摘要
肥胖病是心脏病的危险因素,传统观点认为,在肥胖患者中,由于血流动力学异常和脂代谢异常导致的心脏重构是患者易发展为冠状动脉性疾病和心力衰竭的原因。但最近研究发现,脂肪在心脏沉积可以直接损伤心脏,影响左室重建,导致扩张型心肌病。对肥胖动物模型的研究发现,心肌中脂质过度沉积可导致左室肥厚和缺血性、扩张型心肌病。通过基因治疗或药物干预降低心脏的脂质沉积,可以预防肥胖相关性心脏病的发生。临床研究也提示,心肌的脂质含量可以作为肥胖患者心脏病的生物指标,并且可以成为治疗的靶点。但这方面的研究才刚刚开始,有待进一步的研究。
Obesity is a major risk factor of heart disease. Conventional wisdom suggests that either hemodynamic or metabolic derangements associated with obesity may predispose individuals to coronary artery disease and heart failure. Excessive lipid accumulation within the myocardium is directly cardiotoxic and causes left ventricular remodelling and dilated cardiomyopathy. Studies in animal models of obesity reveal that intracellular accumulation of triglyceride renders organs dysfunctional, which leads to several well-recognized clinical syndromes related to obesity. In these rodent models, excessive lipid accumulation in the myocardium causes left ventricular hypertrophy and non-ischemic, dilated cardiomyopathy. Recent studies in healthy individuals and patients with heart failure reveal that myocardial lipid content increases with the degree of adiposity and may contribute to the adverse structural and functional cardiac adaptations seen in obese persons. These studies provide evidence that myocardial lipid content may be a biomarker and putative therapeutic target for cardiac disease in obese patients.
出处
《心血管病学进展》
CAS
2007年第1期142-145,共4页
Advances in Cardiovascular Diseases
