Abstract 2032: Mechanistic and Prognostic Implications of “Burst” Ventricular Arrhythmias and Their Precise Timing after TIMI 3 Reperfusion in Anterior ST Elevation Myocardial Infarction

Abstract

BACKGROUND Burst ventricular arrhythmias in the presence of TIMI 3 epicardial flow may reflect quality of reperfusion at a cellular level and have previously been shown to correlate with infarct size. This study aims to determine if timing of burst ventricular arrhythmias relative to reperfusion further stratifies the degree of cellular damage. METHODS A total of 229 anterior STEMI pts with final TIMI 3 flow from the EMERALD and CASTEMI primary PCI trials had continuous 24-hr high fidelity 12-lead ECG + Holter monitoring starting prior to PCI. Ventricular ectopy (VPC) burst arrhythmias were defined as a sudden increase over patient-specific baseline VPC rates using statistical outlier detection methodology. The time from reperfusion (defined as attainment of >50% ST recovery and TIMI 3 flow by angiography) to onset of VPC burst arrhythmias was correlated with infarct size by day 7 SPECT imaging. Continuous digital 12-lead ECG + Holter recordings, angiographic films, and SPECT images were analyzed in independent, blinded core labs. RESULTS Reperfusion VPC bursts were seen in 160/229 pts (70%). The presence of reperfusion VPC bursts was significantly associated with a larger infarct size (figure ). Delayed onset reperfusion VPC bursts following epicardial recanalization showed a non-significant trend towards a larger infarct size (figure ). CONCLUSIONS In anterior STEMI pts with successful restoration of TIMI 3 flow, reperfusion burst arrhythmias may be a unique biomarker of cellular injury with delayed burst arrhythmias signaling a worse cellular response to reperfusion. Further characterization of this unique biomarker is important to aid prognostication after reperfusion.