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 (T0P) and from the culprit coronary artery (T0C) 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 (T0p) 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.

Autophagy is a central homeostatic mechanism that preserves intracellular quality control by clearing damaged organelles, aggregated proteins, and excess lipids. Increasing evidence indicates that the lipid-autophagy axis is a critical determinant of chronic inflammatory and metabolic disease. Cholesterol-rich and oxidatively modified lipoproteins, including very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), oxidized LDL, and lipoprotein(a), can impose lysosomal stress, disturb autophagosome maturation, and amplify oxidative and inflammatory signaling, whereas high-density lipoprotein-mediated cholesterol efflux supports cellular lipid clearance and autophagic competence. When chronic lipid overload exceeds lysosomal and autophagic capacity, cells transition from adaptive lipophagy to impaired autophagic flux, leading to lipid-droplet accumulation, mitochondrial dysfunction, inflammasome activation, and sustained cytokine production. This review synthesizes mechanistic insights linking lipid dysregulation and autophagy failure across atherosclerosis, metabolic dysfunction-associated steatotic liver disease/metabolic dysfunction-associated steatohepatitis (MASLD/MASH), and neurocognitive disorders. We further discuss how defective autophagy impairs efferocytosis, phagosome maturation, and inflammasome restraint, thereby contributing to unresolved inflammation and inflammatory cell-death signaling. Translationally, we outline therapeutic strategies that combine metabolic unloading, lipid-lowering interventions, autophagy-lysosome modulation, and flux-based biomarker approaches. Lipid-induced autophagic flux failure provides a unifying framework for understanding how metabolic stress evolves into chronic inflammation and organ dysfunction and identifies actionable targets for precision therapeutic intervention.

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.

Post-viral syndromes are heterogeneous multisystem diseases without a uniform etiology that occur as a result of acute viral infections. During the COVID-19 pandemic, the number of patients increased dramatically due to infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This is known as post-acute sequelae of COVID-19 (PASC), with many cases also meeting the criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), the most severe form of a post-viral disease, characterized by severe fatigue, post-exertional malaise (PEM), unrefreshing sleep, neurocognitive impairment, and autonomic and immune dysregulation. Orexin (OX) neuropeptides, which regulate arousal, metabolism, and neuroendocrine functions, may serve as a central link between stress, immune activation, and metabolic changes in these syndromes. Notable phenotypic similarities between OX system dysfunction and core features of PASC and ME/CFS, including fatigue, sleep issues, impaired glucose metabolism, and neuropsychiatric symptoms, support a mechanistic model in which impaired OX signaling contributes to post-viral endocrine and metabolic dysfunction. This review examines the role of OX in regulating glucose metabolism, HPA axis activity, and systemic homeostasis, with a specific focus on sexually dimorphic expression and function in relation to post-viral syndromes. We also highlight the effect of glucagon-like peptide-1 (GLP-1), another key player in metabolism, which also has neuroprotective, anti-inflammatory, vasoprotective, and immunomodulatory effects. We further emphasize emerging therapeutic strategies, such as GLP-1 receptor agonists (GLP-1RAs) and drugs targeting the OX system. Together, these insights provide an integrated framework for understanding and targeting the neuroendocrine-metabolic underpinnings of PASC, ME/CFS, and other post-viral syndromes.

