Thrombosis is the formation of a blood clot (thrombus) within a blood vessel or a cavity of the heart, reducing or blocking blood flow. Under normal circumstances, clotting is a protective mechanism that stops bleeding when a vessel is damaged. Thrombosis occurs when this process is triggered inappropriately or excessively within an intact vessel.
Three factors (known as Virchow’s triad) predispose to thrombosis: abnormal blood flow (such as turbulence or sluggish circulation), changes to the vessel wall (such as inflammation or atherosclerotic plaque), and changes in the composition of blood that make it more prone to clotting (hypercoagulability).
Thrombosis plays a central role in several life-threatening cardiac events. Coronary thrombosis occurs when an atherosclerotic plaque in a coronary artery ruptures and a clot forms rapidly at the site, potentially blocking the artery completely and causing a heart attack and cardiac arrest. Left ventricular thrombus forms in the left ventricle after a large heart attack where stagnant blood pools in the weakened area, carrying a risk of embolism to the brain or other organs. Deep vein thrombosis (DVT) and pulmonary embolism involve clots forming in leg veins that travel to the lungs, a significant risk in immobilised critical care patients.
Prevention and treatment of thrombosis uses anticoagulant therapy (for most clot types) or antiplatelet therapy (specifically for arterial thrombosis related to coronary artery disease). In acute coronary thrombosis, PCI is used to physically remove or compress the clot and restore blood flow urgently.
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