Exercise training enhances endogenous fibrinolysis in peripheral arterial disease.

Purpose: Acute clinical events resulting from atherosclerosis (myocardial infarction, stroke) are associated with impaired endogenous fibrinolysis, the system by which the body lyses inappropriately formed thrombus. Endurance exercise training improves fibrinolysis in normal subjects and those with coronary artery disease. The hypothesis of this study was that exercise training would improve fibrinolysis in subjects with peripheral arterial disease (PAD).

A single bout of walking exercise enhances endogenous fibrinolysis in stroke patients.

Purpose: Impaired endogenous fibrinolysis is an important predictor for increased risk of stroke and myocardial infarction. Acute exercise can enhance fibrinolysis, primarily by stimulating short-term increases in plasma tissue plasminogen activator (tPA), which is postulated to protect against atherothrombotic events. No prior studies have examined the fibrinolytic response to exercise in stroke survivors despite their high risk for recurrent stroke and myocardial infarction.

The effect of external pneumatic compression on regional fibrinolysis in a prospective randomized trial.

Introduction: External pneumatic compression devices (EPC) prevent deep venous thrombosis (DVT) by reducing lower extremity venous stasis. Early studies suggested they also enhance fibrinolytic activity; however, in a recent study, EPC had no effect on systemic fibrinolysis in patients undergoing abdominal surgery. The hypothesis of this study was that EPCs enhance regional fibrinolysis in these subjects.

External pneumatic compression does not increase urokinase plasminogen activator after abdominal surgery.

External pneumatic compression (EPC) devices prevent lower extremity deep venous thrombosis (DVT) by reducing stasis. There is a widely held belief that they also enhance endogenous fibrinolysis; however, recent studies of tissue plasminogen activator (the primary activator of fibrinolysis) and plasminogen activator inhibitor-1 (the primary inhibitor of fibrinolysis) failed to confirm this. The hypothesis of this study was that EPC devices increase the level of urokinase plasminogen activator (uPA), a second activator of fibrinolysis.