Abstract
The generation of harmful reactive oxygen species (ROS), including hydrogen peroxide, in out-of-hospital cardiac arrest (OHCA) survivors causes systemic ischemia/reperfusion injury that may lead to multiple organ dysfunction and mortality. We hypothesized that the antioxidant enzyme catalase may attenuate these pathophysiological processes after cardiac arrest. Therefore, we aimed to analyze the predictive value of catalase levels for mortality in OHCA survivors. In a prospective, single-center study, catalase levels were determined in OHCA survivors 48 h after the return of spontaneous circulation. Thirty-day mortality was defined as the study end point. A total of 96 OHCA survivors were enrolled, of whom 26% (n = 25) died within the first 30 days after OHCA. The median plasma intensity levels (log2) of catalase were 8.25 (IQR 7.64–8.81). Plasma levels of catalase were found to be associated with mortality, with an adjusted HR of 2.13 (95% CI 1.07–4.23, p = 0.032). A Kaplan–Meier analysis showed a significant increase in 30-day mortality in patients with high catalase plasma levels compared to patients with low catalase levels (p = 0.012). High plasma levels of catalase are a strong and independent predictor for 30-day mortality in OHCA survivors. This indicates that ROS-dependent tissue damage is playing a crucial role in fatal outcomes of post-cardiac syndrome patients.
Highlights
Out-of-hospital cardiac arrest (OHCA) is a major public health concern, affecting annually approximately 300,000 patients in Europe [1]
We enrolled a total of 100 OHCA survivors
We identified a significant association between catalase plasma levels and 30-day mortality in OHCA survivors, with an unadjusted hazard ratio (HR) per one standard deviation (SD) of 2.26 (95% confidence interval (CI) 1.49–3.42; p < 0.001)
Summary
Out-of-hospital cardiac arrest (OHCA) is a major public health concern, affecting annually approximately 300,000 patients in Europe [1] It is associated with substantial morbidity and mortality rates of up to 90% [2]. Patients regaining spontaneous circulation after OHCA suffer from a combination of pathophysiological processes, including brain injury, myocardial dysfunction, systemic ischemia, and reperfusion, and the initial pathology that caused the cardiac arrest. The combination of these ongoing deleterious processes critically affects patient outcome, and is coined as post-cardiac arrest syndrome [5,6]. An optimized risk evaluation in OHCA patients that initially survived the cardiac arrest and are facing the life-threatening postarrest period may have important implications, both for evaluating further therapeutic strategies and clinical judgment of prognosis
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