Publications by authors named "C Sag"
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.
Aims: 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.
Methods And Results: In this study, patients with CS treated with MCS at 15 tertiary care centres in three countries were enrolled.
Background: Acute stimulation of the late sodium current (I) as pharmacologically induced by Anemonia toxin II (ATX-II) results in Na-dependent Ca overload and enhanced formation of reactive oxygen species (ROS). This is accompanied by an acute increase in the amplitude of the systolic Ca transient. Ca transient amplitude is determined by L-type Ca-mediated transsarcolemmal Ca influx (I) into the cytosol and by systolic Ca release from the sarcoplasmic reticulum (SR).
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- VA-ECMO therapy helps patients with cardiogenic shock by restoring circulation but can lead to various complications affecting survival and neurological outcomes.
- A study analyzed data from 501 patients across 16 centers, revealing that over half experienced complications, especially women, with 40% mortality within 30 days.
- The findings indicate a need for better identification of patients at risk for complications to improve treatment strategies, as most adverse events correlate with worse prognosis.
Background: The Bruton tyrosine kinase (BTK) inhibitor Ibrutinib is associated with a higher incidence of cardiotoxic side effects including heart failure (HF).
Objectives: Ibrutinib is capable of inhibiting PI3K/Akt signaling in neonatal rat ventricular cardiomyocytes when stimulated with insulin-like growth factor 1 (IGF-1). We therefore hypothesized that Ibrutinib might disrupt IGF-1-mediated activation of intracellular Ca handling in adult mouse cardiomyocytes by inhibiting PI3K/Akt signaling.