Related Experiment Video
Updated: May 11, 2025
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Pulsed electromagnetic fields treatment ameliorates cardiac function after myocardial infarction in mice and pigs
Shiqi Wang1, Gaiqin Pei1, Jiayu Shen2
1Rehabilitation Medicine Center and Institute of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu 610041, China; Key Laboratory of Rehabilitation Medicine in Sichuan Province, West China Hospital, Sichuan University, Chengdu 610041, China.
Introduction:
Ischemic heart disease (IHD) is a prominent contributor to mortality worldwide, with myocardial infarction (MI) representing its most severe manifestation. Pulsed electromagnetic fields (PEMF) treatment shows promise for treating IHD. Nevertheless, the therapeutic impact and underlying mechanism of PEMF in MI are not fully understood.
Objectives:
To investigate the efficacy, safety, and mechanisms of PEMF for MI.
Methods:
We established MI models in both mice and pigs and performed serial echocardiography and cardiac magnetic resonance follow-up to demonstrate the benefit of PEMF treatment after MI. The pathological environment after myocardial infarction was simulated in vitro to observe changes in various cells exposed to PEMF. Gene knockout (TLR4-/-) mice and inhibitors were used to compare the differences in the efficacy of PEMF treatment relative to that of gene knockout/inhibitor treatments. Agonists were used to further explore the mechanism of PEMF treatment.
Results:
In post-MI mice, PEMF treatment enhanced cardiac function and reduced scar formation. PEMF reduced the macrophage inflammatory response, improved cardiomyocyte survival in an inflammatory environment, and decreased collagen secretion by fibroblasts in vitro. Importantly, in the clinically relevant porcine model, PEMF treatment inhibited the inflammatory response and alleviated adverse left ventricular remodeling. Moreover, PEMF could exert therapeutic effects similar to those of gene knockout or inhibitor treatments. In the presence of TLR4 knockout or pyrrolidine dithiocarbamate (an NF-κB inhibitor) administration, PEMF could still improve cardiac function in post-MI mice. Mechanistically, the anti-inflammatory effect of PEMF was reversed when RS09 (a TLR4 agonist) was administered, and the antifibrotic effect of PEMF was attenuated after treatment with SRI-011381 (a TGF-β signaling pathway agonist).
Conclusions:
PEMF treatment exhibits considerable promise as a noninvasive physical therapy modality, warranting further investigation into its potential implications for managing patients with IHD.
