Taller people might be at an increased risk for atrial fibrillation, according to research set for presentation at the American Heart Association’s Scientific Sessions on Nov. 16.
Lead author Michael Levin, MD, and colleagues at the University of Pennsylvania School of Medicine were able to establish height as a causal—not just correlated—risk factor for AFib, which affects upwards of 33 million people worldwide. Observational studies have linked taller height to an increased risk of AFib before, but those population-level analyses failed to confirm a causal relationship between the two variables.
“Our findings suggest it may be beneficial to incorporate height into risk-prediction tools for AFib,” Levin, a cardiovascular medicine fellow at Penn, said in a release. “While current guidelines advise against widespread screening for AFib, our findings show that a certain group of patients—specifically very tall patients—may benefit from screening.”
Levin and his team leveraged data from the Genetic Investigation of Anthropometric Trials (GIANT) and Atrial Fibrillation Genetics (AFGen) consortiums for their study, considering the combined information of more than 1,200,000 individuals enrolled in the registries. They used a statistical method to estimate the link between genetic variants of height and genetic variants of AFib, ultimately finding that genetic variants associated with height were also strongly associated with AFib.
The relationship between height and arrhythmia remained strong even after adjusting for risk factors like heart disease, high blood pressure and diabetes. Levin et al. replicated their results in an additional individual-level analysis of nearly 7,000 patients in the Penn Medicine Biobank, finding that height correlated strongly with an increased risk of AFib independent of traditional clinical and echocardiographic risk factors.
The researchers said that every one-inch increase in a person’s height over five-foot-seven translated to a 3% increase in their risk of AFib.
“These analyses show how we can use human genetics to help us better understand causal risk factors for common disease,” Scott Damrauer, MD, the study’s senior author, said in the release. “They also illustrate how we can combine summary-level statistics from large published studies with individual-level data from institutional biobanks to further our understanding of human disease.”
Levin will present his team’s findings Saturday, Nov. 16 at 4:30 p.m. in Philadelphia. The AHA’s annual Scientific Sessions last through Nov. 18.