Short-term hypoxia (5 h) decreases Cx43 protein and conduction velocity, thereby contributing to the generation of an arrhythmogenic substrate.

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Background Port‐access (PORT) and robotic (ROBO) mitral repair are well established, but differences in patient selection and outcomes are not well documented. Methods A retrospective analysis was performed on 129 ROBO and 628 PORT mitral repairs at one institution. ROBO patients had 4 cm nonrib spreading incisions with robotic assistance, while PORT patients had 6–8 cm rib spreading incisions with thoracoscopic assistance. Propensity score analysis matched patients for differences in baseline characteristics. Results Unmatched ROBO patients were younger (58 ± 11 vs. 61 ± 13, p = .05), had a higher percentage of males (77% vs. 63%, p = .003) and had less NYHA Class 3–4 symptoms (11% vs. 21%, p < .01), less atrial fibrillation (19% vs. 29%, p = .02) and less tricuspid regurgitation (14% vs. 24%, p = .01). Propensity score analysis of matched patients showed that pump time (275 ± 57 vs. 207 ± 55, p < .0001) and clamp time (152 ± 38 vs. 130 ± 34, p < .0001) were longer for ROBO patients. However, length of stay, postoperative morbidity, and 5‐year survival (97 ± 1% vs. 96 ± 3%, p = .7) were not different. For matched patients with degenerative valve disease, 5‐year incidence of mitral reoperation (3 ± 2% vs. 1 ± 1%), severe mitral regurgitation (MR) (6 ± 4% vs. 1 ± 1%), or ≥2 + MR (12 ± 5% vs. 12 ± 4%), were not significantly different between ROBO versus PORT approaches. Predictors of recurrent moderate MR were connective tissue disease, functional etiology, and non‐White race, but not surgical approach. Conclusions In this first comparison out to 5 years, robotic versus port‐access approach to mitral repair had longer pump and clamp times. Perioperative morbidity, 5‐year survival, and 5‐year repair durability were otherwise similar.

BACKGROUND AND PURPOSE Because myocardial infarction is a major cause of morbidity and mortality worldwide, protecting the heart from the ischaemia and reperfusion (I/R) damage is the focus of intense research. Based on our in vitro findings showing that TVP1022 (the S‐enantiomer of rasagiline, an anti‐Parkinsonian drug) possesses cardioprotective effects, in the present study we investigated the hypothesis that TVP1022 can attenuate myocardial damage in an I/R model in rats. EXPERIMENTAL APPROACH The model consisted of 30‐min occlusion of the left anterior descending artery followed by 4 or 24 h reperfusion. In addition, we investigated the possible mechanisms of cardioprotection in H9c2 cells and neonatal rat ventricular myocytes (NRVM) exposed to oxidative stress induced by H2O2. KEY RESULTS TVP1022 (20 and 40 mg·kg−1) administered 5 min before reperfusion followed by an additional dose 4 h after reperfusion reduced the infarct size and attenuated the decline in ventricular function. TVP1022 also attenuated I/R‐induced deterioration in cardiac mitochondrial integrity evaluated by mitochondrial swelling capacity. In vitro, using H9c2 cells and NRVM, TVP1022 attenuated both serum free‐ and H2O2‐induced damage, preserved mitochondrial membrane potential and Bcl‐2 levels, inhibited mitochondrial cytochrome c release and the increase in cleaved caspase 9 and 3 levels, and enhanced the phosphorylation of protein kinase C and glycogen synthase kinase‐3β. CONCLUSIONS AND IMPLICATIONS TVP1022 provided cardioprotection in a model of myocardial infarction, and therefore should be considered as a novel adjunctive therapy for attenuating myocardial damage resulting from I/R injuries.