Author + information
- Received November 5, 2013
- Revision received January 22, 2014
- Accepted January 23, 2014
- Published online June 1, 2014.
- Johannes Waltenberger, MD∗,†∗ (, )
- Marloes Gelissen, BS∗,‡,
- Sebastiaan C. Bekkers, MD, PhD∗,
- Jindra Vainer, MD∗,
- Vincent van Ommen, MD, PhD∗,
- Filip Eerens, MD∗,
- Alexander Ruiters, MD∗,
- Alexa Holthuijsen, RN∗,
- Paqui Cuesta, PhD§,
- Racho Strauven, MS, MS§,
- Eric Mokelke, MS‖,
- Anton Gorgels, MD, PhD∗ and
- Frits W. Prinzen, MD, PhD‡
- ∗Department of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, the Netherlands
- †Department of Cardiovascular Medicine, University Hospital Münster, Münster, Germany
- ‡Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, the Netherlands
- §Boston Scientific, Diegem, Belgium
- ‖Boston Scientific, St. Paul, Minnesota
- ↵∗Reprint requests and correspondence:
Dr. Johannes Waltenberger, Department of Cardiovascular Medicine, Münster University Hospital, Albert-Schweitzer-Campus 1, Building A1, D-48149 Münster, Germany.
Intermittent dyssynchrony, induced by ventricular pacing, during early reperfusion reduces infarct size in pre-clinical studies. We evaluated cardioprotection by pacing post-conditioning (PPC) in ST-segment elevation myocardial infarction in a randomized, controlled, single-center, single-blinded, first-in-man study. Patients with first ST-segment elevation myocardial infarction received either PPC plus percutaneous coronary intervention (PCI) (n = 30) or PCI (n = 30). PPC consisted of 10 episodes of 30-s right ventricular pacing. Infarct size was measured as the area under the curve of creatine kinase (CK) (primary endpoint) and by contrast-enhanced cardiac magnetic resonance. The CK area under the curve was not significantly different between study groups. Adjusted contrast-enhanced cardiac magnetic resonance data showed ∼25% smaller infarct size in PPC + PCI than in PCI patients after 4 days (p = 0.01), 4 months (p = 0.02), and 1 year of PCI (p = 0.08). In PPC + PCI, (uncomplicated) ventricular fibrillation (n = 3) and paroxysmal atrial fibrillation (n = 4) were observed as opposed to 1 and 0 cases in PCI, respectively. We conclude PPC is feasible and may induce cardioprotection during PCI treatment of ST-segment elevation myocardial infarction, but technical improvements are needed to improve safety. (PROTECT: Pacing to Protect Heart for Damage From Blocked Heart Vessel and From Re-opening Blocked Vessel[s]; NCT00409604)
- acute myocardial infarction
- pacing post-conditioning
- primary PCI
- reperfusion injury
This study was supported by a research grant from Boston Scientific (Dr. Prinzen) and the Cardiovascular Research Institute Maastricht (Drs. Waltenberger and Prinzen). Dr. Cuesta owns shares of Boston Scientific Corporation. Dr. Prinzen has received research grants from Medtronic Inc., EBR Systems, Boston Scientific Corporation, MSD Sharp & Dohme, and Biological Delivery Systems. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received November 5, 2013.
- Revision received January 22, 2014.
- Accepted January 23, 2014.
- American College of Cardiology Foundation