[Quantitative study of myocardial mitochondrial DNA4977 deletion in rheumatic heart disease and its significance].

To better understand the mechaenisms of cardiac function damaged by chronic hypoxemia in rheumatic heart disease, we investigated the level of the 4977 base pair mitochondrial DNA (mtDNA4977) deletion in 16 patients with rheumatic heart disease (RHD) by using polymerase chain reaction (PCR). Myocardial malondialdehyde (SOD) activity was also measured. In control group, mtDNA4977 deletion appeared after 45 years old and reached a maximum of 0.0042%. A higher level of mtDNA4977 deletion (0.02%-1.26%) was found in RHD group. Because mtDNA4977 deletion removes 8 genes coding for subunits of complexes of respiratory chain, its deletion can inhibit oxidative phosphorylation, reduce ATP production and hinder the recovery of cardiac function. In addition, myocardial MDA content increased and SOD activity decreased in the RHD group as compared with the control group. This indicates that the generation of oxygen free radicals enhances and the elimination of free radicals reduces. Oxygen free radical can be an important factor in myocardial mitochondrial DNA injury and lead to mitochondrial DNA deletion.