Heart Failure Risk May Be Written in Your DNA, Study Says

According to a study, it is possible to accurately classify the risk level of heart failure patients by screening for both common and uncommon genetic variations.

A study published in Nature Genetics demonstrated that the risk level of patients with heart failure could be accurately classified by screening for common and uncommon genetic variations.

Researchers from the University of Pennsylvania Perelman School of Medicine and Northwestern University Feinberg School of Medicine conducted a meta-analysis of genome-wide association studies, analyzing data from over 2 million participants without heart failure and more than 207,000 patients with heart failure. 

The study team’s analysis revealed 176 new genetic variations that may increase the risk of heart failure, including coding variations in genes associated with glucose metabolism (GIPR, GLP1R) and cardiomyopathy (MYBPC3, BAG3). 

The research team also performed gene burden studies using data from three biobanks, which included over 27,000 heart failure patients and more than 349,000 individuals without heart failure. 

They reported discovering statistically significant exome-wide correlations between heart failure and rare loss-of-function variations in the FLNC, BAG3, MYBPC3, and TTN genes. 

They emphasized that identifying common and rare genetic variations is vital when assessing the risk of heart failure.

To put it another way, you can determine who is at high risk for heart failure based on their shared genetic background, even if you do not have any rare genetic variants known to cause heart failure.

The research team also stated that the common genetic background significantly modifies disease risk, even in individuals with rare genetic variants.

To better understand the basic biological processes dysregulated in heart failure, they assessed that since they have found that common genetic variants contribute to heart failure risk, they can cluster these to find common pathways between multiple diseases and discover biological pathways shared by these diseases and heart failure.