Author + information
- Received July 27, 2017
- Revision received August 18, 2017
- Accepted August 20, 2017
- Published online August 27, 2017.
- Sandeep Prabhu, MBBSa,b,d,e,
- Andrew J. Taylor, MBBS PhDa,b,f,
- Ben T. Costello, MBBSa,b,
- David M. Kaye, MBBS, PhDa,b,f,
- Alex AJ. McLellan, MBBS, PhDa,b,d,e,
- Aleksandr Voskoboinik, MBBSa,b,d,e,
- Hariharan Sugumar, MBBSa,b,d,e,
- Siobhan M. Lockwood, MBBSc,
- Michael B. Stokes, MBBSc,
- Bhupesh Pathik, MBBSd,e,
- Chrishan J. Nalliah, MBBSd,e,
- Geoff R. Wong, MBBSd,e,
- Sonia M. Azzopardi, RNa,b,
- Sarah Gutman, MBBSa,b,
- Geoffrey Lee, MBBS, PhDd,
- Jamie Layland, MBChB, PhDf,
- Justin A. Mariani, MBBS PhDa,b,e,
- Liang-han Ling, MBBS, PhDa,b,e,
- Jonathan M. Kalman, MBBS, PhDd,e and
- Peter M. Kistler, MBBS, PhDa,b,e,∗ ()
- aThe Baker Heart & Diabetes Institute, Melbourne, Australia
- bThe Alfred Hospital, Melbourne, Australia
- cMonash Heart, Melbourne, Australia
- dRoyal Melbourne Hospital, Melbourne, Australia
- eUniversity of Melbourne, Melbourne, Australia
- fMonash University, Melbourne, Australia
- ↵∗Corresponding author Peter Kistler, MBBS, PhD Baker Heart and Diabetes Institute 75 Commercial Road Melbourne, Victoria, Australia 3004 Telephone: +61 3 8532 1111, Fax: +61 3 8532 1111.
Background Atrial fibrillation (AF) and left ventricular systolic dysfunction (LVSD) frequently co-exist despite adequate rate-control. Existing randomized studies of AF and LVSD of varying etiologies have demonstrated modest benefits with a rhythm control strategy.
Objective To determine whether catheter ablation (CA) for AF could improve LVSD compared to medical rate-control (MRC) where the etiology of the LVSD was unexplained, apart from the presence of AF.
Methods This multi-center randomized clinical trial enrolled patients with persistent AF and idiopathic cardiomyopathy (LVEF ≤45%). After optimization of rate-control, patients underwent cardiac MR (CMR) to assess LVEF and late gadolinium enhancement (LGE), indicative of ventricular fibrosis, before randomization to either CA or ongoing MRC. CA included PVI and posterior wall isolation. AF burden post CA was assessed by implanted loop recorder, and adequacy of MRC by serial Holter-monitoring. The primary endpoint was ΔLVEF on repeat CMR at 6 months.
Results 301 patients were screened and 68 enrolled between November 2013 and October 2016 and randomized with 33 in each arm accounting for two dropouts. The average AF burden post CA was 1.6% ± 5.0% at six months. On intention to treat analysis, absolute LVEF improved by +18 ± 13% in the CA group compared to +4.4 ± 13% in MRC group, (p <0.0001) and normalized (LVEF ≥50%) in 58% vs 9%, p = 0.0002. In those undergoing CA, the absence of LGE predicted greater improvements in absolute LVEF (+10.7%, p = 0.0069) and normalization at 6 months (73% vs 29%, p = 0.0093).
Conclusion AF is an underappreciated reversible cause of LVSD in this population despite adequate rate control. The restoration of sinus rhythm with CA results in significant improvements in ventricular function, particularly in the absence of ventricular fibrosis on CMR. This challenges the current treatment paradigm that rate control is the appropriate strategy in patients with AF and LVSD.
- Catheter ablation
- Medical rate control
- Persistent AF
- Idiopathic cardiomyopathy
- Late gadolinium enhancement
Funding: This was an investigator initiated study. St Jude Medical (St. Paul, Minnesota) provided 14% of ILRs used in this study ex gratia. However, St. Jude provided no funding and had no role in study design, data collection, data analysis, data interpretation, or writing. There were no other industry funding sources. The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication.
Disclosures: While the authors have no conflicts pertaining to this research, the following industry funding sources regarding activities outside the submitted work have been declared in accordance with ICMJE guidelines. Kistler has received funding from St. Jude for consultancy and speaking engagements. Kalman has research and fellowship support from St. Jude, Medtronic, Biosense Webster, Boston Scientific and Abbott and has received payment for advice to Biosense Webster. Mariani has received consultancy and speaking fees from St. Jude, Medtronic, Biotronik and Boehringer Inelheim. He has also received funding from St. Jude, Boston Scientific and Medtronic for fellowship support for a clinical assistant. Ling has received fellowship support from Medtronic, Biotronik and St Jude. Mclellan has received fellowship support from St. Jude. Wong has received consultancy from St. Jude. Sugamar has received fellowship support from St. Jude and Medtronic. Additionally, these non-industry funding sources are also disclosed: Prabhu, Ling, McLellan, Voskoboinik, Nalliah and Pathik receive funding from Australian National Health and Medical Research Council and/or National Heart Foundation of Australia. Prabhu and McLellan also receive funding from the Baker Heart and Diabetes Research Institute (Melbourne, Australia). 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.
Clinical Trial: The trial was registered with the Australia New Zealand Clinical Trials Registry (ACTRN12613000880741).
- Received July 27, 2017.
- Revision received August 18, 2017.
- Accepted August 20, 2017.