Blood clots are believed to occur in the coronary arteries because of platelets that become sticky when they come in contact with the damaged lining of blood vessels, where atheroma formation has commenced. Platelets interact with the damaged surfaces, and chemicals that are produced at the site cause the platelets to clump (platelet aggregation) and form a clot. Chemicals in the body that cause platelets to clump or sludge include collagen from the damaged vessel wall, adrenaline, and a very powerful platelet-clumping chemical called thromboxane A2.
Platelets are small particles present in the blood and circulate as elliptical flat disks. They are the body’s first defense against excessive bleeding. At the site of bleeding, platelets accumulate and stick together to form a clump to plug the seepage of blood. When the platelets clump together, other clotting factors contribute to the final conversion of a blood protein, fibrinogen, which turns into a mesh of fibrin strands that traps red cells and additional platelets, thus forming a firm clot.
Platelets are most sticky when they are newly released from the bone marrow. This may occur 4–10 days after any type of surgery; for example, there is a higher incidence of clots in veins of the legs after surgical operations. The lack of movement of the legs causes a slowing of the circulation in veins and increases the chances of a clot in the deep veins of the legs.

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