Recent studies show that hospitalized COVID-19 patients have an increased incidence of arrhythmia, especially atrial fibrillation (AF). This single-center study included 383 hospitalized patients with positive polymerase chain reaction tests for COVID-19 from March 2020 to April 2021. Patient characteristics were documented, and data were analyzed for episodes of AF on admission or during the hospital stay, intrahospital mortality, need for intensive care and/or invasive ventilation, inflammatory parameters (hs-CRP, IL-6, and procalcitonin), and differential blood count. We demonstrated that in the setting of hospitalized cases of COVID-19 infection, there is an incidence of 9.8% (n = 36) for the occurrence of new-onset AF. Furthermore, it was shown that a total of 21% (n = 77) had a history of episodes of paroxysmal/persistent AF. However, only about one-third of patients with pre-existing AF had relevant documented tachycardic episodes during the hospital stay. Patients with new-onset AF had a significantly increased intrahospital mortality compared to the control and the pre-existing AF without rapid ventricular rate (RVR) group. Patients with new-onset AF required intensive care and invasive ventilation more frequently. Further analysis examined patients with episodes of RVR and demonstrated that they had significantly elevated CRP (p < 0.05) and PCT (p < 0.05) levels on the day of hospital admission compared to patients without RVR.

Background: Despite advances in temporary mechanical circulatory support (tMCS), patients with cardiogenic shock (CS) who are treated with a microaxial flow pump (mAFP; Impella^®, Abiomed) still have a high mortality rate. A dysregulated systemic inflammatory response significantly contributes to multiorgan failure in this population. CytoSorb^® hemadsorption has emerged as a potential adjunctive therapy for modulating inflammation, but data on its use in CS are limited. Methods: This retrospective, single-center study used propensity score matching analysis (1:1 matching; n = 15 per group) to compare the outcomes of patients receiving mAFP support with and without concomitant CytoSorb therapy. Baseline data (T0), including comorbidities and clinical status at ICU admission, were collected for all patients. In the CytoSorb group, data were collected at two additional time points: 24 h before the start of CytoSorb therapy (T1), and 24 h after its completion (T2). At these time points, laboratory values and parameters on respiratory, hemodynamic, and organ function were assessed. Corresponding data were also collected for matched patients in the non-CytoSorb group at equivalent time points relative to their matched counterparts. Results: In the propensity score-matched cohort, patients treated with CytoSorb exhibited significant improvements between T1 and T2. Specifically, reductions were observed in the vasoactive-inotropic score (p = 0.035), procalcitonin levels (p = 0.041), peak inspiratory pressure (p = 0.036), and positive end-expiratory pressure (p = 0.016). Flow rates through the mAFP declined significantly (p = 0.014), suggesting stabilization of hemodynamics. These changes were not observed in the non-CytoSorb group, where most parameters remained unchanged or exhibited less pronounced trends. We observed a lower in-hospital mortality rate in the CytoSorb group (33.3% versus 46.7%), though the difference was not significant, potentially due to limited statistical power. Conclusions: CytoSorb hemadsorption in mAFP-supported CS was associated with improved hemodynamic stability and reduced inflammatory burden. These findings suggest a potential therapeutic benefit of adjunctive hemadsorption in this high-risk population.

Background and Clinical Significance: Fulminant pulmonary embolism (PE) leading to an out-of-hospital cardiac arrest (OHCA) is associated with a high mortality rate and cardiopulmonary resuscitation (CPR) frequently failing to achieve return of spontaneous circulation (ROSC). Extracorporeal CPR (eCPR) has emerged as a potential life-saving intervention. Case Presentation: A 66-year-old woman suffered an OHCA due to massive PE, presenting with pulseless electrical activity (PEA). After 90 min of pre- and in-hospital CPR without sustained ROSC, venoarterial extracorporeal membrane oxygenation (va-ECMO) was initiated as eCPR upon arrival at the hospital. Even after implantation of the va-ECMO, there was initially a pronounced acidosis (pH 6.9) with a high elevated lactate level (>30 mmol/L); these factors, together with the prolonged low-flow period, indicated a poor prognosis. Further diagnostic tests revealed intracranial hemorrhage (subdural hematoma), and systemic lysis was not possible. With persistent right heart failure, surgical thrombectomy was performed during hospitalization. Intensive multidisciplinary management finally led to successful therapy and weaning from mechanical ventilation, as well as to complete neurological recovery (CPC-Score 1-2). Conclusions: This case illustrates that eCPR can facilitate survival with good favorable neurological outcomes despite initially poor prognostic predictors. It underscores the importance of refining patient selection criteria and optimizing management strategies for eCPR in refractory cardiac arrest secondary to PE.

