Search

Background: Abnormal activity of 18F-FDG PET/CT is a major Duke criterion in the diagnostic work-up of infective prosthetic valve endocarditis (IE). We hypothesized that quantitative lesion assessment by 18F-FDG PET/CT-derived standard maximum uptake ratio (SURmax), metabolic volume (MV), and total lesion glycolysis (TLG) might be useful in distinct subgroups of IE patients (e.g. IE-related abscess formation). Methods: All patients (n = 27) hospitalized in our tertiary IE referral medical center from January 2014 to October 2018 with preoperatively performed 18F-FDG PET/CT and surgically confirmed IE were included into this retrospective analysis. Results: Patients with surgically confirmed abscess formation (n = 10) had significantly increased MV (by ~ fivefold) and TLG (by ~ sevenfold) as compared to patients without abscess (n = 17). Receiver operation characteristics (ROC) analyses demonstrated that TLG (calculated as MV × SURmean, i.e. TLG (SUR)) had the most favorable area under the ROC curve (0.841 [CI 0.659 to 1.000]) in predicting IE-related abscess formation. This resulted in a sensitivity of 80% and a specificity of 88% at a cut-off value of 14.14 mL for TLG (SUR). Conclusion: We suggest that 18F-FDG PET/CT-derived quantitative assessment of TLG (SUR) may provide a novel diagnostic tool in predicting endocarditis-associated abscess formation. [ABSTRACT FROM AUTHOR]

Aims Methods and results Conclusion The optimal timing for implementing mechanical circulatory support (MCS) in cardiogenic shock (CS) remains indeterminate. This study aims to evaluate patient characteristics and outcome associated with the time interval between CS onset and veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) implementation.In this study, patients with CS treated with MCS at 15 tertiary care centres in three countries were enrolled. Patients treated with MCS were stratified into early (<2 h), intermediate (2–12 h) and delayed (≥12–24 h) MCS implantation by using the time interval between CS onset and MCS device implementation. Adjusted logistic and Cox regression models were fitted to assess the association between timing of MCS implementation, patient characteristics and 30‐day mortality. A total of 330 patients with CS treated with VA‐ECMO and/or microaxial flow pump were included in this study; 20.9% received early, 55.8% intermediate, and 23.3% delayed MCS. Although crude 30‐day mortality was slightly lower in patients with early MCS (58.1% vs. 64.7% vs. 64.3%), adjusted analyses showed no significant association between timing of MCS implantation and 30‐day all‐cause mortality (hazard ratio [HR] for early vs. intermediate MCS: 0.93, 95% confidence interval [CI] 0.59–1.46, p = 0.74; HR for early vs. delayed MCS: 1.29, 95% CI 0.78–2.13, p = 0.33). Moreover, the incidence of complications, related and unrelated to MCS, did not differ significantly among groups.In this exploratory study of patients with CS treated with MCS, the timing of device implantation within 24 h after CS onset was not associated with mortality. This supports a restrictive MCS approach, reserving its application for patients experiencing CS deterioration despite conventional therapy. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to investigate incidence and predictors of weaning failure and in-hospital death after successful weaning from veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in patients with cardiogenic shock (CS)., Methods and Results: Overall, 685 patients with CS treated with VA-ECMO from 23 tertiary care centres in 7 countries were analysed (median age 57 [interquartile range 49-66] years, 542 [79.1%] male, median lactate 7.6 [interquartile range 4.1-12.7] mmol/L). The cause of CS was acute myocardial infarction in 438 (63.9%) patients, and 431 (62.9%) patients presented with cardiac arrest. A total of 410 patients (59.9%) were successfully weaned from VA-ECMO, whereas in 275 patients (40.1%) weaning failed (i.e. patients died on or within 48 h after VA-ECMO support). Of the successfully weaned patients, 150 (36.6%) died before hospital discharge. On multivariable logistic regression, predictors for both patient groups varied: age (per 10 years, odds ratio [OR] 1.49, 95% confidence interval [CI] 1.25-1.76; p < 0.001) and cardiac arrest before VA-ECMO implantation (OR 1.64, 95% CI 1.01-2.64; p = 0.04) were associated with weaning failure, whereas lactate clearance within 24 h after VA-ECMO initiation was associated with successful weaning (OR 0.21, 95% CI 0.1-0.44; p < 0.001). In-hospital death after successful weaning was more likely with higher age (per 10 years, OR 1.56, 95% CI 1.24-1.97; p < 0.001), renal replacement therapy (OR 2.56, 95% CI 1.4-4.68; p = 0.002) and bleeding events (OR 2.93, 95% CI 1.4-6.14; p = 0.004)., Conclusion: Weaning from VA-ECMO fails in 40% of patients treated with VA-ECMO for CS. When successful, survival after VA-ECMO weaning mostly depends on age and the incidence of device- and shock-related complications., (© 2025 The Author(s). European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: Acute stimulation of the late sodium current (I NaL ) as pharmacologically induced by Anemonia toxin II (ATX-II) results in Na + -dependent Ca 2+ overload and enhanced formation of reactive oxygen species (ROS). This is accompanied by an acute increase in the amplitude of the systolic Ca 2+ transient. Ca 2+ transient amplitude is determined by L-type Ca 2+ -mediated transsarcolemmal Ca 2+ influx (I Ca ) into the cytosol and by systolic Ca 2+ release from the sarcoplasmic reticulum (SR). Type-1 protein kinase A (PKARIα) becomes activated upon increased ROS and is capable of stimulating I Ca , thereby sustaining the amplitude of the systolic Ca 2+ transient upon oxidative stress., Objectives: We aimed to investigate whether the increase of the systolic Ca 2+ transient as acutely induced by I NaL (by ATX-II) may involve stimulation of I Ca through oxidized PKARIα., Methods: We used a transgenic mouse model in which PKARIα was made resistant to oxidative activation by homozygous knock-in replacement of redox-sensitive Cysteine 17 with Serine within the regulatory subunits of PKARIα (KI). ATX-II (at 1 nmol/L) was used to acutely enhance I NaL in freshly isolated ventricular myocytes from KI and wild-type (WT) control mice. Epifluorescence and confocal imaging were used to assess intracellular Ca 2+ handling and ROS formation. A ruptured-patch whole-cell voltage-clamp was used to measure I NaL and I Ca . The impact of acutely enhanced I NaL on RIα dimer formation and PKA target structures was studied using Western blot analysis., Results: ATX-II increased I NaL to a similar extent in KI and WT cells, which was associated with significant cytosolic and mitochondrial ROS formation in both genotypes. Acutely activated Ca 2+ handling in terms of increased Ca 2+ transient amplitudes and elevated SR Ca 2+ load was equally present in KI and WT cells. Likewise, cellular arrhythmias as approximated by non-triggered Ca 2+ elevations during Ca 2+ transient decay and by diastolic SR Ca 2+ -spark frequency occurred in a comparable manner in both genotypes. Most importantly and in contrast to our initial hypothesis, ATX-II did not alter the magnitude or inactivation kinetics of I Ca in neither WT nor KI cells and did not result in PKARIα dimerization (i.e., oxidation) despite a clear prooxidant intracellular environment., Conclusions: The inotropic and arrhythmogenic effects of acutely increased I NaL are associated with elevated ROS, but do not involve oxidation of PKARIα., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Gissibl, Stengel, Tarnowski, Maier, Wagner, Feder and Sag.)