线粒体脱氧核糖核酸缺失与病毒性心肌疾病患者心功能损伤的关系

The Deletion of Mitochondrial DNA in Patients with Viral Myocardial Disease and Its Relation to Heart Function

目的：探讨不同心功能状态病毒性心肌疾病患者外周淋巴细胞线粒体脱氧核糖核酸（ｍｔＤＮＡ）缺失率，为进一步 明确ｍｔＤＮＡ损伤在病毒性心肌疾病发病中的作用提供分子依据。 方法：将８３例病毒性心肌疾病患者分为病毒性心肌炎组（ＶＭＣ组，ｎ＝５０）和扩张型心肌病组（ＤＣＭ组，ｎ＝３３）， ２３例健康献血者为对照组。用定量多聚酶链反应（ＰＣＲ）法检测患者外周淋巴细胞ｍｔＤＮＡ９７７碱基对（ｍｔＤＮＡ４９７７）和 ｍｔＤＮＡ７４３６碱基对（ｍｔＤＮＡ７４３６）缺失率，并分析ｍｔＤＮＡ缺失程度与心脏扩大及心功能状态的关系。 结果：ＶＭＣ组和ＤＣＭ组外周淋巴细胞ｍｔＤＮＡ缺失率显著高于对照组（Ｐ＜０．００１）；ｍｔＤＮＡ缺失率的高低与心 功能损害呈一致性改变，ＮＹＨＡ心功能 Ｉ级与Ⅳ级者 ｍｔＤＮＡ缺失率分别比对照组高 １２．４倍和 １１０．３倍；ｍｔＤＮＡ缺 失率与心功能分级、心胸比率及心腔内径呈正相关，与左心室射血分数（ＬＶＥＦ）呈负相关；ｍｔＤＮＡ４９７７和ｍｔＤＮＡ７４３６缺 失率与 ＬＶＥＦ的相关系数分别为－０．６８１和－０．６７５（Ｐ均＜０．０５）。 结论：ｍｔＤＮＡ缺失突变与病毒性心肌疾病患者心功能的损伤密切相关，可能在该病?

Objective: To investigate mitochondrial DNA (mtDNA)deletion rates of peripheral lymphocytes in patients with viral my-ocardial disease, and its relation to heart function. Methods: mtDNA 4977 base pair (mtDNA4977)and mtDNA 7436 base pair (mtDNA7436)deletion rates of peripheral lym- phocytes were measured by the method of quantitative polymerase chain reaction (PCR)in 83 patients with viral myocardial dis- ease (50 with viral myocarditis and 33 with dilated cardiomyopathy)and 23 control cases. Results: mtDNA4977and mtDNA7436deletions were observed in both controls (0.031 % )and patients with viral myocardial disease (0.490% in viral myocarditis and 2.682% in dilated cardiomyopathy), (p < 0.001). The degree of mtDNA deletion rates showed well accordance with the severity of heart function, which was 0.415% in patients with NYHA class I and ele- vated to3.451% in patients with NYHA class IV.mtDNA deletion rate correlated positively with NYHA classification, cardio- thoratic ratio and left atrial or left ventricular diameter, and correlated negatively with left ventricular ejection fraction (LVEF). The correlation coefficient (r value)of mtDNA4977and mtDNA7436 deletion rates with LVEF is - 0.681 and - 0.675, respectively (p<0.05). Conclusion: The degree of mtDNA deletion in patients with viral myocardial disease is closely related to the impairment of heart function, which might play an important role in the pathogenesis of viral myocardial disease.