Thrombolytic therapy of massive pulmonary embolism during prolonged cardiac arrest using recombinant tissue-type plasminogen activator

1989 ◽  
Vol 18 (6) ◽  
pp. 678-680 ◽  
Author(s):  
Robert W Langdon ◽  
William R Swicegood ◽  
David A Schwartz
2008 ◽  
Vol 14 (2) ◽  
pp. 238-240
Author(s):  
Thomas W. Stief

A life-threatening thrombus in massive pulmonary embolism has to be eliminated within minutes. Extremely activated plasmatic fibrinolysis destroys such thrombi in time: 50 µL plasma clots were incubated with urokinase or tissue-type plasminogen activator and 50 µL pooled normal plasma. The microtiter plate clot lysis assay was performed. The time point at which 50% of the clot has been lysed is 4 minutes for 8333 IU/mL urokinase or an equimolar concentration of tissue-type plasminogen activator (52498 IU/mL = 105 µg/mL). The effective dose 50% at 5 minutes lysis time is about 800 nM (4320 IU/mL) urokinase or (27220 IU/mL = 54 µg/mL) tissue-type plasminogen activator. Addition of plasminogen to the plasmatic clot supernatant improves thrombolysis if 65 IU/mL of urokinase acts for 10 minutes. The risk for severe intracranial hemorrhage in massive thrombolysis might be much lower than the lethality of a massive pulmonary embolism. Extremely activated plasmatic thrombolysis could be clinically indicated.


1987 ◽  
Author(s):  
M Verstraete

Recombinant tissue-type plasminogen activator (rt-PA) was given to 34 patients with acute massive pulmonary embolism of less than five days and with an angiographic Miller index greater than 15. The regimen was 50 mg rt-PA over 2 hours followed by repeat angiography, and, if the Miller index was judged still to be above 15, by an additional dose of 50 mg over 5 hours. Heparin was given in a bolus of 5000 IU followed by 1000 IU per hour. The rt-PA preparation (Boehringer Ingelheim GmbH, G 11021) contained mainly two-chain rt-PA. The infusion route was at random in a peripheral vein (IV) or in the pulmonary artery (PA). Pulmonary angiographs were assessed blindly by a panel of five radiologists according to the protocol developed by Miller (Br Med J 1971). 19 patients were given rt-PA via the pulmonary artery, 15 patients received rt-PA intravenously. Eleven patients were postoperative (PA 9, mean 13± ]] SD days, IV 4, 7±3 daysSixteen patients (66%) received two infusions (PA 14; IV 8). The Miller index decreased from 25 ± 3 to 22 ± 6 (−12%) in the PA group and from 26 ± 2 to 22 ± 5 (−15%) in the IV group after the first infusion. In the patients who received a second infusion, the Miller index decreased to 16 ± 6 (−38%) after 100 mg in the PA group and to 16±;6 (−38%) in the IV group. The mean pulmonary artery pressure decreased from 30 ± 7 to 22 ± 6 (−27%) and further to 14 ± 5 (−53%) in the PA group and from 29 ± 7 to 22 ± 9 (−24%) after 50 mg and to 13 ± 5 (−55%) after 100 mg in the IV group. All these differences are significant (p < 0.01)Fibrinogen levels dropped 46% from baseline after 50 mg and 66% from baseline after 100 mg. Bleeding occurred in 16 patients, 5 of whom had recent surgery (mean 8 days, range 2-13)This pilot trial indicates that a prolonged infusion of rt-PA over 7 hours (100 mg) is superior to a single infusion over 2 hours (50 mg) and that infusion in the pulmonary artery does not offer a significant clinical benefit over the intravenous route. In case of life-threatening massive pulmonary embolism, treatment with rt-PA could be envisaged as early as from the third day after major surgery


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