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心血管疾病主要死因是致命性心律失常,对它的治疗仍是一个问题。当前Ⅰ类及Ⅲ类药均不推荐用于控制室性心律失常,由于药效差及增加死亡率,对病变心脏有毒性。梗死心脏中非梗死区(NIZ)中形成易损基质(VS),如去甲肾上腺素耗竭,SOD活性降低,心肌肥大,APD延长及QT离散度增加等。慢性给左甲状腺素可形成心肌肥大及加重缺血/再灌注性心律失常,此模型有VS的特点。离子通道的病变类型在先天性LQTS与后天性心脏病中有明显的不同。先天性LQTS是单一离子通道的改变。我们发现在HERG中一个新突变-提前终止密码,使QT延长。而后天性心脏病的心肌肥大是多离子通道病变而非特殊性。后天性心脏病中离子通道病变是继发于VS病变对脂质膜的影响。VS及多离子通道的病变可作为药物治疗病变心脏心律失常的新靶点。
The main cause of cardiovascular disease is fatal arrhythmias, the treatment of which is still a problem. The current class I and class III drugs are not recommended for the control of ventricular arrhythmias, due to poor efficacy and increased mortality, the lesion heart toxicity. Vulnerable stroma (VS) is formed in non-infarcted zone (NIZ) of infarcted heart, such as norepinephrine depletion, decreased SOD activity, cardiac hypertrophy, prolonged APD and increased QT dispersion. Chronic left levothyroxine can form myocardial hypertrophy and aggravate ischemia / reperfusion arrhythmias, this model has the characteristics of VS. The pathological types of ion channels are significantly different between congenital LQTS and acquired heart disease. Congenital LQTS is a single ion channel change. We found a new mutation in HERG - ending the code early and prolonging the QT. Myocardial hypertrophy of acquired heart disease is a multi-ion channel lesion rather than a particular one. Ion channel lesions in acquired heart disease are secondary to VS lesions on the lipid membrane. VS and multi-ion channel lesions can be used as a new target for the treatment of disease-induced cardiac arrhythmia.