Pro-arrhythmic effects of the cardiac sympathetic co-transmitter, neuropeptide-Y, during ischemia-reperfusion and ST elevation myocardial infarction

Beta-blockers are the only anti-arrhythmic drugs that improve mortality post myocardial infarction (MI), but a significant risk of ventricular arrhythmia remains. We have shown that ventricular fibrillation threshold is reduced following high-level sympathetic stimulation even in the presence of a beta-blocker due to release of the sympathetic co-transmitter neuropeptide-Y (NPY). We hypothesized that exogenous NPY would increase the prevalence of ventricular arrhythmias following ischemia reperfusion in the isolated rat heart. Moreover, we hypothesized that plasma NPY levels would correlate with ventricular arrhythmias following primary percutaneous intervention (PPCI) in patients being treated for ST-elevation MI (STEMI). In the isolated Langendorff perfused (10ml/min) rat heart NPY (250nM, n=10) significantly increased the prevalence of ventricular arrhythmias (90% v’s 20%, p19 pg/ml) were significantly older (68.0±2.2 v’s 58.2±2.5 year old, p