Background:Transcatheter edge-to-edge mitral valve repair (mTEER) is an established treatment for patients with mitral regurgitation (MR) at prohibitive surgical risk. However, predictors of optimal MR reduction remain insufficiently defined. Methods:We retrospectively analyzed all patients who underwent mTEER treatment at four German cardiac centers between 2011 and 2022. Patients were categorized by residual MR ≤ I° or II°. Univariable and multivariable logistic regression analyses revealed predictors of residual MR ≤ I°. Long-term survival was assessed via Kaplan-Meier analysis and adjusted through propensity-score matching (PSM). Results:Among 821 patients, 724 (88.2%) achieved residual MR ≤ I°, whereas 97 (11.8%) achieved residual MR of II°. Patients with residual MR of II° were younger, exhibited higher morbidity, and required longer procedures with more clips. Age <65 years, prior implantable cardioverter defibrillator (ICD), and left ventricular end-diastolic diameter >62 mm served as inverse predictors of residual MR ≤ I° in univariable analysis. In contrast, only age <65 years remained a significant inverse predictor of residual MR ≤ I° in the multivariable model (odds ratio 0.39, 95% confidence interval 0.19-0.84, p = 0.01). Long-term survival did not differ significantly in the overall cohort between patients with residual MR ≤ I° and those with residual MR of II° before or after PSM. Conclusion:Residual MR of II° occurred in 12% of patients and was more common in younger, comorbid individuals with complex MR anatomy. While survival was unaffected in the overall cohort, age <65 years emerged as a key predictor of suboptimal MR reduction. These findings highlight the need for critical patient selection and may inform individualized treatment strategies in contemporary mTEER practice.

Background : Acute myocardial infarction-related cardiogenic shock (AMI-CS) remains associated with high mortality. We investigated early hemodynamic and metabolic changes following adjunctive extracorporeal hemadsorption in a real-world AMI-CS cohort. Methods : This retrospective single-center landmark analysis included adult intensive care unit (ICU) patients with AMI-CS classified as Society for Cardiovascular Angiography and Interventions (SCAI) stage C or higher between January 2017 and July 2025. Patients who died within 24 h of ICU admission were excluded; among patients receiving hemadsorption, only those treated for at least 24 h were included. Propensity score matching was performed using sex, prior cardiopulmonary resuscitation (CPR), temporary mechanical circulatory support (tMCS), continuous renal replacement therapy (CRRT), admission lactate, admission vasoactive-inotropic score (VIS), and admission Horovitz index. The principal analysis compared pretreatment values with those at 24 h after treatment initiation; corresponding pseudo-timepoints were assigned in matched controls. Serial assessments at 12 h, 24 h, and 48 h characterized VIS and lactate trajectories. Results : Of 479 screened patients with AMI-CS, 398 met eligibility criteria for the 24-h landmark analysis, including 57 treated with adjunctive hemadsorption and 341 controls. Propensity score matching yielded 35 matched pairs and improved balance across the prespecified covariates, although residual imbalance persisted for prior CPR, CRRT, admission lactate, and admission VIS. In the matched cohort, hemadsorption-treated patients showed early within-group reductions in VIS (56.2 to 23.0; P=0.009) and lactate (2.0 to 1.5 mmol/L; P<0.001) as well as declines in aspartate aminotransferase (P=0.031) and lactate dehydrogenase (P=0.018). In matched controls, lactate likewise decreased significantly, whereas VIS remained unchanged, and tissue-injury markers did not show a comparable early decline. Although VIS and lactate improved over time overall, no significant time-by-treatment interaction was observed over 48 h for VIS (P=0.834) or lactate (P=0.427). Exploratory subgroup and multivariable analyses revealed no evidence of a differential mortality benefit. In-hospital mortality was similar between matched groups (45.7% vs. 42.9%; P=1.000), and hemadsorption was not independently associated with mortality (odds ratio=1.05, 95% CI: 0.36–3.08; P=0.934). Conclusions : In this exploratory propensity score-matched landmark analysis of AMI-CS, hemadsorption-treated patients showed early within-group hemodynamic and metabolic changes, but subsequent VIS and lactate trajectories did not differ significantly from matched controls, and in-hospital survival was not improved. Residual imbalance and the observational design limit causal interpretation. These findings should be considered hypothesis-generating and require prospective validation.

