim; and has received funding from Abbott, Boston Scientific, and Medtronic for fellowship support for a clinical assistant. Dr. Ling has received fellowship support from Medtronic, Biotronik. and Abbott. Dr. McLellan has received fellowship support from Abbott. Dr. Sugumar has received fellowship support from St Jude Medical and Medtronic. Mr. Prabhu, Drs. Ling and McLellan, Mr. Voskoboinik, Mr. Nalliah, and Mr. Pathik have received funding from the NHMRC and/or National Heart Foundation of Australia. Mr. Prabhu and Dr. McLellan have received funding from the Baker Heart and Diabetes Research Institute (Melbourne, Australia). Drs. Kalman, Lee, and Kistler are in part supported by the NHMRC. This research is supported in part by the Victorian Government’s Operational Infrastructure Funding. Francis Marchlinski, MD, served as Guest Editor for this paper.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received March 5, 2018.
- Revision received April 26, 2018.
- Accepted April 27, 2018.
- 2018 American College of Cardiology Foundation
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