Embolization itself stimulates thrombus propagation in pulmonary embolism

1 Department of Medicine, Division of Pulmonary/Critical Care Medicine and 2 Department of Family and Preventative Medicine, Division of Biostatistics, University of California San Diego, San Diego, California 92093 Submitted 6 October 2003 ; accepted in final form 23 March 2004 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 U/kg bolus, then 90 U·kg –1 ·h –1 infusion) was administered before embolization to prevent subsequent thrombotic activity. Plasma FPB concentrations were significantly suppressed in the heparinized group relative to the nonheparinized group for 1 h postembolization ( P = 0.038). We conclude that pulmonary embolization itself causes preexisting venous thrombi to greatly intensify their thrombotic activity and that embolization-associated thrombus propagation can be prevented by heparin. thrombosis; anticoagulants; heparin Address for reprint requests and other correspondence: T. A. Morris, UCSD Medical Ctr., 200 West Arbor Dr., San Diego, CA 92103-8378 (E-mail: t1morris{at}ucsd.edu ).