LAUSR

Introduction: Sympathetic nerve overactivity plays a critical role in the pathogenesis of heart failure (HF). Renal denervation (RDN) is currently under evaluation for the treatment of resistant hypertension and reduces blood pressure by disruption of sympathetic pathways that modulate cardiovascular function. We have demonstrated cardioprotective actions of RDN in rodent models of acute myocardial infarction and HF. We sought to determine if RDN treatment could improve cardiac function in a clinically relevant large animal model of HF. Methods: Yucatan miniswine (n=14) underwent 75 min of proximal left anterior descending coronary artery balloon-occlusion followed by 18 wks of reperfusion to generate large transmural infarcts and heart failure. Cardiac function was measured every 3 wks by 2-D echocardiography. HF was defined as left ventricular ejection fraction (LVEF) TM Multi-Electrode System (St. Jude Medical, St. Paul, MN). RDN was performed from distal to proximal in each renal artery, with at total of 24 ablation points separated both longitudinally and rotationally under fluoroscopic guidance. Results: At 3 wks of reperfusion following myocardial ischemia, LVEF was reduced in all pigs (SHAM RDN, 29.92.7%; RDN, 31.41.9%) with no further decline at the 6 wk treatment timepoint. At 6 wks of reperfusion, SHAM RDN and RDN treatments were performed without complication. Three wks after RDN treatment, LVEF was increased compared to SHAM (33.52.5 and 48.04.6%, respectively). LVEF was further increased 6 wks after RDN treatment compared to SHAM (31.51.5 vs. 62.00.6%, respectively). Interestingly, LVEF was higher 6 wks post-RDN compared to 3 wks post-RDN ( p =0.047). Conclusions: Preliminary results demonstrate that RDN significantly improves cardiac function in a clinically relevant swine model of HF.