Predicting outcomes in patients with low ejection fraction undergoing coronary artery bypass graft.

Introduction: Reduced left ventricular ejection fraction (LVEF) is a well-known predictor of adverse events after cardiac surgery. We aimed to assess the outcomes in patients with low LVEF undergoing coronary artery bypass graft. Methods: In this retrospective cohort, we included all patients with left ventricular ejection fraction ≤ 40 who underwent coronary artery bypass grafting between March 2007 and March 2016 (with a median follow-up of nine years) at Tehran Heart Center. Demographics and clinical characteristics were extracted from the data registry. Akaike information criterion (AIC) was used. The univariate Cox regression was performed. We investigated the predictors of mortality and major adverse cardiac and cerebrovascular events (MACCE) using Cox multivariable regression. Results: In total, 5,532 cases (79 % male) with a mean age of 65.58 were included in the study. The nine-year overall survival was calculated at 68 %, and more than half of the patients had MACCE (55 %). In adjusted multivariable Cox regression analysis, moderate to severe mitral valve regurgitation, glomerular filtration rate ≤ 60, mild right ventricular dysfunction, and valvular heart disease independently predicted higher mortality. The abovementioned predictors and peripheral vascular disease significantly increased MACCE. Conclusion: Our study indicates the clinical significance of mitral regurgitation, valvular heart disease, and renal function in patients with low ejection fraction treated by coronary artery bypass grafting surgery. Identifying predictors of adverse events can help with clinical decision-making and risk stratification, ultimately improving patient outcomes.

Bariatric surgery mitigated electrocardiographic abnormalities in patients with morbid obesity.

Obesity can lead to cardiovascular dysfunctions and cause electrocardiographic disruptions. Bariatric surgery plays a significant role in weight loss. To assess its benefits, this study investigated electrocardiographic changes before and after bariatric surgery. The present article describes a retrospective cohort study with a 6-month follow-up period. Electrocardiograms were interpreted and compared before and six months after surgery. The relationships between weight loss, type of surgery, and electrocardiographic alterations were analyzed. A total of 200 patients participated in the study, with 34 (17%) men and 166 (83%) women. The mean age of the participants was 44.6 ± 8.6, and their mean body mass index was 43.8 ± 5.5 kg/m2. The mean of QTc decreased after the surgery, while the Sokolow-Lyon scores increased. The statistical analysis showed that QTc dispersion (> 40) (P < 0.001), right ventricular hypertrophy (P < 0.001), abnormal R wave progression (P < 0.001), QTc (P < 0.001) and Sokolow-Lyon criteria (P < 0.001) significantly changed postoperatively. In conclusion, bariatric surgery can reduce QTc, correct poor R wave progression, and resolve right ventricular hypertrophy (RVH) in patients with morbid obesity.

Understanding the Role of Galectin-1 in Heart Failure: A Comprehensive Narrative Review.

Heart failure (HF) is the fastest-growing cardiovascular condition worldwide. The immune system may play a role in the development of HF since this condition is associated with elevated pro-inflammatory cytokine levels. HF is a life-threatening disease, and there is an increasing demand for diagnostic biomarkers, prognostic factors, and therapeutic agents that can help treat it. Galectin-1 (Gal-1) is the prototype galectin of the lectin family. Multiple signal transduction pathways are regulated by Ras proteins, which act as a molecular switch in cells. Gal-1 regulates T and B cell activation, differentiation, and survival. Gal-1 has been linked to inflammation. Activated T cells produce Gal-1 through an autocrine apoptotic mechanism involving MEK1/ERK and p38 MAPK. In the cardiovascular system, atherosclerosis is facilitated by Gal-1. Heart disease, myocardial infarction, hypertension, and stroke can be caused by atherosclerotic plaque. HF and heart hypertrophy are caused by decreased cardiac L-type Ca2+ channel activity. Deregulation of Gal-1 and CaV1.2 in pathological cardiac hypertrophy suggests a possible target for anti-hypertrophic therapy. Rat hypertrophic cardiomyocytes express Gal-1 and CaV1.2 channels simultaneously. It has been reported that diastolic dysfunction (DD) is associated with elevated Gal-1 levels. The high Gal-1 level in subjects led to the lowest cumulative survival as a composite endpoint. Incidences of HF, DD, and serum Gal-1 levels correlated significantly. The ejection fraction was negatively correlated with Gal-1 and CRP concentrations. Based on two different approaches in mice and humans, Gal-1 was identified as a potential mediator of HF.