Zusammenfassend wird im ESC-Konsensuspapier die Bedeutung von Impfungen als essenzieller Bestandteil der kardiovaskulären Prävention überzeugend dargestellt. Dennoch bleiben zahlreiche Fragen offen, insbesondere hinsichtlich der Wahl des optimalen Impfstoffs, der Mechanismen der Impfstoffwirkung sowie spezifischer Strategien für besondere Risikogruppen. Weiterführende Forschung ist notwendig, um diese Evidenzlücken zu schließen und die Grundlage für evidenzbasierte Empfehlungen zu erweitern. Trotz dieser Einschränkungen basieren die aktuellen Empfehlungen für bestimmte Impfstoffe, insbesondere für Influenza‑, Pneumokokken- und SARS-CoV-2-Impfstoffe, auf einer soliden Studienlage. Für andere Indikationen und spezielle Patientengruppen ist jedoch künftig spezifische klinische und experimentelle Forschung notwendig, um die kardiovaskuläre Prävention durch Impfstrategien weiter zu verbessern [1]. Eine interdisziplinäre, translational ausgerichtete Forschungsagenda für Impfstoffe und Impfstrategien ist notwendig, die klinisch-immunologische, epidemiologische und gesundheitsökonomische Aspekte verbindet. Ziel muss es sein, das volle Potenzial der Impfprävention in der Kardiologie auszuschöpfen und dadurch die Versorgung sowie die Prognose kardiovaskulärer Erkrankungen zu verbessern. Die konsequente Anwendung evidenzbasierter Impfstrategien unter Berücksichtigung von Sicherheitsaspekten, vulnerablen Gruppen, praktischen Zeitplänen, Impfstoffvielfalt und immunologischen Wirkmechanismen, ist entscheidend für die moderne kardiovaskuläre Prävention und ein integraler Bestandteil der klinischen Versorgung.

Die kardiovaskuläre Intensivmedizin ist ein zentraler Pfeiler in der Versorgung kritisch erkrankter Patienten. Während sich die frühen Koronarstationen der 1960er-Jahre im Wesentlichen auf das Monitoring von Rhythmusstörungen konzentrierten, erfordert die gegenwärtige medizinische Versorgung den Umgang mit einer Patientendemografie, die zunehmend durch fortgeschrittenes Alter, multiple Komorbiditäten sowie eine gesteigerte Prävalenz von Multiorganversagen geprägt ist [1, 2]. Mit den Fortschritten in interventionellen Verfahren haben sich die therapeutischen Möglichkeiten zwar erheblich erweitert; zugleich wächst jedoch der Bedarf an strukturierten Vorgaben und Standards, wie es die G‑BA-Zentrumsregelungen sowie die Empfehlungen der Fachgesellschaften und der Deutschen Interdisziplinären Vereinigung für Intensiv- und Notfallmedizin (DIVI) verdeutlichen [3–6]. Für Hochrisikopatienten in der kardiovaskulären Intensivmedizin jedoch – insbesondere bei kardiogenem Schock, schwerer Herzinsuffizienz, ausgeprägter hämodynamischer Instabilität, drohendem Multiorganversagen, Hochrisikolungenembolie, septischer Kardiomyopathie oder im Rahmen des Post-Cardiac-Arrest-Syndroms (PCAS) – reichen derartige, allgemein formulierte Standards nicht aus, da ihre Versorgung ein durchgängiges strukturiertes Behandlungskontinuum von der klinischen Akut- und Notfallmedizin über die intensivmedizinische Stabilisierung bis zur Organunterstützung und Netzwerksteuerung erfordert. Es braucht spezialisierte Strukturen, optimierte Prozesse und Outcome-Messungen für eine funktionierende multidisziplinäre Versorgung. Zudem sind zentrale Strukturvorgaben obligat, inklusive der Definition besonderer Anforderungen – von der 24/7-Katheterbereitschaft über die Integration von Shock-Teams bis hin zur Indikationsstellung mechanischer Organunterstützung und dem Einsatz einer mobilen extrakorporalen Membranoxygenierung(ECMO)-Therapie. Darüber hinaus muss eine interdisziplinäre Roadmap für Ausbildung, Netzwerkbildung und Integration innovativer Versorgungsstrukturen (inklusive Telemedizin und Artificial Intelligence) die Weiterentwicklung der kardiovaskulären Intensivmedizin ergänzen und zukunftsorientiert ausrichten. Nur so kann auch perspektivisch eine multidisziplinäre hoch spezialisierte Versorgung jener zunehmend kritisch erkrankten Patienten unter Einhaltung einer bestmöglichen Versorgungsqualität gelingen.

