The Role of Inflammatory Cytokines in Cardiac Arrest.

INTRODUCTION: Post-cardiac arrest syndrome (PCAS) is characterized by systemic ischemia/reperfusion injury, anoxic brain injury, and post-arrest myocardial dysfunction superimposed on a precipitating pathology. The role of inflammatory cytokines in cardiac arrest remains unclear. AIMS: We aimed to describe, with an emphasis on clinical applications, what is known about the role of inflammatory cytokines in cardiac arrest. DATA SOURCES: A PubMed literature review was performed for relevant articles. Only articles in English that studied cytokines in patients with cardiac arrest were included. RESULTS: Cytokines play a crucial role in the pathogenesis of PCAS. Following cardiac arrest, the large release of circulating cytokines mediates the ischemia/reperfusion injury, brain dysfunction, and myocardial dysfunction seen. Interleukins, tumor necrosis factor, and matrix metalloproteinases all play a unique prognostic role in PCAS. High levels of inflammatory cytokines have been associated with mortality and/or poor neurologic outcomes. Interventions to modify the systemic inflammation seen in PCAS continue to be heavily studied. Currently, the only approved medical intervention for comatose patients following cardiac arrest is targeted temperature management. Medical agents, including minocycline and sodium sulfide, have demonstrated promise in animal models. CONCLUSIONS: The role of inflammatory cytokines for both short- and long-term outcomes is an important area for future investigation.

Impact of right ventricular dysfunction on mortality in adults with cardiac arrest undergoing coronary angiogram.

OBJECTIVE: We sought to identify the impact of echocardiographic right ventricular (RV) systolic dysfunction on mortality in adults with cardiac arrest (CA). METHODS: The study population included 147 adults hospitalized with CA who underwent both echocardiogram and coronary angiogram at an academic tertiary medical center. The primary outcome of interest was all-cause in-hospital mortality. RESULTS: Of the 147 patients studied, 20 (13.6%) had evidence of RV systolic dysfunction while 127 (86.4%) did not. Patients with RV dysfunction had higher rates of prior surgical and percutaneous coronary revascularization. They also had higher rates of mechanical ventilation, therapeutic hypothermia, vasopressor and inotrope use, and a trend towards higher rates of mechanical support. Coronary angiogram revealed higher rates of multivessel disease, right coronary artery intervention, and glycoprotein IIb-IIIa inhibitor use in those with RV dysfunction, alongside with lower echocardiographic left ventricular ejection fraction. In-hospital mortality rates were higher in adults with RV dysfunction compared to those without (55% vs 11%, p < 0.001). In multivariate analysis, RV dysfunction was the strongest independent predictor of higher mortality [odds ratio 4.71, 95% confidence interval 1.27-17.50]. CONCLUSIONS: In this observational contemporary study, RV dysfunction was independently associated with higher mortality in adults with CA undergoing coronary angiogram. RV dysfunction may be useful for risk stratification and management in this high-mortality population.