Improvement of Left Ventricular Ejection Fraction by a Novel Electrical Microcurrent Therapy in a Sheep Model of Chronic Heart Failure

Purpose The burden of systolic heart failure (HF) is ever increasing, and the need for novel HF treatment strategies is huge. Direct application of electrical microcurrent to the heart triggers reverse remodeling and reduces myocardial inflammation. The aim of the present study was to test the efficacy of chronic application of microcurrent by a dedicated implantable generator for the first time in a sheep model of chronic heart failure. Methods Twelve sheep were subjected to implantation of the microcurrent system, which consists of (a) an extremely thin patch electrode on the epicardium of the left ventricle (LV), (b) a transvenous counter electrode in the right ventricle and (c) a subcutaneous microcurrent generator connected to both electrodes. Whereas in five sheep the surgical procedure and the electrode design were optimized, in the remaining seven sheep HF was induced by injection of 90 µm microspheres directly into the left coronary artery. Microembolization was repeated until a sustained reduction of LV ejection fraction (LVEF) was achieved, which was defined as a stable mean reduction by 25% as confirmed by echocardiography. Thereafter the device was activated to continuously apply transmyocardial microcurrent to the failing LV. LVEF was repeatedly measured after microcurrent treatment by echocardiography until 12 weeks after start of therapy. Results LVEF strongly decreased after microembolization (baseline, 70.9 ± 5.0%; after embolization, 44.2 ±13.4%, P Conclusion Continuous microcurrent therapy applied over several weeks is associated with a strong improvement of LVEF in a sheep model of chronic systolic HF. As demonstrated earlier, a mitigated inflammatory response to ischemia may be one of the underlying reasons. Future trials are warranted to further test this promising novel therapy, with the intention to induce and sustain intrinsic myocardial recovery and to ultimatively establish a novel treatment strategy for systolic HF.