Comparison of original EuroSCORE, EuroSCORE II and STS risk models in a Turkish cardiac surgical cohort

OBJECTIVESThe aim of this study was to compare additive and logistic European System for Cardiac Operative Risk Evaluation (EuroSCORE), EuroSCORE II and the Society of Thoracic Surgeons (STS) models in calculating mortality risk in a Turkish cardiac surgical population.METHODSThe current patient population consisted of 428 patients who underwent isolated coronary artery bypass grafting (CABG) between 2004 and 2012, extracted from the TurkoSCORE database. Observed and predicted mortalities were compared for the additive/logistic EuroSCORE, EuroSCORE II and STS risk calculator. The area under the receiver operating characteristics curve (AUC) values were calculated for these models to compare predictive power.RESULTSThe mean patient age was 74.5 ± 3.9 years at the time of surgery, and 35.0% were female. For the entire cohort, actual hospital mortality was 7.9% (n = 34; 95% confidence interval [CI] 5.4-10.5). However, the additive EuroSCORE-predicted mortality was 6.4% (P = 0.23 vs observed; 95% CI 6.2-6.6), logistic EuroSCORE-predicted mortality was 7.9% (P = 0.98 vs observed; 95% CI 7.3-8.6), EuroSCORE II- predicted mortality was 1.7% (P = 0.00 vs observed; 95% CI 1.6-1.8) and STS predicted mortality was 5.8% (P = 0.10 vs observed; 95% CI 5.4-6.2). The mean predictive performance of the analysed models for the entire cohort was fair, with 0.7 (95% CI 0.60-0.79). AUC values for additive EuroSCORE, logistic EuroSCORE, EuroSCORE II and STS risk calculator were 0.70 (95% CI 0.60-0.79), 0.70 (95% CI 0.59-0.80), 0.72 (95% CI 0.62-0.81) and 0.62 (95% CI 0.51-0.73), respectively.CONCLUSIONSEuroSCORE II significantly underestimated mortality risk for Turkish cardiac patients, whereas additive and logistic EuroSCORE and STS risk calculators were well calibrated. © 2013 The Author 2013

Primary Left Cardiac Angiosarcoma with Mitral Valve Involvement Accompanying Coronary Artery Disease

We report here on a 43-year-old female patient presenting with non-ST elevation myocardial infarction, severe mitral regurgitation, and mild mitral stenosis secondary to encroachment of the related structures by a primary cardiac angiosarcoma. A coronary angiography revealed significant stenosis in the left main and left circumflex arteries and at exploration, the tumour was arising from posterior left atrial free wall, invading the posterior mitral leaflet, and extending into all of the pulmonary veins and pericardium. Therefore, no further intervention was performed, except for left internal mammarian artery to left anterior descending artery anastomosis and biopsy. As far as we know, this case is unique with respect to its presentation

Effects of off-pump and on-pump coronary-artery bypass grafting at 1 year

BACKGROUND: Previously, we reported that there was no significant difference at 30 days in the rate of a primary composite outcome of death, myocardial infarction, stroke, or new renal failure requiring dialysis between patients who underwent coronary-artery bypass grafting (CABG) performed with a beating-heart technique (off-pump) and those who underwent CABG performed with cardiopulmonary bypass (on-pump). We now report results on quality of life and cognitive function and on clinical outcomes at 1 year. METHODS: We enrolled 4752 patients with coronary artery disease who were scheduled to undergo CABG and randomly assigned them to undergo the procedure off-pump or on-pump. Patients were enrolled at 79 centers in 19 countries. We assessed quality of life and cognitive function at discharge, at 30 days, and at 1 year and clinical outcomes at 1 year. RESULTS: At 1 year, there was no significant difference in the rate of the primary composite outcome between off-pump and on-pump CABG (12.1% and 13.3%, respectively; hazard ratio with off-pump CABG, 0.91; 95% confidence interval [CI], 0.77 to 1.07; P=0.24). The rate of the primary outcome was also similar in the two groups in the period between 31 days and 1 year (hazard ratio, 0.79; 95% CI, 0.55 to 1.13; P=0.19). The rate of repeat coronary revascularization at 1 year was 1.4% in the off-pump group and 0.8% in the on-pump group (hazard ratio, 1.66; 95% CI, 0.95 to 2.89; P=0.07). There were no significant differences between the two groups at 1 year in measures of quality of life or neurocognitive function. CONCLUSIONS: At 1 year after CABG, there was no significant difference between off-pump and on-pump CABG with respect to the primary composite outcome, the rate of repeat coronary revascularization, quality of life, or neurocognitive function. (Funded by the Canadian Institutes of Health Research; CORONARY ClinicalTrials.gov number, NCT00463294.)

Activation of histone deacetylase-6 induces contractile dysfunction through derailment of α-tubulin proteostasis in experimental and human atrial fibrillation

BACKGROUND: Atrial fibrillation (AF) is characterized by structural remodeling, contractile dysfunction, and AF progression. Histone deacetylases (HDACs) influence acetylation of both histones and cytosolic proteins, thereby mediating epigenetic regulation and influencing cell proteostasis. Because the exact function of HDACs in AF is unknown, we investigated their role in experimental and clinical AF models. METHODS AND RESULTS: Tachypacing of HL-1 atrial cardiomyocytes and Drosophila pupae hearts significantly impaired contractile function (amplitude of Ca(2+) transients and heart wall contractions). This dysfunction was prevented by inhibition of HDAC6 (tubacin) and sirtuins (nicotinamide). Tachypacing induced specific activation of HDAC6, resulting in α-tubulin deacetylation, depolymerization, and degradation by calpain. Tachypacing-induced contractile dysfunction was completely rescued by dominant-negative HDAC6 mutants with loss of deacetylase activity in the second catalytic domain, which bears α-tubulin deacetylase activity. Furthermore, in vivo treatment with the HDAC6 inhibitor tubastatin A protected atrial tachypaced dogs from electric remodeling (action potential duration shortening, L-type Ca(2+) current reduction, AF promotion) and cellular Ca(2+)-handling/contractile dysfunction (loss of Ca(2+) transient amplitude, sarcomere contractility). Finally, atrial tissue from patients with AF also showed a significant increase in HDAC6 activity and reduction in the expression of both acetylated and total α-tubulin. CONCLUSIONS: AF induces remodeling and loss of contractile function, at least in part through HDAC6 activation and subsequent derailment of α-tubulin proteostasis and disruption of the cardiomyocyte microtubule structure. In vivo inhibition of HDAC6 protects against AF-related atrial remodeling, disclosing the potential of HDAC6 as a therapeutic target in clinical AF