Extracorporeal low-energy shock-wave therapy exerts anti-inflammatory effects in a rat model of acute myocardial infarction.

Abstract

It has been previously demonstrated that extracorporeal low-energy shock-wave (SW) therapy ameliorates left ventricular (LV) remodeling through enhanced angiogenesis after acute myocardial infarction (AMI) in pigs in vivo. However, it remains to be examined whether SW therapy also exerts anti-inflammatory effects on AMI. METHODS AND RESULTS: AMI was created by ligating the proximal left anterior descending coronary artery in rats. They were randomly assigned to 2 groups: with (SW group) or without (control group) SW therapy (0.1 mJ/mm(2), 200 shots, 1 Hz to the whole heart at 1, 3 and 5 days after AMI). Four weeks after AMI, SW therapy significantly ameliorated LV remodeling and fibrosis. Histological examinations showed that SW therapy significantly suppressed the infiltration of neutrophils and macrophages at days 3 and 6, in addition to enhanced capillary density in the border area. Molecular examinations demonstrated that SW therapy enhanced the expression of endothelial nitric oxide synthase and suppressed the infiltration of transforming growth factor-β1-positive cells early after AMI. SW therapy also upregulated anti-inflammatory cytokines and downregulated pro-inflammatory cytokines in general. These results suggest that low-energy SW therapy suppressed post-MI LV remodeling in rats in vivo, which was associated with anti-inflammatory effects in addition to its angiogenic effects, and demonstrated a novel aspect of the therapy for AMI.