Biomedical subjects
Publications and source records attributed to V Tilsner.
Urokinase is a potent fibrinolytic agent. Its good tolerance and the close correlation to the dosage render the treatment well governable and reduce the possible side effects. However, the comparatively high costs have to be taken into account. Up to now, urokinase is an indispensable tool for long-term lysis.
Fibrinolytic therapy of pulmonary emboli is indicated in persistent pulmonary hypertension or acute shock. If possible, diagnosis should be confirmed by pulmonary angiography - in our hands digital subtraction angiography has proved of value. Emboli of such size that spontaneous lysis is unlikely can be actively removed by lysis therapy so as to minimize late damage. Small or insignificant emboli do not require such therapy. As lysis therapy does not reduce early mortality it follows that mortality is not a suitable parameter for evaluating the results of treatment. Rapid clinical improvement and fall in pulmonary arterial pressure and oxygen tension some 24 to 48 hours later should not lead to erroneous conclusion that the thrombus mass has been lysed. Pulmonary angiography demonstrates that lysis takes 48 hours to 13 days. Large thrombi require a mean duration of treatment of 6 days. Only complete elimination of the vascular occlusion leads to permanent improvement. Obviously, the duration of therapy in cases of demonstrable phlebothrombosis will also depend upon the results of phlebography. In the case of contraindications lytic therapy should only be initiated where the risk from the emboli is greater than the possible haemorrhagic risk from the contraindication. Under such circumstances urokinase therapy with 40,000 to maximal 60,000 units/hour is preferable.
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To achieve reperfusion early, an intravenous bolus of 2 million units of urokinase was administered in 50 patients with transmural acute myocardial infarction (AMI) 1.8 +/- 2.5 hours after the onset of symptoms. Coronary angiography performed 1.1 +/- 0.6 hours after urokinase therapy revealed patent coronary arteries in 30 patients (60%), with no significant difference between those with anterior and those with inferior AMI. Reocclusion occurred in only 1 of 24 patients restudied. Failure to achieve reperfusion was not related to the degree of systemic fibrinolytic activity, which was equally high in patients who did and those who did not achieve reperfusion, as evident from serially obtained fibrinogen measurements (77 +/- 52 vs 84 +/- 24 mg/dl, difference not significant). Plasmin activity, measured serially from 15 minutes to 24 hours after urokinase in 7 patients, was maximal at 15 minutes and undetectable after 3 hours. Wall motion at the infarct site measured from contrast ventriculograms was significantly better at follow-up only in patients in whom reperfusion was achieved and who received urokinase within 2 hours after the onset of symptoms as compared with patients in whom reperfusion was not achieved (-1.2 +/- 1.4 vs -2.4 +/- 0.9 standard deviations from normal, p less than 0.05). Peak serum creatine kinase level was significantly lower in patients in whom reperfusion was achieved than in those in whom it was not or those who had rethrombosis (802 +/- 763 vs 1,973 +/- 1,071 U/liter, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
In 16 patients with recent myocardial infarction (3 to 12 week old) and with large left ventricular thrombi systemic thrombolysis with urokinase was performed. Left ventricular thrombi were diagnosed by two-dimensional echocardiography; in all patients the mural thrombus was located in the area of recent myocardial infarction. Each of three patients suffered an embolic episode before the initiation of thrombolytic therapy and the episode caused a stroke in one. Urokinase was infused intravenously at a rate of 60,000 U/hr for 2 to 8 days in combination with intravenous heparin (200 units/kg X 12 hr). Left ventricular thrombi were successfully lysed in 10 of 16 patients, as determined by two-dimensional echocardiography. In four of the six remaining patients only partial thrombolysis was achieved and in two thrombolytic treatment failed. There was no evidence of embolic events during thrombolysis in any of the 16 patients. The success of thrombolysis seemed to depend on the age of the thrombus: the thrombus was dissolved in eight of nine patients undergoing thrombolysis within 4 weeks of the acute myocardial infarction vs in two of seven patients receiving treatment later (p = .057). The presence of a left ventricular aneurysm or depressed left ventricular function also appeared to reduce the likelihood of successful thrombolysis. All patients were discharged on oral anticoagulants. At 6 months follow-up (n = 9) no recurrence of left ventricular thrombus was found. These results show that left ventricular thrombi can be safely lysed by intravenous urokinase. However, for better definition of the risk and benefit of this new therapy further investigation is necessary.
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Clinical Experience with the Urokinase Therapy Although all the biochemical details of fibrinolytic therapy are not yet clear, this type of treatment has found its place. Due to its lower risk of haemorrhage and non-existent allergenic properties urokinase is usually preferred and in certain cases must be used exclusively, although it is still the more expensive. It is to be hoped, that the promising experiments for cheaper production of urokinase by bacteria, will bring financial relief.
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Bleeding through the pores of thoracic vascular grafts sealed with bioadhesive has been eliminated without inducing additional defects in the coagulation system. This has been true regardless of whether additional valve replacement or aorto-coronary bypass procedures were performed. The operative risk and the need for blood transfusions has been lowered significantly thus reducing the cost of these procedures. Bioadhesive has been also applied successfully in a variety of perioperative bleeding complications.
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