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Background: To compare surgical outcomes after mitral valve replacement via either minimally invasive thoracoscopic (MIs) or traditional median sternotomy (MS) surgery and determine the short-and mid-term clinical outcomes of the MI approach.Methods: All patients who received either MIs (n=405) or MS (n=691) mitral valve replacement surgery at the Guangdong Cardiovascular Institute between January 2012 and July 2015 were analyzed for outcome differences due to surgical approach using propensity score matching. The best 202 matches from the MI group and the MS group were analyzed. The clinical data of the two groups were collected, including preoperative cardiac function, operative data, postoperative complications, and follow-up.Results: A final total of 404 patients were included in this study after propensity score matching; the MIs group and the MS group each contained 202 patients. The two groups were similar in age, weight, pathological changes, and surgical approach. Compared with the MS group, the MIs group had a longer cardiopulmonary bypass time (P<0.001), aortic cross-clamping time (P<0.001), and total procedure time (P<0.001). There were no significant differences between the groups regarding in-hospital mortality, stroke, pneumonia, acute renal failure, arrhythmia, and chylothorax. The MS group had significantly more patients with poor wound healing than the MIs group (P=0.004). The MI group had a lower rate of transfusion (P=0.037), shorter ventilation time (P=0.041), shorter ICU stay (P=0.033), reduced chest tube drainage and length of chest tube stay (P<0.001), and shorter hospital stay (P<0.001). There was no significant difference between the groups in hospital re-admission for bleeding, but the total hospitalization cost was higher in the MIs group (P=0.002). The mean follow-up was 26.59±12.33 months, the 1-year postoperative survival rate was 98.86%, and the overall survival rate was 97.44%. Compared with the MS group, the MIs group recovered earlier (P<0.05), and returned to work or study earlier (P<0.05). More patients in the MIs group were satisfied with the wound (P<0.001). The MS group had a higher incidence of postoperative osteomyelitis than the MIs group (P=0.028). There were no significant differences between groups in rates of mortality, stroke, pacemaker, reoperation, or 36-item Short Form Health Survey score.Conclusions: Compared with the MS approach, the MIs method of mitral valve replacement has longer cardiopulmonary bypass time and aortic cross-clamp time; however, it does not increase the risk of mortality Liu et al. MVR via MICS versus traditional approach

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BackgroundWe previously demonstrated that endothelial microparticles (EMPs) are increased in mitral valve diseases and impair valvular endothelial cell function. Perioperative systemic inflammation is an important risk factor and complication of cardiac surgery. In this study, we investigate whether EMPs increase in congenital heart diseases to promote inflammation and endothelial dysfunction.MethodsThe level of plasma EMPs in 20 patients with atrial septal defect (ASD), 23 patients with ventricular septal defect (VSD), and 30 healthy subjects were analyzed by flow cytometry. EMPs generated from human umbilical vascular endothelial cells (HUVECs) were injected into C57BL6 mice, or cultured with HUVECs without or with siRNAs targeting P38 MAPK. The expression and/or phosphorylation of endothelial nitric oxide synthase (eNOS), P38 MAPK, and caveolin-1 in mouse heart and/or in cultured HUVECs were determined. We evaluated generation of nitric oxide (NO) in mouse hearts, and levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cultured HUVECs and in mice.ResultsEMPs were significantly elevated in patients with ASD and VSD, especially in those with pulmonary hypertension when compared with controls. EMPs increased caveolin-1 expression and P38 MAPK phosphorylation and decreased eNOS phosphorylation and NO production in mouse hearts. EMPs stimulated P38 MAPK expression, TNF-α and IL-6 production, which were all inhibited by siRNAs targeting P38 MAPK in cultured HUVECs.ConclusionsEMPs were increased in adult patients with congenital heart diseases and may contribute to increased inflammation leading to endothelial dysfunction via P38 MAPK-dependent pathways. This novel data provides a potential therapeutic target to address important complications of surgery of congenial heart disease.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1087-2) contains supplementary material, which is available to authorized users.