A study recommends a hereditary link between depression and heart problem through inflammation, suggesting that combined medication could prevent heart muscle degeneration. Credit: SciTechDaily.comResearch reveals that treating anxiety and cardiovascular disease together could lower the threat of heart muscle disease.Coronary artery disease and major depression might be genetically connected by means of inflammatory paths to an increased risk for cardiomyopathy, a degenerative heart muscle disease, researchers at Vanderbilt University Medical Center and Massachusetts General Hospital have found.Their report, published recently in the journal Nature Mental Health, recommends that drugs recommended for coronary artery disease and anxiety, when used in combination, possibly may reduce swelling and prevent the development of cardiomyopathy.”This work suggests that chronic low-level swelling may be a significant contributor to both depression and cardiovascular disease,” stated the papers corresponding author, Lea Davis, PhD, associate teacher of Medicine in the Division of Genetic Medicine and Vanderbilt Genetics Institute.Corresponding author, Lea Davis, PhD, associate professor of Medicine in the Division of Genetic Medicine and Vanderbilt Genetics Institute. Credit: Vanderbilt University Medical CenterInflammation as a Common FactorThe connection between depression and other serious health conditions is popular. As lots of as 44% of patients with coronary artery disease (CAD), the most common type of cardiovascular illness, also have a medical diagnosis of significant depression. The biological relationship in between the two conditions remains badly understood.A possible connection is swelling. Modifications in the levels of inflammatory markers have been observed in both conditions, recommending that there might be a typical biological pathway connecting neuroinflammation in anxiety with atherosclerotic swelling in CAD.Research Findings and ImplicationsIn the present study, the researchers used a method called transcriptome-wide association scans to map single nucleotide polymorphisms (hereditary variations) associated with controling the expression of genes related to both CAD and depression.The method identified 185 genes that were significantly connected with both depression and CAD, and which were “enriched” for biological roles in swelling and cardiomyopathy. This recommends that predisposition to both depression and CAD, which the scientists called (major) depressive CAD, or (m)dCAD, may further incline people to cardiomyopathy.However, when the scientists scanned big electronic health record databases at VUMC, Mass General, and the National Institutes of Healths All of Us Research Program, they found the real occurrence of cardiomyopathy in patients with the enriched genes for (m)dCAD was lower than in clients with CAD alone.One possible explanation is that medications recommended for CAD and depression, such as statins and antidepressants, might prevent development of cardiomyopathy by lowering swelling, the researchers concluded.Future Directions in Treatment”More research is needed to examine optimum treatment mechanisms,” Davis included, “but at a minimum this work suggests that client heart and brain health ought to be thought about together when developing management plans to treat depression or cardiovascular disease.”Reference: “Genes connected with anxiety and coronary artery illness are enriched for cardiomyopathy and inflammatory phenotypes” by Kritika Singh, Hyunjoon Lee, Julia M. Sealock, Tyne Miller-Fleming, Peter Straub, Nancy J. Cox, Quinn S. Wells, Jordan W. Smoller, Emily C. Hodges and Lea K. Davis, 5 April 2024, Nature Mental Health.DOI: 10.1038/ s44220-024-00219-zKritika Singh, PhD, the papers first author, is a former college student in the Davis laboratory who is now a postdoctoral Innovation Fellow at Novartis in Cambridge, Massachusetts.Other VUMC co-authors are Tyne Miller-Fleming, PhD, Peter Straub, MS, Nancy Cox, PhD, establishing director of the Vanderbilt Genetics Institute, and institute members Quinn Wells, MD, PharmD, MSCI, associate teacher of Medicine in the Division of the Cardiovascular Medicine, and Emily Hodges, PhD, assistant professor of Biochemistry.The research study was supported by National Institutes of Health grants R56MH120736, 1F31MH124306, r01h118233, and 1r01hl140074, and an American Heart Association Fellowship.
