Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area.

Abstract

Because efferent autonomic pathways to the right ventricle (RV) differ from the efferent autonomic projections to the left ventricle (LV), we assessed the effects of RV infarction on this innervation. We measured the ventricular effective refractory period (ERP) shortening in response to bilateral ansae subclaviae stimulation and ERP lengthening induced by bilateral vagal stimulation as markers of autonomic innervation before and after RV myocardial infarction (RVMI) produced by coronary ligation (n=28 dogs) or intracoronary latex injection (n=18 dogs) into a marginal branch of the right coronary artery in open-chest anesthetized dogs. In each dog, ERPs measured in viable peri-infarct area at two RV outflow tract (RVOT) sites and two septal and four lateral sites at the RV free wall after RVMI showed reduced or absent ERP shortening during bilateral ansae subclaviae stimulation laterally, septally, and at RVOT sites 3 hours after RVMI. ERP shortening in response to infused norepinephrine was still present. Bilateral vagal stimulation during background norepinephrine infusion (0.10 to 0.25 microg/kg per minute) lengthened the ERP at all test sites before latex injection. After transmural RVMI, vagally induced ERP prolongation was attenuated or lost at lateral, septal, and RVOT test sites. RVMI causes sympathetic and vagal denervation at viable sites at the RVOT, lateral, and, to a lesser extent, septal sides of the viable peri-infarct area. Autonomic denervation in the RVOT might contribute to the development of ventricular tachyarrhythmias after the acute stage of myocardial infarction involving the RV.