Mitochondrial DNA Copy Count Associated With VTE Risk

According to authors of a recent study, venous thromboembolism (VTE) is the third most common cardiovascular disease. While VTE can occur in all age groups, risk significantly increases with age. The researchers cited studies that suggested roles of mitochondrial dysfunction and telomere shortening in cardiovascular aging and set out to evaluate whether these biomarkers were related to risk of VTE.

In their findings, published in Thrombosis Research, the study’s lead author, Rafaela  Vostatek, reported that patients with VTE had lower human mitochondrial DNA copy numbers (mtDNA) compared with healthy controls in their population.

Mitochondrial Dysfunction Associated With Increased VTE Risk

The study included 116 patients with a history of VTE and 128 age- and sex-matched controls. Patients with VTE had at least one recorded unprovoked VTE event and were enrolled within 3 months of the latest VTE event. Researchers assessed mtDNA and telomere length in isolated blood samples using a quantitative PCR-based assay kit.

Reportedly, patients with VTE had a median mtDNA copy number of 663 per diploid cells (interquartile range [IQR], 78.75-2204.5) compared with 2823 per diploid cells (IQR, 724-4350) in healthy control patients (P<.001). Of note, mtDNA copy numbers differed significantly between men and women at 893 (IQR, 152-3154) and 2375 (IQR, 455-3737), respectively (P<.001).

The researchers further noted that mtDNA copy number showed an independent association with risk of VTE after adjusting for confounders including age, sex, body mass index, and smoking (odds ratio for each 400 mtDNA increase per diploid cells, 0.889; 95% CI, 0.834-0.946). Comparatively, telomere length did not significantly differ between the two groups and was not associated with risk of VTE.

Ultimately, the authors summarized “mtDNA copy numbers were significantly lower in VTE patients than in healthy controls, suggesting an association of biological aging with risk of VTE.”

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