Center for Cardiology/Cardiology 1, Laboratory of Molecular Cardiology of the Johannes Gutenberg University, Mainz, Germany.
Department of Heart, Thoracic and Vascular Surgery of the Johannes Gutenberg University, Mainz, Germany.
Oxid Med Cell Longev. 2018 Dec 17;2018:6598326. doi: 10.1155/2018/6598326. eCollection 2018.
Obesity is one of the major cardiovascular risk factors and is associated with oxidative stress and myocardial dysfunction. We hypothesized that obesity affects cardiac function and morbidity by causing alterations in enzymatic redox patterns.
Sixty-one patients undergoing coronary artery bypass grafting (CABG) were included in the study. Excessive right atrial myocardial tissue emerging from the operative connection to the extracorporeal circulation was harvested. Patients were assigned to control ( = 19, body mass index (BMI): <25 kg/m), overweight ( = 25, 25 kg/m < BMI < 30 kg/m), or obese ( = 17, BMI: >30 kg/m) groups. Oxidative enzyme systems were studied directly in the cardiac muscles of patients undergoing CABG who were grouped according to BMI. Molecular biological methods and high-performance liquid chromatography were used to detect the expression and activity of oxidative enzymes and the formation of reactive oxygen species (ROS).
We found increased levels of ROS and increased expression of ROS-producing enzymes (i.e., p47phox, xanthine oxidase) and decreased antioxidant defense mechanisms (mitochondrial aldehyde dehydrogenase, heme oxygenase-1, and eNOS) in line with elevated inflammatory markers (vascular cell adhesion molecule-1) in the right atrial myocardial tissue and by trend also in serum (sVCAM-1 and CCL5/RANTES).
Increasing BMI in patients undergoing CABG is related to altered myocardial redox patterns, which indicates increased oxidative stress with inadequate antioxidant compensation. These changes suggest that the myocardium of obese patients suffering from coronary artery disease is more susceptible to cardiomyopathy and possible damage by ischemia and reperfusion, for example, during cardiac surgery.
肥胖是主要的心血管危险因素之一，与氧化应激和心肌功能障碍有关。我们假设肥胖通过改变酶的氧化还原模式影响心脏功能和发病率。
本研究纳入了 61 例行冠状动脉旁路移植术（CABG）的患者。从与体外循环的手术连接处采集过多的右心房心肌组织。根据体重指数（BMI）将患者分为对照组（ = 19，BMI：<25kg/m）、超重组（ = 25，25kg/m < BMI < 30kg/m）或肥胖组（ = 17，BMI：>30kg/m）。根据 BMI 将接受 CABG 的患者分组，直接研究心脏肌肉中的氧化酶系统。采用分子生物学方法和高效液相色谱法检测氧化酶的表达和活性以及活性氧（ROS）的形成。
我们发现，随着右心房心肌组织中 ROS 产生酶（即 p47phox、黄嘌呤氧化酶）的表达增加和抗氧化防御机制（线粒体乙醛脱氢酶、血红素加氧酶-1、eNOS）的减少，ROS 水平升高，并且炎症标志物（血管细胞黏附分子-1）升高，同时血清中也存在升高趋势（sVCAM-1 和 CCL5/RANTES）。
接受 CABG 的患者 BMI 的增加与心肌氧化还原模式的改变有关，这表明氧化应激增加而抗氧化补偿不足。这些变化表明，患有冠心病的肥胖患者的心肌更容易受到心肌病和缺血再灌注损伤的影响，例如在心脏手术期间。
