The current study focused on 977 patients with cardiovascular disease who had either a 50 percent or higher blockage in at least one major coronary artery or a documented heart attack. Of these patients, 21 percent were female and the average age was 59 years. Symptoms of depression were measured using a standardized self-reported questionnaire recommended by the National Heart, Lung and Blood Institute (NHLBI).
Researchers targeted 59 different candidate genes because of their relevance to a biological pathway of interest or their prior association with depression in medical literature. The genes include those related to inflammation; platelet aggregation, or clumping; endothelial function involving the cells that line the inner surface of blood vessels; and omega-3 fatty acid metabolism, which can affect the hardening of the arteries.
Following genotyping and statistical analyses, the research team discovered that genetic variations involving endothelial dysfunction a hallmark for vascular diseases, such as atherosclerosis and platelet aggregation appear to contribute to depressive symptoms.
Specifically, they identified one marker within the vonWillebrand factor (vWF) gene that appears to have a significant association. vWF is a protein produced by the endothelium that is critical to the initial stages of blood clotting by helping platelets stick to damaged blood vessels. When elevated in concentration, VWF is a strong predictor of endothelial dysfunction and a risk factor for atherosclerosis.
"Although further study is needed, our findings suggest that endothelial dysfunction may be a novel mechanism contributing to depressive symptoms among heart disease patients," said McCaffery, who is also an assistant professor of psychiatry and human behavior at The Warren Alpert Medical School of Brown University.
Researchers note that the candidate gene approach used in the study is limited by the cu
|Contact: Jessica Collins Grimes|