Submitted on January 6, 2004
Accepted on March 23, 2004
Embolization Itself Stimulates Thrombus Propagation in Pulmonary Embolism
Timothy A. Morris1*, James J. Marsh1, Peter G. Chiles1, Craig A. Pedersen1, Ronald G. Konopka1, Anthony C. Gamst2, and Oralia Loza2
1 Department of Medicine, Division of Pulmonary/Critical Care Medicine, University of California, San Diego, San Diego, California, USA
2 Department of Family and Preventative Medicine, Division of Biostatistics, University of California, San Diego, San Diego, California, USA
* To whom correspondence should be addressed. E-mail: t1morris{at}ucsd.edu.
The role of active thrombosis in the pathophysiology of pulmonary embolism is unclear. We tested the hypothesis that venous thrombi significantly increase their thrombotic
activity once they embolize into the high-flow circulation of the pulmonary arteries. Thrombotic activity was measured using an immunoassay that measures both fibrinopeptide B (FPB) as well as its most abundant metabolite, des-arginine FPB. Thrombi were formed in the femoral veins of adult dogs. In one group, the thrombi were embolized without anticoagulation. In the second group, heparin (300 units/kg bolus, then 90 units/kg/hour infusion) was administered prior to embolization to prevent subsequent thrombotic activity. Plasma FPB concentrations were significantly
suppressed in the heparinized group relative to the non-heparinized group for one hour post-embolization (p = 0.038). We conclude that pulmonary embolization itself causes pre-existing venous thrombi to greatly intensify their thrombotic activity, and that embolization-associated thrombus propagation can be prevented by heparin.
