The hemodynamic status of patients with pulmonary embolism was essentially unaltered 24 hours after initiation of heparin therapy. However, 24 hours after initiation of urokinase therapy a significant lowering of right ventricular systolic and diastolic pressures, as well as of pulmonary arterial and right atrial mean pressures, was observed. Total pulmonary resistance also fell significantly after urokinase. These changes indicate that the resolution of pulmonary embolic obstruction was accelerated by urokinase therapy.
Massiveness of embolism appeared to be a determinant of the efficacy of urokinase therapy, inasmuch as the hemodynamic treatment effect was more pronounced in patients with massive embolism than in those with submassive embolism.
Patients also appeared to have a more favorable response to urokinase if their preinfusion chest roentgenogram was free of infiltrate. Previous history of cardiopulmonary disease did not appear to influence response to urokinase therapy.
Therapeutic interventions other than urokinase did not influence hemodynamic responses, nor did acute bleeding complications (which were more frequent in patients treated with urokinase).
- © 1973 American Heart Association, Inc.