Julian Kreutz

Background: Despite advances in temporary mechanical circulatory support, the mortality rate for patients with cardiogenic shock (CS) remains high. Current shock frameworks rely on hemodynamic parameters and fail to capture ongoing biological injury. Our study aimed to investigate cytokine trajectories during support and their association with clinical outcomes. Methods: This single-center retrospective cohort study analyzed 113 patients with CS in SCAI stage ≥ C who were treated with microaxial flow pump (mAFP). Serial cytokine levels were measured from the time of mAFP implantation until day 7 afterwards. Time-point-specific multivariable logistic regression was used to identify independent predictors of 30-day mortality. The incremental prognostic value of cytokine levels was evaluated in relation to age, lactate, and vasoactive-inotropic score (VIS), with interaction analyses conducted in relation to hemodynamic severity and blood culture positivity. Results: The overall 30-day mortality rate in the study cohort was 26.5%. IL-6 trajectories diverged progressively between survivors and non-survivors during mAFP support, with the greatest separation at 72 h. At this time point, log-transformed IL-6 was independently associated with 30-day mortality. ROC analysis at 72 h showed moderate discriminatory performance (AUC 0.745) and identified an optimal cut-off of 164.5 pg/mL (sensitivity 68.0%; specificity 82.1%). Patients with IL-6 levels ≥ 164.5 pg/mL presented with lower 30-day survival in exploratory landmark-type Kaplan–Meier analysis (log-rank p < 0.001). This association was not modified by blood culture positivity, although infection, culture-negative inflammatory complications, and vasoplegic/distributive physiology cannot be excluded as contributors to IL-6 elevation. Conclusions: In patients with CS supported by mAFP, persistent IL-6 elevation at 72 h was associated with increased 30-day mortality and provided additional prognostic information alongside established clinical severity markers. These findings suggest that ongoing inflammatory activity may provide additional prognostic information and support further evaluation of serial IL-6 measurements for risk stratification.

Background: Moderate-to-severe tricuspid regurgitation (TR) and renal dysfunction are each associated with adverse outcomes after transcatheter aortic valve replacement (TAVR). We investigated whether their coexistence identifies a clinically relevant high-risk group. Methods: In this retrospective two-centre cohort, patients undergoing TAVR were classified into four groups according to moderate-to-severe TR and preprocedural estimated glomerular filtration rate < 45 mL/min/1.73 m². The primary outcome was one-year all-cause mortality. Multivariable logistic regression adjusted for prespecified clinical covariates, and multiplicative interaction between TR and renal dysfunction was assessed. Results: Among 2227 patients, 1456 had neither condition, 324 isolated renal dysfunction, 315 isolated TR, and 132 both conditions. Patients with the combined phenotype had the highest rates of in-hospital mortality, 30-day mortality, acute kidney injury, and renal replacement therapy (all p < 0.001). One-year mortality increased progressively across groups (6.7%, 10.6%, 11.3%, and 22.9%; p < 0.001). After adjustment (n = 1704), the combined phenotype was associated with higher one-year mortality compared with neither condition (OR 2.91, 95% CI 1.62–5.23; p < 0.001), isolated TR (OR 2.17, 95% CI 1.16–4.07; p = 0.015), and isolated renal dysfunction (OR 2.32, 95% CI 1.16–4.61; p = 0.017). No significant multiplicative interaction was observed (p = 0.187). Conclusions: Coexisting moderate-to-severe TR and renal dysfunction identify a clinically relevant high-risk group after TAVR, with higher adjusted one-year mortality than either condition alone. Combined assessment of TR and renal function may improve preprocedural risk stratification.

(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.

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.

Intermediate monocytes (CD14⁺⁺CD16⁺), a highly pro-inflammatory subset, are linked to endothelial activation, thrombus formation, and poor outcomes in acute coronary syndrome (ACS), suggesting a role in the transition to plaque vulnerability. MicroRNA-92a (miR-92a) promotes vascular inflammation by repressing the transcription factors Kruppel-like factors (KLFs) 2/4, thereby inducing endothelial dysfunction and increasing leukocyte adhesion. Because both intermediate monocytes and miR-92a contribute to plaque instability, their expression profiles appear relevant in acute ischemia. We investigated whether miR-92a is differentially regulated in monocyte subpopulations in ACS compared to chronic coronary syndrome (CCS). Patients with ACS (STEMI/NSTEMI) undergoing urgent coronary angiography and patients with CCS were enrolled. Blood samples were collected peripherally (T_0P) and from the culprit coronary artery (T_0C) during catheterization. Additional peripheral samples were collected 48 h after intervention (T₁) and at the 3-month follow-up (T₂). Peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll density-gradient centrifugation. Monocytes were sorted by fluorescence-activated cell sorting (FACS) into classical (CD14⁺⁺CD16^–), intermediate (CD14⁺⁺CD16⁺), and non-classical (CD14⁺CD16⁺⁺) subsets. MiR-92a expression was measured using real-time PCR and analyzed across predefined time points. In classical and non-classical monocytes, miR-92a levels remained stable throughout the observation period and did not differ between ACS and CCS patients. No spatial expression gradient was observed between intracoronary and peripheral samples at baseline. In contrast, intermediate monocytes in the ACS cohort showed a transient increase in miR-92a expression at T₁ compared with baseline (T_0p) and the 3-month follow-up (T₂). No comparable temporal changes were observed in CCS patients. These findings indicate a temporary alteration of miR-92a expression in intermediate monocytes during the early post-interventional phase following ACS. However, given the exploratory nature of this study and the limited sample size, the biological significance of this observation requires confirmation in larger cohorts.

