Pathophysiology of coronary thrombosis

Abstract

Detailed knowledge of the pathophysiology as well as the dynamic nature of coronary thrombus formation provides a valuable tool for correct management and proper adjunctive therapy in patients with acute coronary syndromes. Coronary thrombosis is in the majority of cases caused by disruption or fissuring of an atherosclerotic plaque. At the lesion thrombogenic material will be exposed to the flowing blood leading to activation of platelets and the formation of a platelet clot. Simultaneously, the coagulation system is activated resulting in increased thrombin formation. Thrombin is a key mediator in arterial thrombosis, due to its effect on both platelets and fibrin generation. Thrombin contributes to the stabilization of an initially loose platelet clot by generating cross-bound fibrin within the thrombus. During the course of an acute coronary syndrome, the patient presents changing chest pain and dynamic ischaemic ECG findings. This is likely to be related to the dynamic nature of the pathophysiology. The presence of a non-occlusive coronary thrombus may deprive the myocardium its normal blood flow and oxygen supply, leading to ischaemic pain. During lysis or embolization, blood supply may be restored, but the presence of thrombus fragments in the microcirculation holds the potential to sustained interference with myocardial metabolism. The emboli contain activated platelets which release vasoconstrictors that may compromise the microcirculation. Recurrent thrombus formation at the lesion site may result in occlusion of the artery adding to the dynamic nature of the clinical presentation. In conclusion, platelets, the coagulation system, and the endothelium cause a dynamic process of intermittent occlusion, vasospasm and embolization of thrombus material.