Abstract 200: Temporal Relationship Between Left Ventricular Dysfunction and Plasma High-Sensitivity Cardiac Troponin T Levels in a Rat Model of Cardiac Arrest and Resuscitation

Abstract

Introduction. Post resuscitation left ventricular (LV) dysfunction is one of the leading causes of death after return of spontaneous circulation (ROSC). Impairment in cardiac myofilament cross-bridge cycling and the associated degradation and release of cardiac troponins (cTn) concur to depressed contractile function. We hypothesized that the severity of myocardial dysfunction would be associated with plasma cTn levels following cardiac arrest in rats. Methods. Ventricular fibrillation was induced in 17 rats and was untreated for 6 min. CPR, including mechanical chest compressions, ventilation, and epinephrine, was then initiated and continued for additional 6 min prior to defibrillations. Two, 4, and 72 hr following ROSC, LV morphology, systolic and diastolic function were assessed by echocardiography. Animals were then sacrificed, plasma collected and high sensitivity cTnT (hs-cTnT) assayed. Additional 5 rats were not subjected to cardiac arrest and served as controls. Results. At 2 and 4 hr post ROSC, LV end-diastolic volume was enlarged compared to controls (+22% and +25%, respectively) but similar at 72 hr. LVEF was lower than in control rats at 2 and 4 hr following ROSC (Fig., left pannel), but similar at 72 hr. Post ROSC deceleration time (DT) of the E wave showed similar trends (Fig., middle pannel). Plasma release of hs-cTnT increased at 2 and 4 hr post ROSC compared to controls, but was similar at 72 hr (Fig., right pannel). LVEF and DT were significantly inversely correlated with hs-cTnT (r=-0.89, p<0.0001 and r=-0.53, p=0.014). Conclusions. A strong relationship between LVEF and circulating hs-cTnT was observed at different time points following ROSC. Normal LV function at 72 hr post ROSC indicates that myocardial viability was preserved even after remarkable TnT release.