BACKGROUND:In physician-staffed emergency medical services (EMS) systems, emergency physicians may differ in postgraduate specialist and critical care training. Whether such differences are associated with outcomes after out-of-hospital cardiac arrest (OHCA) remains uncertain. We investigated the association between emergency physician qualification and outcomes after non-traumatic OHCA. METHODS:This retrospective cohort study included adult patients with non-traumatic OHCA from the Marburg-Biedenkopf EMS region from 2018 to 2024. Patients were treated by residents, specialists without additional critical care training, or specialists with additional critical care training. The primary outcome was survival to discharge. Secondary outcomes included return of spontaneous circulation (ROSC), hospital admission with ROSC, 24-h survival, and favorable neurological outcome. Multivariable logistic regression was performed for each endpoint with residents as reference. RESULTS:Among 1426 patients, any ROSC did not differ significantly between groups (39.9%, 42.5%, and 45.7%; p = 0.211). Operational response times and time to first ROSC were comparable. Specialists with additional critical care training achieved faster vascular access and earlier vasopressor administration, with fewer access failures. Survival to discharge increased across groups (12.2%, 14.4%, and 18.0%; p = 0.047). In adjusted analyses, specialists with additional critical care training had higher odds of hospital admission with ROSC (OR 1.42, 95% CI 1.05-1.93) and survival to discharge (OR 1.59, 95% CI 1.05-2.40) compared with residents. CONCLUSIONS:Additional critical care training was associated with selected prehospital procedural measures and higher odds of hospital admission with ROSC and survival to discharge. These observational findings are hypothesis-generating and do not establish causality.

BackgroundTranscatheter aortic valve replacement (TAVR) has become a widely used treatment option for severe aortic stenosis (AS), particularly in elderly and multimorbid patients. The New York Heart Association (NYHA) classification, which assesses the severity of heart failure (HF), is a key factor influencing TAVR outcomes. However, its impact on procedural success, complications, and outcomes remains underrepresented in recent studies.MethodsIn this multicenter study, data from 2,256 patients who underwent TAVR between 2017 and 2022 at two high-volume German Heart Centers were analyzed. Demographics, comorbidities, and peri-procedural parameters were evaluated to determine the influence of pre-procedural NYHA classification on complications, hospital stay, and outcomes. Multivariable logistic regression analyses were performed to assess the independent prognostic impact of pre-procedural NYHA class on 30-day and 1-year mortality.ResultsNYHA class III/IV prior to the procedure was associated with higher peri-procedural complication rates, prolonged hospital stays, and increased mortality compared to class NYHA I/II. In particular, the rates for cardiopulmonary resuscitation (5.3% vs. 0.7%; p < 0.001), acute coronary intervention (1.9% vs. 0.0%; p = 0.006), vasopressor use >6 h (11.7% vs. 1.6%; p < 0.001), and renal replacement therapy (6.8% vs. 0.2%; p < 0.001) were higher. Procedure-related complications like vascular closure device failure (4.9% vs. 1.3%; p = 0.008), need for vascular surgery (9.0% vs. 6.3%; p = 0.002), and blood transfusion (9.4% vs. 4.7%; p = 0.017) were more common in NYHA IV. Median hospital stay was longer in NYHA IV (10.0 vs. 6.0 days; p < 0.001). The 30-day mortality rate was 8.3% (NYHA IV) vs. 1.4% (NYHA I/II), and 1-year mortality was 19.2% vs. 5.2% (p < 0.001). After multivariable adjustment for relevant clinical confounders, NYHA class IV remained independently associated with both 30-day and 1-year mortality.ConclusionsPre-procedural NYHA class provides important prognostic information in patients undergoing TAVR, with higher symptom burden associated with increased peri-procedural risk and mortality. These findings highlight the relevance of comprehensive pre-procedural evaluation and optimized timing of intervention. Incorporating functional status into pre-procedural assessment may support risk stratification and individualized patient management.

