by Bill Snyder
A study by researchers at Vanderbilt University Medical Center has strengthened the link between thyroid function and atrial fibrillation (AF), an irregular heart rhythm that increases the risk of stroke and other heart-related complications.
The phenome-wide association study scanned the medical records of more than 37,000 people for a link between genetically determined variation in thyroid stimulating hormone levels (a measure of thyroid function) and AF risk.
Previous observational studies have found that subclinical hyperthyroidism, an overactive thyroid which does not meet the clinical threshold for diagnosis or treatment, nevertheless can increase the risk of AF. But whether to treat subclinical hypo- or hyperthyroidism to reduce AF risk remains a matter of debate in the medical community.
The current study, published last week in the journal JAMA Cardiology, found that genetically determined variations in thyroid function, even among individuals whose levels fall within a physiologically accepted “normal” range, still can increase the risk for AF.
The decision to treat subclinical thyroid disease thus should account for this new evidence, as “antithyroid medications to treat hyperthyroidism may reduce AF risk (while) thyroid hormone replacement for hypothyroidism (low thyroid function) may increase AF risk,” the researchers concluded.
The paper’s senior author, Jonathan Mosley, MD, PhD, is assistant professor of Medicine and Biomedical Informatics at Vanderbilt University School of Medicine. First author and adjunct professor of Medicine Joe-Elie Salem, MD, PhD, is on the faculty of a Sorbonne University teaching hospital in Paris, France.
Other Vanderbilt faculty members who contributed to the study were Lea Davis, PhD, Joshua Denny, MD, MS, Todd Edwards, PhD, Bjorn Knollmann, MD, PhD, Dan Roden, MD, Benjamin Shoemaker, MD, MSCI, Digna Velez Edwards, PhD, Thomas Wang, MD, and Quinn Wells, MD, PharmD, MSCI.