Introduction: Blood purification techniques are being investigated as adjunctive options in critically ill patients not only to treat severe inflammation but also to remove harmful substances such as myoglobin in rhabdomyolysis. Yet, the available evidence is limited, and further research is needed to clarify their clinical benefits. Methods: The international prospective COSMOS Registry (NCT05146336, 23 Nov 2021) tracks CytoSorb® (CS) utilization patterns and outcomes in critical care settings. Clinical assessment was performed before, during, and after CS treatment, with a 90-day follow-up. Device-related adverse effects were reported by investigators as the safety evaluation. Data were analyzed according to a pre-specified statistical plan using descriptive statistics and paired tests to compare pre- and post-treatment values, with subgroup and safety analyses performed. Results: A total of 300 adult patients (30.3% female, mean age 59 ± 15 years) from 22 sites were included in this analysis. The most common indications for CS therapy (multiple indications possible per patient) were septic shock (48.3%), rhabdomyolysis (12.8%), cardiogenic shock (11.5%), liver failure (11.5%), and acute respiratory distress syndrome (ARDS; 5.0%). On average, each patient received 3.3 ± 3.3 adsorbers, with 27.9% of patients receiving 4 or more adsorbers. CS was integrated in conjunction with kidney replacement therapy (75.6%), standalone hemoperfusion (7.1%), intermittent hemodialysis (IHD; 10.6%), extracorporeal membrane oxygenation (ECMO; 3.9%), and sustained low-efficiency daily dialysis (SLEDD; 4.9%). At baseline, median (interquartile range, IQR) APACHE II and SOFA scores were 24 [18, 30] and 12 [9, 15], respectively. Fluid balance improved from +1675 [141, 3348] mL pre-CS to +115 [−1100, 1495] mL post-CS, and norepinephrine requirements decreased from 0.21 [0.09, 0.40] µg/kg/min to 0.08 [0.02, 0.22] µg/kg/min ( p < 0.0001 for both). Ratio of partial pressure of oxygen in arterial blood to the fraction of inspiratory oxygen concentration (P/F ratio) improved from 120 [72, 208] to 176 [115, 255] ( p < 0.0001). Platelet counts decreased from 123 [76, 185] to 72 [42, 118] × 10 ⁹ /L ( p < 0.0001), while albumin levels remained stable from 2.6 [2.3, 3.1] to 2.5 [2.3, 3.0] g/dL ( p = 0.112). ICU mortality was 33.1%, which was lower than mortality estimates historically associated with comparable APACHE II and SOFA scores. No serious adverse effects related to the device or device deficiencies were reported. Conclusions: Real-world CytoSorb® use as part of standard care in critically ill patients was associated with improvements in several clinical and laboratory parameters; however, these findings should be interpreted cautiously given the observational design and absence of a control group. Observed mortality was lower than mortality estimates historically associated with established severity scores.

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: Left atrial appendage aneurysm (LAAA) is a rare cardiac abnormality associated with thromboembolic events and arrhythmias. This systematic review aimed to provide a comprehensive evaluation of literature reports on the demographics, clinical presentation, electrocardiographic and imaging findings, treatment, and outcomes of patients with LAAA. Methods: A literature search was conducted using the PubMed, MEDLINE, and Scopus databases through September 2025. Only case reports and series explicitly describing LAAA were included. Extracted data included age, sex, clinical symptoms, electrocardiogram (ECG) characteristics, imaging findings, associated cardiac abnormalities, treatment modalities, and outcomes. Results: A total of 216 cases were included. The mean age at diagnosis was 30.41 ± 22.39 years, with a slight predominance of males (50.5%). Symptoms included palpitations (32.4%), dyspnoea (17.2%), and thromboembolic events (7.8%). Atrial fibrillation and flutter were the most commonly detected arrhythmias. Echocardiography was the most frequently used initial diagnostic tool, with computed tomography (CT) and magnetic resonance imaging (MRI) providing additional anatomical details. Chest X-rays often yielded non-specific findings. The mean aneurysm diameter was 6.87 ± 2.64 cm. Surgical treatment, mainly aneurysm resection, was the most commonly used approach (72.7%), while conservative and device-based therapies were applied selectively. Concomitant cardiac anomalies were present in 13.7% of cases and influenced case management. The mortality rate was 4.6%, although significant morbidity was observed. Multivariate logistic regression analysis revealed that atrial fibrillation/flutter was the sole variable significantly linked with clot formation/embolism (p < 0.05). Conclusion: LAAA is a rare, although clinically significant, entity with variable presentation and management challenges. However, early recognition and individualized treatment are essential. Further research is needed to define standardized diagnostic criteria and treatment guidelines.