Analyzing mitochondrial DNA copy numbers (mtDNA-CN) in patients at risk for cardiovascular disease could help clinicians predict sudden cardiac death and heart failure in patients up to a decade before anything happens, a study published in JAMA: Cardiology reports.
These findings pave the way for improved outcomes in cardiac patients, the study stated, since blood testing for mitochondrial DNA measurements could lead to early detection of cardiovascular disease (CVD) and, therefore, allow at-risk patients to take preventative measures against developing heart problems in the future.
Mitochondrial DNA-CN is a statistic derived from the number of mitochondria per cell and the number of mitochondrial genomes per mitochondria, Dan E. Arking, PhD, and colleagues wrote in their recent findings. Because mitochondrial dysfunction relates directly to the aging process and has been suggested as playing a role in atherosclerotic cardiovascular disease, Arking and his team pulled data from more than 20,000 patients and monitored their mitochondrial DNA-CN over an average of 13 and a half years.
Of the 21,870 participants who were drawn from the databases of the Cardiovascular Health Study, Atherosclerosis Risk in Communities Study and Multiethnic Study of Atherosclerosis, 92 percent were CVD-free at baseline. Arking and colleagues measured mitochondrial DNA levels against nuclear DNA levels in these patients, and input that number into the American College of Cardiology/American Heart Association Heart Risk Calculator.
The researchers were adding a new value to the risk calculator, which is widely used to predict cardiac risk and uses a patient’s cholesterol levels, blood pressure, smoking history, family medical history, weight and more to predict a 10-year risk for heart attacks and other adverse cardiac events.
Arking said in a news release from Johns Hopkins Medicine that mitochondrial DNA could be a more accurate predictor of future heart disease than other variables.
“Essentially two out of every three people who experience sudden cardiac death show no symptoms that could have warned their physician of their risk,” he said. “That is why our group fervently looked for genetic markers to identify those people at higher risk.”
Arking’s team correctly predicted by the end of the study that six patients who otherwise wouldn’t have been recommended for heart treatment went on to have a life-threatening heart event, and 139 patients who would have been recommended for statin treatment under current guidelines actually didn’t suffer from CVD. The researchers found that the lower mitochondrial DNA-CN numbers were, the more at-risk a patient was for suffering an adverse CVD event.
Still, though this information showed a significant improvement in risk classification and specificity for heart disease, Arking said the research is new and needs further development.
“It’s a promising biomarker, but we need to learn how it is actually functioning to determine if it is causal,” he said.