Author + information
- Received December 23, 2019
- Revision received June 10, 2020
- Accepted June 12, 2020
- Published online September 16, 2020.
- Tomos E. Walters, MD, PhD,
- Judit Szilagyi, MD,
- Christina Alhede, MD, PhD,
- Richard Sievers, BS,
- Qizhi Fang, MD,
- Jeffrey Olgin, MD and
- Edward P. Gerstenfeld, MS, MD∗ (, )@ed_gerst
- Section of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California
- ↵∗Address for correspondence:
Dr. Edward P. Gerstenfeld, MU-East 4th Floor, Section of Cardiac Electrophysiology, University of California- San Francisco, 505 Parnassus Avenue, San Francisco, California 94143.
Objectives This study sought to prospectively study the development and then regression of premature ventricular contraction (PVC)-induced cardiomyopathy, with the hypothesis that structural left ventricular (LV) changes that are of potential clinical significance may endure beyond the period of exposure to PVCs.
Background Recovery of LV function after eradication of PVCs in PVC-induced cardiomyopathy is incompletely defined.
Methods Fifteen swine were exposed to: 1) 50% paced PVCs from the LV lateral epicardium for 12 weeks (LV PVC, n = 5); 2) no pacing for 12 weeks (Control, n = 5); or 3) 50% paced LV PVCs for 12 weeks followed by pacing cessation for 4 weeks (Recovery, n = 5). LV function was quantified biweekly in sinus rhythm with echocardiography. Dyssynchrony was measured from pressure-volume loops at baseline and terminal studies. LV fibrosis was quantified after sacrifice.
Results LV ejection fraction during sinus rhythm fell between baseline and terminal studies in the LV PVC group (65.8 ± 3.0 to 39.3 ± 3.2; p < 0.05), whereas there was no significant change in the Control group (69.6 ± 3.0 to 72.2 ± 3.0; p = NS) or after Recovery (64.5 ± 3.4% to 61.4 ± 3.4%; p = NS) groups. There was a significant increase in LV dyssynchrony measured during sinus rhythm between baseline and terminal studies in the LV PVC group (4.0 ± 1.5% to 9.0 ± 1.5%; p < 0.05); there was a similar increase in dyssynchrony that persisted 4 weeks after PVC cessation in the Recovery group (4.4 ± 1.7% to 12.8 ± 1.7%; p < 0.05). After sacrifice, percent fibrosis was higher in the LV PVC group compared with Control (5.7 ± 0.3% vs. 3.0 ± 0.3%; p < 0.05) and remained elevated in Recovery (4.1 ± 0.3% vs. 3.0 ± 0.3%; p < 0.05) despite return to baseline LV ejection fraction.
Conclusions In a swine model of PVC-induced cardiomyopathy, cessation of PVCs for 4 weeks leads to normalization of LV systolic function but significant changes in myocardial fibrosis and LV dyssynchrony during sinus rhythm persist.
Dr. Walters was supported, in part, by a Heart Rhythm Society fellowship grant. Pacemakers and leads were donated by Medtronic, Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The 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 December 23, 2019.
- Revision received June 10, 2020.
- Accepted June 12, 2020.
- 2020 American College of Cardiology Foundation
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