Quantification of mitochondrial sublimons in human fibrillating atria

Supraventricular tachycardias, including AF (atrial fibrillation), and mtDNA (mitochondrial DNA) deletions may lead to dilated cardiomyopathy. It is unknown whether mtDNA function is impaired in the human atrium in AF. In the present study, we investigated the role of rearranged mtDNA 'sublimons' in the pathogenesis of AF. Right atrial biopsies were collected from 38 patients in AF and 35 patients with SR (sinus rhythm) undergoing elective cardiac surgery. Total DNA was extracted by standard methods. The break-point regions of the two most prevalent classes of sublimon were amplified by PCR using fluorescent oligonucleotides for the 3.75 kb partial duplication and the 2.83 kb deletion. Multiplex reactions included additional primers to amplify an internal genomic standard for semi-quantitative analysis. Reaction products were quantified as peak areas in the electrophoretogram and ratios computed of the sublimon abundance relative to the genomic standard. There was no difference in SCN (sublimon copy number) between AF and SR patients [19.09+/-28.29 compared with 10.25+/-24.68, the difference was 0.28 (95% confidence interval, -0.04 and +0.61; P =0.08)]. SCN did not increase with age ( P =0.207) and was unrelated to AF duration ( P =0.661), left atrial diameter ( P =0.560), post-operative AF ( P =0.52), underlying disease ( P =0.94), medication and gender (2.84+/-0.72 in females vs 2.97+/-0.67 in males; P =0.431). In conclusion, our findings do not indicate any role of mtDNA in the pathophysiology of AF.