Mechanical circulatory support reduces directly recorded cardiac sympathetic nerve activity in ovine acute myocardial infarction

Abstract

Acute myocardial infarction (AMI) of the left ventricle activates cardiac sympathetic nerve activity (CSNA) as a compensatory mechanism to improve tissue perfusion.1 An elevation in CSNA increases heart rate and myocardial contractility, both of which operate to improve cardiac output. Although this may be benef icial in the short term, continued activation of CSNA is detrimental to cardiac recovery as increases in CSNA can result in fatal cardiac arrhythmias and sudden cardiac death. This elevation in CSNA can propel AMI to incipient cardiogenic shock, and once established, the cardiogenic shock downward cascade, if there is no intervention. Mechanical circulatory support (MCS) is currently used in the management of left ventricular systolic dysfunction following AMI. Previous studies have indicated that MCS can reduce ventricular strain and improve coronary blood flow (CoBF).2 A preclinical study has suggested that MCS using Impella can also reduce induction of atrial arrhythmias in a porcine model of myocardial infarction3 although this has not been directly tested in a clinical cohort. While there is good evidence that heightened CSNA can elevate arrhythmia risk, how CSNA is modulated during MCS is not known. We tested the hypothesis that MCS using Impella would inhibit CSNA in an ovine model of AMI.