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 The axillary artery is an alternative access- site for transcatheter aortic valve implantation (TAVI) when femoral arteries are unfavourable. Simplified transaxillary-TAVI (TAx-TAVI) is performed completely percutaneously, using vascular closure device (VCD) techniques for arteriotomy closure. Concerns exist regarding major vascular complications with this technique. This registry-study describes off-label VCD use during simplified TAx-TAVI.Methods Consecutive severe aortic stenosis patients unsuitable for both surgery and transfemoral access were enrolled in our heart valve registry and underwent simplified TAx-TAVI using VCDs for arteriotomy closure. At the operator’s discretion, closure was performed with a collagen-based plug (MANTA) or a suture-based system (double ProGlide). The primary endpoint was axillary access-related major vascular complications in hospital and at 30 days according to Valve Academic Research Consortium (VARC-3) definitions. Secondary endpoints included axillary access-site bleeding and all-cause mortality during hospitalisation to 30 days post-TAx-TAVI.Results From January 2022 to January 2024, 32 patients (mean age 77 years, 31.3% female) underwent simplified TAx-TAVI using VCDs. MANTA and ProGlide were each used in 50.0% of cases (n=16). Local anaesthesia with conscious sedation was used in 21.9% (n=7). Overall VARC-3 device success was 96.9% (31/32). VCD failure occurred in 25.0% (8/32) and was numerically more frequent with ProGlide (31.3%) than MANTA (18.8%). A covered stent was required for definitive axillary haemostasis in 12.5% (4/32). The 30-day axillary major vascular complication rate was 3.1% (1/32). No major bleeding complications occurred. All-cause 30-day mortality was 3.1% (1/32). New permanent pacemaker implantation occurred in 12.5% (4/32). At 30 days, New York Heart association (NYHA) class improved by at least one category in 68.8% (22/32).Conclusions In these simplified TAx-TAVI cases, MANTA and ProGlide VCDs performed well in terms of vascular and bleeding complications. Simplified TAx-TAVI requires advanced access-site management skills, including covered stent use. We found VCDs approved for femoral use safe with axillary access.

Quadricuspid aortic valve (QAV) is a rare congenital anomaly with an estimated incidence of 0.008% to 0.043% based on autopsy and echocardiographic studies. Although often asymptomatic, it can lead to progressive aortic regurgitation (AR), left ventricular (LV) dysfunction, and arrhythmias such as atrial fibrillation (AF). Due to its rarity, QAV is often misdiagnosed or discovered incidentally, highlighting the need for advanced cardiac imaging in young patients presenting with unexplained heart failure symptoms and arrhythmias. We present the case of a 41-year-old female patient who was admitted with new-onset dyspnea classified as New York Heart Association (NYHA) class III and palpitations due to persistent AF with a European Heart Rhythm Association (EHRA) symptom class 2b. There was no family history of congenital or structural heart disease, with arterial hypertension being the only identified predisposing condition. Initial transthoracic echocardiography revealed moderate AR, but more detailed transesophageal echocardiography performed before pulmonary vein isolation incidentally revealed a QAV. Further cardiac magnetic resonance imaging confirmed normal aortic root dimensions with early LV remodeling. The patient was managed conservatively with rate control, anticoagulation, and regular follow-up to monitor disease progression. This case highlights the importance of advanced imaging techniques in the diagnosis of rare structural heart abnormalities in young patients presenting with unexplained heart failure symptoms and arrhythmias. Early identification of QAV allows for timely medical intervention, optimal patient monitoring, and prevention of long-term complications. Regular follow-up is essential to monitor disease progression and determine the need for surgical intervention.

