MG是一种自身免疫性疾病,主要损害骨骼肌,造成神经肌肉接头处递质传递障碍,表现为受累骨骼肌易疲劳,劳累后加重,休息或服用抗胆碱酯酶药减轻,随着临床与神经免疫研究的进展,近来研究提示重症肌无力为一种全身性免疫性疾病,除骨骼肌受累外,还可累及运动神经系统、植物神经系统、胃肠道平滑肌、心肌等。尤其合并的心肌损害临床易造成心源性猝死。病因和发病机制:MG造成的心肌损害,原因有以下方面:①自身免疫机制造成的心肌损害,国外早在1962年Beutner等用免疫荧光技术首先发现MG患者血清中存在一种可与心肌细胞发生特异结合的抗体;1990年Connor等用PHA法监测到此种抗体在MG患者血液中阳性率为53％,并发现抗心肌抗体滴度的高低及其结合心肌抗原的多少对心功能产生直接影响。国内刘氏、陈氏等于1999年报道,对56例MG MG is an autoimmune disease that mainly damages skeletal muscle and causes neurotransmitter neurotransmission at the neuromuscular junction. It manifests as fatigue of affected skeletal muscle, aggravating after fatigue, rest or taking anticholinesterase drugs, Recent progress in neuroimmunity research suggests that myasthenia gravis is a systemic autoimmune disease. In addition to skeletal muscle involvement, it may also involve the motor nervous system, autonomic nervous system, gastrointestinal smooth muscle, and myocardium. In particular, combined myocardial damage easily lead to sudden cardiac death. Etiology and pathogenesis: Myocardial damage caused by MG, the following aspects: ① autoimmune mechanism of myocardial damage, as early as 1962 Beutner and other immunofluorescence technology first found in serum of MG patients there is a cardiomyocyte can occur Specific binding antibody; Connor et al in 1990 by PHA method to detect this antibody was 53% positive in patients with MG blood, and found that the level of anti-myocardium antibody titers and the level of myocardial antigen binding has a direct impact on cardiac function . Domestic Liu, Chen equal reported in 1999, 56 cases of MG