Thrombosis, physical activity, and acute coronary syndromes

Abstract

Acute coronary syndromes (ACS) are common, life-threatening cardiac disorders that typically are triggered by rupture or erosion of an atherosclerotic plaque. Platelet deposition and activation of the blood coagulation cascade in response to plaque disruption lead to the formation of a platelet-fibrin thrombus, which can grow rapidly, obstruct coronary blood flow, and cause myocardial ischemia and/or infarction. Several clinical studies have examined the relationship between physical activity and ACS, and numerous preclinical and clinical studies have examined specific effects of sustained physical training and acute physical activity on atherosclerotic plaque rupture, platelet function, and formation and clearance of intravascular fibrin. This article reviews the available literature regarding the role of physical activity in determining the incidence of atherosclerotic plaque rupture and the pace and extent of thrombus formation after plaque rupture.

Fig. 1.

Atherosclerotic plaque rupture and thrombosis. A: coronary atherosclerotic plaque with thin-walled fibrous cap and thrombogenic necrotic core. B: plaque rupture. C: thrombotic response. If thrombus formation is not extensive (black thrombus), there is no obstruction to blood flow and event does not cause clinical symptoms. If thrombus formation is extensive (gray thrombus), blood flow is obstructed and acute coronary syndrome develops.

Fig. 2.

Blood coagulation cascade. The tissue factor and contact activation pathways converge at factor X, whose activation initiates the common pathway. HMWK, high-molecular-weight kininogen.

Fig. 3.

Fibrinolytic system. Actions of fibrinolysis inhibitors are indicated by dashed lines. PA, plasminogen activator; PAI-1, PA inhibitor-1.