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), characterized by inadequate tissue perfusion due to cardiac dysfunction, has a high mortality rate despite advances in treatment. Systemic inflammation and organ failure exacerbate the severity of CS. Extracorporeal hemadsorption techniques such as CytoSorb® have been introduced to control inflammation. However, evidence of their efficacy, particularly in patients on various mechanical circulatory support (MCS) systems, remains limited. Methods: This retrospective study analyzed data from 129 CS patients treated with CytoSorb® at the University Hospital of Marburg between August 2019 and December 2023. Those patients receiving MCS were grouped according to MCS type: (1) Impella, (2) VA-ECMO, and (3) ECMELLA. The hemodynamic parameters of circulatory support (e.g., MCS flow rates and vasoactive inotropic score, VIS) and laboratory and ventilation parameters were assessed 24 h before start of CytoSorb® therapy (T1) and 24 h after completion of CytoSorb® therapy (T2). Results: Of 129 CS patients (mean age: 64.7 ± 13.1 years), 103 (79.8%) received MCS. Comparing T1 and T2, there was a significant reduction in VIS in the entire cohort (T1: 38.0, T2: 16.3; p = 0.002), with a concomitant significant reduction in the level of MCS support in all subgroups, indicating successful weaning. Analysis of laboratory parameters showed significant reductions in lactate (T1: 2.1, T2: 1.3 mmol/L; p = 0.014), myoglobin (T1: 1549.0, T2: 618.0 µg/L; p < 0.01), lactate dehydrogenase (T1: 872.0, T2: 632.0 U/L; p = 0.048), and procalcitonin (T1: 2.9, T2: 1.6 µg/L; p < 0.001). However, a significant decrease in platelets (T1: 140.0, T2: 54.0 tsd/µL; p < 0.001) and albumin (T1: 25.0, T2: 22.0 g/dL; p < 0.001) was also documented. The median SOFA score of the entire cohort was 15.0 (IQR 12.0–16.0), predicting a mortality rate of >80%, which could be reduced to 60.5% in the present study. Conclusions: During CytoSorb® therapy in CS, a significant reduction in VIS was demonstrated, resulting in improved organ perfusion. Therefore, the results of this study underline that CytoSorb® therapy can be considered a useful “component” in the complex management of CS, especially when combined with MCS. To refine and optimize treatment strategies in CS, prospective studies are needed to better define the role of hemadsorption.

BACKGROUND: Epinephrine administration during cardiopulmonary resuscitation (CPR) has been a long-standing recommendation, but the evidence is controversial. This study investigated effects of epinephrine administration in a physician-staffed emergency medical service (EMS) system and for the first time addressed the quality of chest compressions. METHODS: Complete datasets of adult patients who suffered out-of-hospital cardiac arrest (OHCA) and received CPR were retrospectively analysed. Factors (time of collapse, bystander CPR, EMS arrival, initial cardiac rhythm, suspected cause of OHCA, and for the first time also quality of chest compressions) that may influence outcome (return of spontaneous circulation [ROSC], survival to discharge, neurological status) and epinephrine administration (time of first administration, total dose, route of administration) were analysed after adjustment. RESULTS: A total of 1141 patients were identified; 1090 patients were included. Patient data (age, gender, pre-existing conditions, initial electrocardiographic rhythm, suspected cause) were comparable to those reported in international studies. Mean chest compression depth was 5.5 cm (SD: 0.8 cm). Median compression rate was 115/min (SD: 12/min). The first epinephrine dose was administered after a mean period of 6:43 min after EMS arrival (SD: 9:30 min) and 18:23 min after collapse (SD: 11:13 min). Earlier epinephrine administration was associated with increased rates of ROSC and survival to discharge. Patients who achieved ROSC and survived to discharge received less than 6 mg of epinephrine. Early administration was associated with improved outcomes, especially in patients with asystole. Neurological outcomes, however, deteriorated with increasing epinephrine doses. CONCLUSIONS: This study supports the benefit of early administration of limited doses of epinephrine in OHCA patients. Higher epinephrine doses may be associated with poorer outcomes. Further randomised controlled studies that investigate the administration of medications within fifteen minutes after collapse and also address the quality of basic life support measures are required to assess the actual benefits of epinephrine during CPR.

