Impairment of myocardial mitochondria in viral myocardial disease and its reflective window in peripheral cells.

Abstract

BACKGROUND: Viral myocardial disease (VMD) is a common disease inducing heart failure. It has not been clear the roles of mitochondrial damage in the pathological changes of cardiomyocytes in VMD. METHODS: Myocardial tissues and lymphocytes were collected from 83 VMD patients. Control groups included 12 cases of healthy accidental death with myocardial autopsy and 23 healthy blood donors. The mouse model of viral myocarditis (VMC) was established by Coxsackie virus B3 infection and myocardial tissues and skeletal muscle were collected. Mitochondrial DNA (mtDNA) deletion rate was quantitatively determined using polymerase chain reaction. RESULTS: There was significantly difference of myocardial mitochondrial DNA deletion rate between VMD or VMC group and control group (P<0.05). Moreover, the loss of mitochondrial membrane phospholipids was significantly different between VMD or VMC group and control group. In VMC mice, there were negative correlations between myocardial mtDNA3867 deletion rate and left ventricular peak systolic pressure (LVPSP) (r = -0.66, P<0.05), and between myocardial mtDNA3867 deletion rate and +dp/dtmax (r = -0.79, P<0.05), while there was positive correlation between myocardial mtDNA3867 deletion rate and -dp/dtmax (r = 0.80, P<0.05). CONCLUSION: Mitochondrial damage is an important pathophysiological mechanism leading to myocardial injury and cardiac dysfunction. The mitochondrial damage in the skeletal muscle and lymphocytes reflect a "window" of myocardial mitochondrial damage.