Search

Objective: To summarize the experience with surgical treatment of coronary artery disease with severe ischemic mitral valve regurgitation (IMR)., Methods: From January 2006 to December 2009, 45 patients (35 males, 10 females aged 32-74 years) with the diagnosis of coronary artery disease complicated by IMR underwent coronary artery bypass grafting (CABG) combined with mitral valve plasty (MVP, 24 cases) or mitral valve replacement (MVR, 21 cases)., Results: Perioperative deaths occurred in 2 cases due to multiple organ failure (MOF). Echocardiography showed a significant reduction of the mitral regurgitation area (from 11.80∓2.45 cm(2) to 2.83∓0.98 cm(2), t=22.80, P=0.00) after CABG combined with mitral valve surgery, with also significantly reduced postoperative left ventricular end diastolic diameter (LVEDD) (from 57.61∓10.06 mm to 51.84∓8.98 mm, t=2.85, P=0.005). No significant difference was detected in the left ventricular ejection fraction after the operation [(52.7∓15.4)% vs (53.2∓13.2)%, t=0.16, P=0.87)]., Conclusions: CABG combined with mitral valve surgery can improve early postoperative left ventricular function in patients with ischemic coronary heart disease complicated by severe mitral regurgitation, but further follow-up study is still needed for evaluation of the long-term results.

Objectives: The etiology of myocardial ischemia/reperfusion (I/R) injury is multifactorial, but activation of the innate immune system and the resulting inflammatory response are important components of I/R injury. The aim of this study was to investigate the protective effect of a hemoglobin-based oxygen carrier (HBOC) on cold I/R heart and to explore the underlying mechanisms. Methods: Isolated Sprague-Dawley rat hearts were perfused in the Langendorff mode. After 30 min of basal perfusion, rat hearts were arrested with histidine-tryptophan-ketoglutarate solution (HTKs) with or without an HBOC and hypothermically stored (4°C) for 9 or 14 h, followed by 2 h of reperfusion. Results: Compared with HTKs alone, the HBOC in HTKs greatly improved heart contraction and decreased infarct size, necrosis and apoptosis, which was related to the reduced expression of Toll-like receptor 2 (TLR 2), TLR 4, TNF-α, IL-1β and nuclear factor-κB (NF-κB) activation. Conclusions: Our results demonstrated that the HBOC protected isolated rat heart from cold I/R injury and this protection was associated with attenuation of the expression of the TLR 2 and TLR 4/NF-κB signaling pathway, which may down-regulate the inflammatory response. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aims: Myocardial ischemia is the most common form of cardiovascular disease and the leading cause of morbidity and mortality. Understanding the mechanisms is very crucial for the development of effective therapy. Therefore, this study aimed to investigate the functional roles and mechanisms by which ELAVL1 regulates myocardial ischemia and reperfusion (I/R) injury. Methods: Mouse myocardial I/R model and cultured myocardial cells exposed to hypoxia/reperfusion (H/R) were used in this study. Features of ferroptosis were evidenced by LDH activity, GPx4 activity, cellular iron, ROS, LPO, and GSH levels. The expression levels of autophagy markers (Beclin-1, p62, LC3), ELAVL1 and FOXC1 were measured by qRT-PCR, immunostaining and western blot. RIP assay, biotin-pull down, ChIP and dual luciferase activity assay were employed to examine the interactions of ELAVL1/Beclin-1 mRNA and FOXC1/ELAVL1 promoter. CCK-8 assay was used to examine viability of cells. TTC staining was performed to assess the myocardial I/R injury. Results: Myocardial I/R surgery induced ferroptosis and up-regulated ELAVL1 level. Knockdown of ELAVL1 decreased ferroptosis and ameliorated I/R injury. Si-ELAVL1 repressed autophagy and inhibition of autophagy by inhibitor suppressed ferroptosis and I/R injury in myocardial cells. Increase of autophagy could reverse the effects of ELAVL1 knockdown on ferroptosis and I/R injury. ELAVL1 directly bound with and stabilized Beclin-1 mRNA. Furthermore, FOXC1 bound to ELAVL1 promoter region and activated its transcription upon H/R exposure. Conclusion: FOXC1 transcriptionally activated ELAVL1 may promote ferroptosis during myocardial I/R by modulating autophagy, leading to myocardial injury. Inhibition of ELAVL1-mediated autophagic ferroptosis would be a new viewpoint in the treatment of myocardial I/R injury. [ABSTRACT FROM AUTHOR]