Gene type accounted for 7.3 percent of variance in Factor VII levels, while environmental factors such as blood levels of a type of fat called triglyceride or smoking accounted for another 12.3 percent. However, unlike prior studies, this study did not detect an interaction between the polymorphism and traditional risk factors such as cholesterol levels or fasting triglycerides. DaLi Feng, M.D., a research fellow in cardiology at Deaconess who presented the results, said the study provides evidence of a genetic component in blood clotting. However, this needs to be studied further. The second study, reported by Christopher O'Donnell, M.D., medical officer and cardiologist at the National, Heart, Lung and Blood Institute and the Framingham Heart Study, compared blood platelet aggregation in 848 pairs of siblings and 387 unrelated spouses.
Platelets are small disk-shaped blood cells that clump together to form blood clots.
Receptors, located on the platelet surface, act like docking sites and determine the stickiness, or aggregation ability of platelets. Some individuals may have hyperactive receptors, which can accelerate platelet aggregation, causing them to stick to each other more readily, often forming clots. Platelet hyperreactivity has been associated with increased cardiovascular risk, but until now scientists have believed environmental factors were primarily responsible. The reactivity of platelets of Framingham siblings was tested with agents that lead to platelet aggregation. It is conceivable that a substantial portion of platelet aggregation in individuals is really due to genetic differences in receptors.