ANG II induces O2- release in HVECs via activation of membrane-bound NADH-/NADPH-oxidase, an effect, that is mediated by both AT-1 and AT-2 receptors. This suggests that acceleration of AS and MI in ANG II-mediated hypertension may at least be due to ANG II-induced O2- generation from vascular endothelial cells. In this case, the ACE inhibitors and the ANG receptor antagonists may act as causative "antioxidants".

Background: Cardiac surgery often represents the only treatment option in patients with infective endocarditis (IE). However, IE surgery may lead to a sudden release of inflammatory mediators, which is associated with the severity of postoperative organ dysfunction. We investigated the impact of hemoadsorption during IE surgery on postoperative organ dysfunction. Methods: This multi-center, randomized, non-blinded, controlled trial assigned patients undergoing cardiac surgery for IE to hemoadsorption [integration of CytoSorb® to cardiopulmonary bypass (CPB)] or control. The Primary outcome (ΔSOFA) was defined as the difference between the mean total postoperative sequential organ failure assessment score (SOFA), calculated maximally to the 9th postoperative day, and the basal SOFA score. The analysis was by modified intention-to-treat. A predefined inter-group comparison was done using a linear mixed model for ΔSOFA including surgeon and baseline SOFA as fixed effect covariates and with the surgical center as random effect. The SOFA score assesses dysfunction in six organ systems, each scored from zero to four. Higher scores indicate worsening dysfunction. Secondary outcomes were 30-day mortality, durations of mechanical ventilation, vasopressor and renal replacement therapy. Cytokines were measured in the first 50 patients. Results: Between January 17, 2018 and January 31, 2020, A total of 288 patients were randomly assigned to hemoadsorption (n=142) or control (n=146). Four patients in the hemoadsorption and two in the control group were excluded as they did not undergo surgery. The primary outcome ΔSOFA did not differ between the hemoadsorption and the control group (1.79 ± 3.75 and 1.93 ± 3.53, respectively, 95% CI: −1.30 to 0.83, p=0.6766). Mortality at 30 days (21% hemoadsorption vs 22% control, p=0.782), the durations of mechanical ventilation, vasopressor and renal replacement therapy did not differ between groups. Levels of IL-1β and IL-18 at the end of CPB were significantly lower in the hemoadsorption than in the control group. Conclusions: This randomized trial failed to demonstrate a reduction in postoperative organ dysfunction through intraoperative hemoadsorption in patients undergoing cardiac surgery for IE. Although hemoadsorption reduced plasma cytokines at the end of CPB, there was no difference in any of the clinically relevant outcome points.

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Cardiac ejection is detectable by cbPPG under pathophysiologic conditions of cardiovascular disease and perioperative medicine. cbPPG measurements can be seamlessly integrated into the clinical work flow of critical care patients.

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