Background: Cardiogenic shock (CS) and post-cardiac arrest syndrome (PCAS) are frequently associated with a systemic inflammatory response resulting from ischemia–reperfusion injury, endothelial dysfunction, and microcirculatory impairment. This inflammatory biology may be further amplified by temporary mechanical circulatory support (tMCS) through blood–surface interactions and shear-related hemolysis. Extracorporeal cytokine adsorption has therefore been proposed as an adjunctive strategy to attenuate hyperinflammation and facilitate shock reversal in selected patients. Methods: We conducted a narrative review, guided by a targeted PubMed and Scopus search and reference screening, to summarize the current pathophysiological concepts and clinical evidence on extracorporeal cytokine adsorption in CS-, PCAS-, and tMCS-supported states. Results: Across porous polymer hemoadsorption cartridges (e.g., CytoSorb^®), membrane-based or hybrid filters with adsorptive properties (e.g., oXiris^®), and selective approaches targeting inflammatory mediators (e.g., PentraSorb^® CRP), available studies most consistently report short-term physiological effects, including reduced vasopressor demand, improved metabolic stabilization, and modulation of inflammatory markers. However, evidence of benefits to clinically relevant endpoints remains inconsistent in various clinical settings, and randomized data are limited. Conclusions: Extracorporeal cytokine adsorption is a biologically plausible adjunct in inflammation-driven acute cardiovascular syndromes, but current evidence does not support routine use. Phenotype-guided patient selection, early timing, and adequately powered, mechanism-informed randomized trials are required to define clinical efficacy and safety in defined patient populations.

Background: Post-cardiac arrest syndrome (PCAS) following out-of-hospital cardiac arrest (OHCA) is driven by global ischemia–reperfusion injury, endothelial dysfunction, and a dysregulated inflammatory response. This cascade frequently culminates in profound vasoplegia and multiorgan failure, even when guideline-directed post-resuscitation management is applied. Hemoadsorption using the CytoSorb device may attenuate hyperinflammation and vasoplegia by removing circulating inflammatory and injury-related mediators. Methods: This single-centre, retrospective cohort study compared adults with PCAS following OHCA who received hemoadsorption with propensity score-matched controls (1:1 matching; n = 50 per group). For patients treated with hemoadsorption, data were analyzed within predefined intervals covering the 24 h preceding therapy initiation (T1) and the 24 h following the completion of the hemoadsorption treatment period (T2). Controls were evaluated at time points aligned to those of their matched hemoadsorption counterparts. Hemodynamic, metabolic, respiratory, and organ injury markers were assessed. Results: Formal between-group comparisons of temporal change between T1 and T2 showed no statistically significant differences between hemoadsorption-treated patients and matched controls across key parameters, including VIS (Δ −18.7 vs. −7.7; p = 0.183) and lactate (Δ −1.8 vs. −1.25 mmol/L; p = 0.780), as well as markers of organ injury, pH, and oxygenation. In exploratory ANCOVA models, only base excess was associated with treatment group (p = 0.035). Survival to hospital discharge was comparable (48% vs. 40%; p = 0.423), with similar neurological outcomes. Within the hemoadsorption group, pre–post comparisons around hemoadsorption initiation (T1–T2) demonstrated marked improvements, including reduced vasoactive support (VIS 70.0 to 12.1; p = 0.039), substantial lactate clearance (4.1 to 1.1 mmol/L; p < 0.001), and declines in organ injury markers (AST, ALT, LDH, myoglobin), alongside more pronounced platelet reduction compared with controls (129 to 57 × 10³/µL vs. 189 to 123 × 10³/µL). However, adjusted analyses indicated that these changes were primarily driven by baseline shock severity rather than a treatment-specific effect. Conclusions: In this propensity score-matched cohort of PCAS patients after OHCA, hemoadsorption was associated with within-group physiological changes but showed no detectable advantage over matched controls, with similar survival. These findings are hypothesis-generating and warrant prospective studies with standardized timing and phenotype-guided patient selection.

(1) Background: The association between microaxial flow pump (mAFP) timing and outcomes in acute myocardial infarction-related cardiogenic shock (AMI-CS) remains uncertain. (2) Methods: We conducted a retrospective single-center study of patients with AMI-CS admitted between January 2017 and July 2025. Prespecified 24 h landmark analyses included patients alive 24 h after intensive care unit (ICU) admission. The primary analysis compared patients with ST-segment elevation myocardial infarction (STEMI) receiving mAFP within 6 h with STEMI patients managed without temporary mechanical circulatory support (tMCS). Later STEMI implantation (>6–≤24 h) and both non-ST-segment elevation myocardial infarction (NSTEMI) timing cohorts were exploratory. The primary endpoint was subsequent in-hospital mortality from the landmark onward. Associations were assessed using multivariable logistic regression and propensity score-weighted models. (3) Results: In the primary STEMI cohort, 106 patients received mAFP within 6 h and 59 received no-tMCS. Subsequeunt in-hospital mortality was 17.0% versus 23.7%, respectively (p = 0.293). Early mAFP implantation was associated with lower mortality in the fully adjusted model (OR, 0.25 [95% CI, 0.06–0.99]; p = 0.048). Propensity score-based estimates were directionally consistent, with significance in the doubly robust weighted model (OR, 0.22 [95% CI, 0.06–0.85]; p = 0.028) but not in all weighted models. Later-timing and NSTEMI estimates did not reach statistical significance and were imprecise. (4) Conclusions: Among patients with STEMI who survived the first 24 h after ICU admission, mAFP implantation within 6 h was associated with lower subsequent in-hospital mortality. Exploratory later-timing and NSTEMI estimates were inconclusive. These observational findings are hypothesis-generating and require prospective validation.