Author + information
- Received March 14, 2014
- Revision received June 6, 2014
- Accepted June 10, 2014
- Published online September 9, 2014.
- Martin H. Ruwald, MD, PhD∗,†∗ (, )
- Suneet Mittal, MD‡,
- Anne-Christine Ruwald, MD∗,†,
- Mehmet K. Aktas, MD∗,
- James P. Daubert, MD§,
- Scott McNitt, MS∗,
- Amin Al-ahmad, MD‖,
- Christian Jons, MD, PhD†,
- Valentina Kutyifa, MD, PhD∗,
- Jonathan S. Steinberg, MD‡,
- Paul Wang, MD¶,
- Arthur J. Moss, MD∗ and
- Wojciech Zareba, MD, PhD∗
- ∗Heart Research Follow-up Program, University of Rochester Medical Center, Rochester, New York
- †Department of Cardiology, Gentofte Hospital, Hellerup, Denmark
- ‡Arrhythmia Institute, Valley Health System of New York and New Jersey, New York, New York and Ridgewood, New Jersey
- §Cardiology Division, Department of Medicine and Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina
- ‖Texas Cardiac Arrhythmia Institute, Austin, Texas
- ¶Division of Cardiovascular Medicine, Stanford University, Stanford, California
- ↵∗Reprint requests and correspondence:
Dr. Martin H. Ruwald, Heart Research Follow-up Program, University of Rochester Medical Center, 265 Crittenden Boulevard, Rochester, New York 14642.
Background A high percentage of biventricular pacing is required for optimal outcome in patients treated with cardiac resynchronization therapy (CRT), but the influence of ectopic beats on the success of biventricular pacing has not been well established.
Objectives This study sought to determine if increased ectopic beats reduce the chance of high biventricular pacing percentage and are associated with subsequent adverse outcomes.
Methods From the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy), 801 patients with an implanted CRT-defibrillator device with data available on biventricular pacing percentage and pre-implantation 24-h Holter recordings were included. Using logistic regression, we estimated the influence of ectopic beats on the percentage of biventricular pacing. Reverse remodeling was measured as reductions in atrial and left ventricular end-systolic volumes (LVESV) at 1 year. Cox models were used to assess the influence of ectopic beats on the outcomes of heart failure (HF) or death, ventricular tachyarrhythmias (VTAs), and death.
Results In the pre-implantation Holter recording, ectopic beats accounted for a mean 3.2 ± 5.5% of all beats. The probability of subsequent low biventricular pacing percentage (<97%) was increased 3-fold (odds ratio: 3.37; 95% confidence interval: 1.74 to 6.50; p < 0.001) in patients with 0.1% to 1.5% ectopic beats and 13-fold (odds ratio: 13.42; 95% confidence interval: 7.02 to 25.66; p < 0.001) in patients with >1.5% ectopic beats compared with those with <0.1% ectopic beats. Patients with ≥0.1% ectopic beats had significantly less reverse remodeling (percent reduction in LVESV 31 ± 15%) than patients with <0.1% ectopic beats (percent reduction in LVESV 39 ± 14%; p < 0.001). The risk of HF/death and VTA was increased significantly in those with 0.1% to 1.5% ectopic beats (hazard ratio: 3.13 and 1.84, respectively) and for >1.5% ectopic beats (hazard ratio: 2.38 and 2.74, respectively).
Conclusions Relatively low frequencies of ectopic beats (≥0.1%) dramatically increase the probability of low biventricular pacing (<97%), with reduced CRT efficacy by less reverse remodeling and higher risk of HF/death and VTA. This supports pre-implantation Holter monitoring of patients selected for CRT for optimal outcome. (MADIT-CRT: Multicenter Automatic Defibrillator Implantation With Cardiac Resynchronization Therapy; NCT00180271)
- biventricular pacing
- cardiac resynchronization therapy
- ectopic beats
- Holter monitoring
- reverse remodeling
The MADIT-CRT Holter substudy was funded by an unrestricted research grant provided to the University of Rochester Medical Center from Boston Scientific. Dr. Zareba was the Primary Investigator for this research grant. Dr. Ruwald has received unrestricted funding from the Danish Heart Foundation (12-04-R90-A3806-22701) and the Lundbeck Foundationhttp://dx.doi.org/10.13039/501100003554 (R108A104415) unrelated to this study. Dr. Mittal is a consultant to Boston Scientific. Ms. Ruwald is a Mirowski-Moss awardee; and has received unrestricted grants from the Lundbeck Foundationhttp://dx.doi.org/10.13039/501100003554 and Falck Denmark. Dr. Daubert has received research grants from Biosense Webster, Medtronichttp://dx.doi.org/10.13039/100004374, Boston Scientific, ARCA biopharma, and Gilead Sciences, Inc.; and honoraria from Medtronic, Boston Scientific, Sorin, Biotronik, St. Jude Medical, CardioFocus, Premier Healthcare Alliance, Gilead Sciences, Inc., Biosense Webster, Sanofi-Aventis, Northwestern University, and VytronUS; as well as fellowship support to Duke University provided by Biotronik, Biosense Webster, Medtronic, and Boston Scientific. Dr. Al-ahmad has received honoraria from Boston Scientific, Medtronic, and St. Jude Medical. Dr. Steinberg has received research grants from Boston Scientific and Medtronichttp://dx.doi.org/10.13039/100004374; and serves as a consultant for Medtronic, Boston Scientific, St. Jude Medical, and Cameron Health. Dr. Wang has received fellowship support from Medtronichttp://dx.doi.org/10.13039/100004374 and St. Jude Medicalhttp://dx.doi.org/10.13039/100006279; and honoraria from Medtronic and St. Jude Medical. Dr. Moss has received a research grant from Boston Scientific. Dr. Zareba has received a research grant from Boston Scientific. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 14, 2014.
- Revision received June 6, 2014.
- Accepted June 10, 2014.
- American College of Cardiology Foundation