Suleiman M-S, Hancock M, Shukla R, Rajakaruna C, Angelini G D
Faculty of Medicine & Dentistry, Bristol Heart Institute, University of Bristol, Bristol, UK.
Perfusion. 2011 Sep;26 Suppl 1(Suppl 1):48-56. doi: 10.1177/0267659111420607.
Cardioplegic arrest and cardiopulmonary bypass are key triggers of myocardial injury during aortic valve surgery. Cardioplegic ischaemic arrest is associated with disruption to metabolic and ionic homeostasis in cardiomyocytes. These changes predispose the heart to reperfusion injury caused by elevated intracellular reactive oxygen species and calcium. Cardiopulmonary bypass is associated with an inflammatory response that can generate systemic oxidative stress which, in turn, provokes further damage to the heart. Techniques of myocardial protection are routinely applied to all hearts, irrespective of their pathology, although different cardiomypathies respond differently to ischaemia and reperfusion injury. In particular, the efficacy of cardioprotective interventions used to protect the hypertrophic heart in patients with aortic valve disease remains controversial. This review will describe key cellular changes in hypertrophy, response to ischaemia and reperfusion and cardioplegic arrest and highlight the importance of optimising cardioprotective strategies to suit hypertrophic hearts.
心脏停搏和体外循环是主动脉瓣手术期间心肌损伤的关键触发因素。心脏停搏缺血性停搏与心肌细胞代谢和离子稳态的破坏有关。这些变化使心脏易受细胞内活性氧和钙升高引起的再灌注损伤。体外循环与炎症反应相关，炎症反应可产生全身氧化应激，进而对心脏造成进一步损害。心肌保护技术常规应用于所有心脏，无论其病理情况如何，尽管不同的心肌病对缺血和再灌注损伤的反应不同。特别是，用于保护主动脉瓣疾病患者肥厚心脏的心脏保护干预措施的疗效仍存在争议。本综述将描述肥厚、对缺血和再灌注的反应以及心脏停搏中的关键细胞变化，并强调优化心脏保护策略以适应肥厚心脏的重要性。
