Activating transcription 3 (ATF3) is a member of the basic leucine zipper family of transcription factors. ATF3 is an immediate early gene expressed following various cellular stresses. ATF3 acts through binding to cyclic AMP response elements found in the promoters of key regulatory proteins that determine cell fate. In the heart, multiple cardiac stresses result in chronic ATF3 expression. Transgenic mice with ATF3 expression in cardiomyocytes clearly demonstrate that ATF3 serves a leading role in heart hypertrophy, cardiac fibrosis, cardiac dysfunction and death. In contrast, the use of ATF3 whole body knockout mice resulted non-conclusive results. The heart is composed of various cell types such as cardiomyocytes, fibroblasts, endothelial and immune cells. The question that we addressed in this study is whether ablation of ATF3 in unique cell types in the heart results in diverse cardiac phenotypes. ATF3-flox mice were crossed with αMHC and Postn specific promoters directing CRE expression and thus ATF3 ablation in cardiomyocytes and myofibroblast cells. Mice were challenged with transverse aortic constriction (TAC) for eight weeks and heart function, ventricle weight, hypertrophic markers, fibrosis markers and ATF3 expression were assessed by qRT-PCR. The results of the study show that ATF3 deletion in cardiomyocytes followed by TAC resulted in reduced heart growth and dampened fibrosis response while ATF3 ablation in myofibroblasts displayed a reduced hypertrophic gene program. TAC-operation results in increased ATF3 expression in both myofibroblasts and cardiomyocytes that promotes a hypertrophic program and fibrotic cardiac growth, respectively.

Background: Sex-based differences in mortality have been previously observed in patients with surgically treated infective endocarditis. We sought to evaluate the risk factors leading to this difference. Methods: A retrospective cohort from three centers in Israel comprising 376 surgically treated patients, comparing short- and long-term mortality rates and risk factors between female and male patients. Results: Compared to male patients, female patients had higher rates of hypertension (62% vs. 48%), higher rates of Gram-negative infections (20% vs. 11%), and more mitral valve replacement (55% vs. 42%). Diabetes and age were the most significant predictors for mortality and did not differ between female and male patients. In-hospital mortality rates did not differ between female and male patients (29% vs. 26%), and the difference in long-term mortality was not statistically significant (46% vs. 36% p = 0.088). Conclusions: No statistical difference was observed in short- and long-term mortality between female and male patients, most likely due to a lack of difference in the rates of important risk factors such as diabetes and age. Mortality rates decreased in the last 10 years, and a good prognosis is observed for patients surviving the initial 30 days after surgery.

Background: High-sensitivity Troponin I (hs-cTnI) has largely replaced conventional troponin assays in an effort to improve detection of myocardial infarction. However, the mean displacement of hs-cTnI following coronary artery bypass graft (CABG) and the optimal threshold to detect perioperative myocardial infarction (MI) is unclear. Our objective is to describe mean hs-cTnI values at 6–12 h post-CABG and to determine the highest specificity while maintaining 100% sensitivity hs-cTnI cut-off values for diagnosis of perioperative or type-5 MI. Methods: Between 2016 and 2018, 374 patients underwent non-emergent, isolated CABG. Pre-operative and 6 h post-operative hs-cTnI values were recorded as well as ECG, echocardiographic and angiographic data. Results: Of 374 patients, 151 (40.3%) had normal and 224 (59.7%) had elevated preoperative hs-cTnI. Patients with normal preoperative hs-cTnI had a mean 6 h hs-cTnI of 9193 ng/l or 270X the upper normal value. Eleven patients (7.3%) presented with post-operative MI with a mean 6 h hs-cTnI of 50,218 ng/l or 1477X the upper normal value. Patients with elevated preoperative hs-cTnI had a mean 6 h hs-cTnI of 9449 ng/l or 292X the upper normal value. Eleven patients (4.9%) who presented with post-operative MI had a mean 6 h hs-cTnI of 26,823 ng/l or 789X the upper normal value. Conclusions: We suggest hs-cTnI threshold of 80-fold in patients with normal pre-operative hs-cTnI and 2.7-fold in patients with elevated pre-operative hs-cTnI. These results have important implications for perioperative care and for surgical trial reporting.

Objectives: Current guidelines advise stopping clopidogrel at least 5 days prior to coronary artery bypass grafting (CABG) in patients with acute coronary syndrome to lower bleeding risk. However, this delay may increase the risk of cardiovascular events. This study evaluated the impact of clopidogrel discontinuation timing on bleeding and postoperative outcomes. Methods: This retrospective single‐center study analyzed data from 472 patients treated with clopidogrel who underwent CABG. Patients were grouped based on the duration between clopidogrel cessation and surgery: 1–2 days ( n = 42), 3–4 days ( n = 89), and ≥ 5 days ( n = 341). Outcomes included bleeding complications and transfusion requirements. Results: No significant difference was found in clinically substantial bleeding (defined as chest tube drainage > 800 mL within 12 h postsurgery) among the groups ( p = 0.45). However, earlier surgery was associated with greater transfusion requirements. Patients operated on within 1–2 days had 2.52 times higher odds of requiring blood product transfusion (95% CI: 1.32–4.83), and those at 3–4 days had 1.69 times higher odds (95% CI: 1.05–2.71), compared to those with ≥ 5 days. Conclusions: In this single‐center cohort, a waiting period of at least 5 days between clopidogrel cessation and CABG was associated with lower transfusion requirements, without a clear increase in early clinically substantial bleeding, thereby supporting current guideline recommendations for stable patients.