ECLS-SHOCK and DanGer Shock: Implications for optimal temporary mechanical circulatory support use for cardiogenic shock due to acute myocardial infarction.

Despite concerted efforts to rapidly identify patients with cardiogenic shock complicating acute myocardial infarction (AMI-CS) and provide timely revascularization, early mortality remains stubbornly high. While artificially augmenting systemic flow through the use of temporary mechanical circulatory support (tMCS) devices would be expected to reduce the rate of progression to multi-organ dysfunction and thereby enhance survival, reliable evidence for benefit has remained elusive with lingering questions regarding the appropriate selection of both patients and devices, as well as the timing of device implantation relative to other critical interventions. Further complicating matters are the resource-intensive multidisciplinary systems of care that must be brought to bear in this complex patient population.

Canadian Cardiovascular Society 2023 Guidelines on the Fitness to Drive.

Cardiovascular conditions are among the most frequent causes of impairment to drive, because they might induce unpredictable mental state alterations via diverse mechanisms like myocardial ischemia, cardiac arrhythmias, and vascular dysfunction. Accordingly, health professionals are often asked to assess patients' fitness to drive (FTD). The Canadian Cardiovascular Society previously published FTD guidelines in 2003-2004; herein, we present updated FTD guidelines.

Intraoperative and Early Postoperative Management of Heart Transplantation: Anesthetic Implications.

The gold standard treatment for end-stage heart failure, with 50% mortality within 5 years of diagnosis, is considered heart transplantation. Despite the improvements in immunosuppression, the period of highest mortality risk in the heart transplantation population is during the first year post-transplantation, with primary graft dysfunction being the leading cause of mortality. After adequate preoperative assessment of the recipient, including patients on mechanical support, the intraoperative care of heart transplantation patients requires extensive monitoring followed by proficient management of anesthesia induction and maintenance, ventilation, and fluid therapy.

Knockout of Canopy 2 activates p16 pathway to impair cardiac repair.

Background: Cardiac repair depends on angiogenesis and cell proliferation. Previously we identified Canopy 2 (CNPY2) as a secreted angiogenic growth factor which promotes neovascularization. We investigated the role of CNPY2 in cardiac repair following myocardial infarction (MI) and the possible mediators involved using Cnpy2 knockout (KO) mice and human cardiac tissue.

Tricuspid Valve Annular Dilation as a Predictor of Right Ventricular Failure After Implantation of a Left Ventricular Assist Device.

Background: Tricuspid annular (TA) dilation has been suggested as a more reliable marker of concomitant advanced right ventricular failure (RVF) than severity of tricuspid regurgitation (TR). Our objective was to examine the impact of TA dilation on occurrence of RVF and in-hospital mortality following left ventricular assist device (LVAD) implant.

Methods: Consecutive patients undergoing implantation of a continuous-flow LVAD implant were grouped according to the presence or absence of preoperative dilated TA.

Transcatheter aortic valve implantation and left ventricular assist device: a word of caution.

Aortic valve disease in the setting of a left ventricular assist device presents unique challenges. We present the case of a patient who underwent transcatheter aortic valve implantation to replace a stenotic aortic valve to facilitate left ventricular assist device explantation. Thirty-three days later, the porcine pericardial valve cusps were fused and a thick pseudomembrane had occluded the left ventricular outflow tract, forcing the explant to be aborted.

Defective liver formation and liver cell apoptosis in mice lacking the stress signaling kinase SEK1/MKK4.

The stress signaling kinase SEK1/MKK4 is a direct activator of stress-activated protein kinases (SAPKs; also called Jun-N-terminal kinases, JNKs) in response to a variety of cellular stresses, such as changes in osmolarity, metabolic poisons, DNA damage, heat shock or inflammatory cytokines. We have disrupted the sek1 gene in mice using homologous recombination. Sek1(-/- )embryos display severe anemia and die between embryonic day 10.

Brca2 is required for embryonic cellular proliferation in the mouse.

Mutations of the tumor suppressor gene BRCA2 are associated with predisposition to breast and other cancers. Homozygous mutant mice in which exons 10 and 11 of the Brca2 gene were deleted by gene targeting (Brca2(10-11)) die before day 9.5 of embryogenesis.