Spontaneous fibrinolysis in pulmonary embolism

James E. Wilson; Eugene P. Frenkel; Alan K. Pierce; Robert L. Johnson; Edward R. Winga; George C. Curry; Donald S. Mierzwiak

doi:10.1172/JCI106515

Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235

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Published in Volume 50, Issue 3 on March 1, 1971
J Clin Invest. 1971;50(3):474–480. https://doi.org/10.1172/JCI106515.
© 1971 The American Society for Clinical Investigation

Published March 1, 1971 - Version history

This study correlated levels of activated fibrinolysis with the presence, extent, and rate of resolution of angiographically documented pulmonary emboli. Pulmonary emboli demonstrable by angiography were associated with detectable fibrin split products in the serum of 24 of 25 patients. In the absence of increased fibrin split products, pulmonary emboli large enough to be demonstrated by angiography were found in only 2 of 25 positive pulmonary angiograms. Spontaneous resolution of pulmonary emboli could not be correlated with the the concentration or persistence of fibrin split products but did correlate well with the presence of a reversible precipitating cause.

Thrombophlebitis in the absence of clinical evidence of pulmonary embolism was not associated with increased concentrations of fibrin split products in eight of nine patients. The one patient with increased fibrin split product concentration had evidence on lung scan of silent pulmonary embolism.