Background: Emerging evidence suggests the role of mechanical circulatory support (MCS) devices in the therapy of refractory cardiogenic shock (CS). However, largerandomized trials addressing the role of Impella in the therapy of infarct-associated CS are sparse. As such, evidence coming from comprehensive retrospective studies or meta-analyses is of major importance in order to clarify the role of the Impella device in this setting. Methods: Only clinical trials involving patients receiving Impella 2.5 and Impella CP for treatment of CS caused in terms of acute coronary syndrome (ACS) were included in this meta-analysis. The primary endpoint was 30-day mortality, with major bleeding and ischemic vascular complications serving as secondary endpoints. Results: A total of 18 observational retrospective studies (2617 patients with CS and Impella implantation) were included in this analysis. The mean age of the total participants was 64.7 ± 2.93 years. A mean mortality incidence of 45% was found between all included participants. The ischemia rate was in total 8.5 ± 4.4%, and the incidence of bleeding was 13.9 ± 5.6%. Conclusions: The 30-day mortality rate for patients with ACS-associated CS treated with Impella remains high. The high complication rates underline the importance of Impella use in only a very well-selected population of patients.

Background Current guidelines recommend transcatheter aortic valve implantation (TAVI) for patients with aortic stenosis and porcelain aorta (PA). Neurological outcomes of patients with PA undergoing TAVI with modern valves require clarification as most trials examined balloon-expandable valves (BEV) and self-expandable valves in intermediate or high-risk patients, but not specifically in patients with PA. Our aim was to compare outcomes, including stroke and mortality, in well-matched patients with and without PA who received BEV during transfemoral TAVI procedures.Methods Consecutive patients undergoing TAVI were entered into a registry. For this single-centre (Zentralklinik Bad Berka, Germany), retrospective analysis, we only selected patients who received BEV. PA diagnosis was made when non-contrast axial CT images fulfilled Valve Academic Research Consortium-2 criteria for PA. There was 2:1 nearest neighbour matching of patients without and with PA. The primary outcome measure was 30-day mortality or stroke within 72 hours. Secondary outcome measures were 30-day mortality, stroke within 72 hours, technical success and 30-day device success.Results After matching patients with (n=141) and without PA (n=282), the primary outcome of mortality at <30 days or stroke within 72 hours was higher in PA versus non-PA (7.8% vs 2.5%; OR 3.32 (95% CI 1.25 to 8.85); p=0.019). With regard to secondary outcomes, PA was not associated with mortality at 30 days (4.3% vs 2.1%; OR 2.04 (95% CI 0.65 to 6.48); p=0.23); however, stroke within 72 hours was significantly higher in PA versus non-PA (3.5% vs 0.4%; OR 10.33 (95% CI 1.17 to 91.12); p=0.017). Technical and device success were uninfluenced by PA.Conclusions Transfemoral TAVI with BEV in patients with PA was associated with a higher risk of the primary combined endpoint of mortality at 30 days or stroke within 72 hours, which was primarily driven by stroke within 72 hours. These findings might influence cerebral embolic protection device use in patients with PA.

The steadily increasing number of transcatheter aortic valve replacement (TAVR) procedures being performed on a heterogeneous patient population highlights the need for robust risk assessment. While EuroSCORE II is well established for surgical risks, it is less effective for TAVR, and the newer STS/ACC TAVR score has so far been validated mainly for in-hospital and 30-day mortality. This study aims to improve risk stratification for TAVR patients by identifying real-time predictors of 30-day and 1-year mortality that incorporate comprehensive, procedure-specific factors. Five-year data from 2256 transfemoral TAVR procedures performed at two German Heart Centers (2017–2022) were retrospectively analyzed. Predictors of 1-year and 30-day mortality were assessed using multivariable logistic and LASSO regression, considering a broad spectrum of patient demographics, comorbidities, and peri-procedural factors. The analyses revealed a predictor model (PRE-TAVR predictors) for 1-year mortality (AUC 0.770; 95

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.