Patients with acute coronary syndromes (ACS) with depression are at greater risk for subsequent major adverse coronary events (MACE: myocardial infarctions, revascularization procedures, strokes, and death). Depressive symptoms are associated with increased inflammatory protein levels, but only in certain individuals. Proposed is to test if inflammatory protein gene polymorphisms interact with depression resulting in even greater increases in inflammatory protein levels than those caused by either gene polymorphisms or depression alone, increasing risk of subsequent MACE.
Specific aims are to determine 1) whether depression is associated with the risk of MACE; 2) whether inflammatory protein levels during ACS differ between those with and without depression; 3) whether selected genetic polymorphisms are related to the level of inflammatory proteins; 4) whether genetic polymorphisms and depressive symptoms interact to influence the level of inflammatory proteins; and 5) and whether genetic polymorphisms and depressive symptoms interact to influence risk of MACE. Inflammatory proteins and genes include: Interleukin (IL) 6, C-reactive protein (CRP), Tumor Necrosis Factor Alpha (TNFa), E-Selectin (SELE) and Monocyte Chemoattractant Protein-1 (MCP-1). From about 1300 ACS patients, blood samples for genetic and protein work will be collected once shortly after hospital admission before cardiac intervention, and depression will be assessed once within 2-5 days post admission. Occurrence of MACE will be followed for 2 years. Data will be analyzed using logistic regression and survival analysis.
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