Research suggests a genetic link between depression and inflammation-mediated heart disease, and shows that combination therapy may prevent degeneration of the heart muscle. Credit: SciTechDaily.com

Research has revealed that treating depression and heart disease together may reduce the risk of heart muscle disease.

Coronary artery disease and major depression may be genetically linked to an increased risk of cardiomyopathy, a degenerative heart muscle disease, through inflammatory pathways, researchers at Vanderbilt University Medical Center and Massachusetts General Hospital have found. discovered.

Their report recently published in a magazine natural mental healthsuggests that a combination of drugs prescribed for coronary artery disease and depression may reduce inflammation and prevent the development of cardiomyopathy.

“This study suggests that chronic low-level inflammation may be a significant cause of both depression and depression. cardiovascular disease” said Lee Davis, Ph.D., corresponding author of the paper and associate professor of medicine in the Department of Medical Genetics and the Vanderbilt Genetics Institute.

Corresponding author, Dr. Lee Davis, Associate Professor of Medicine, Department of Medical Genetics and Vanderbilt Genetics Institute.Credit: Vanderbilt University Medical Center

Inflammation as a common factor

The relationship between depression and other serious health conditions is well known. As many as 44% of patients with coronary artery disease (CAD), the most common form of cardiovascular disease, are diagnosed with major depression. However, the biological relationship between these two conditions remains poorly understood.

Inflammation may be involved. Changes in the levels of inflammatory markers have been observed in both conditions, suggesting that there may be a common biological pathway linking neuroinflammation in depression and atherosclerotic inflammation in CAD.

Research results and implications

In the current study, the researchers used a technique called transcriptome-wide association scanning to map single nucleotide polymorphisms (genetic variations) involved in regulating the expression of genes associated with both CAD and depression. .

This technique identified 185 genes that were significantly associated with both depression and CAD and were “enriched” with biological roles in inflammation and cardiomyopathy. This suggests that predisposition to both depression and CAD, which researchers term (major) depressive CAD, or (m)dCAD, may make individuals more susceptible to cardiomyopathy. are doing.

But when researchers scanned VUMC, a large electronic medical records database at Massachusetts General Hospital, National Institutes of HealthThe All of Us Research Program found that the actual incidence of cardiomyopathy in patients enriched for the (m)dCAD gene was lower than in patients with CAD alone.

One possible explanation is that drugs prescribed for CAD and depression, such as statins and antidepressants, may prevent the development of cardiomyopathy by reducing inflammation, researchers say. concluded.

Future direction of treatment

“Further research is needed to investigate the optimal treatment mechanism, but this study at least suggests that patients’ heart and brain health should be considered together when developing treatment plans for depression and cardiovascular disease.” ,” Dr. Davis added.

Reference: “Genes associated with depression and coronary artery disease are enriched for cardiomyopathy and inflammatory phenotypes” Kritika Singh, Hyunjoon Lee, Julia M. Sealock, Tyne Miller-Fleming, Peter Straub, Nancy J Cox, Quinn S. Wells, Jordan W. Smoller, Emily C. Hodges, Lee K. Davis, April 5, 2024. natural mental health.
DOI: 10.1038/s44220-024-00219-z

The paper’s first author, Dr. Kritika Singh, is a former graduate student in the Davis lab and currently a postdoctoral innovation fellow at Novartis in Cambridge, Massachusetts.

Other VUMC co-authors are Tyne Miller-Fleming, Ph.D., Peter Straub, M.S., Nancy Cox, Ph.D., founding director of the Vanderbilt Genetics Institute, and institute member Quinn Wells, MD, Pharm.D., associate professor of medicine in the MSCI Division. Dr. Emily Hodges, PhD in Cardiovascular Medicine, Assistant Professor of Biochemistry.

This research was supported by National Institutes of Health grants R56MH120736, R01H118233, 1F31MH124306, and 1R01HL140074, and an American Heart Association Fellowship.