[Arterial permeability, objective of thrombolytic therapy].
The effects of thrombolytic therapy in acute myocardial infarction are related exclusively to coronary arterial reperfusion. This is the main factor which influences myocardial salvage, the conservation of left ventricular function and, ultimately, the reduction in mortality. From the beginning of the 80s, the patency (or reperfusion) rate was arbitrarily assesses at 90 minutes. However, arterial reperfusion is a progressive phenomenon and the patency rate in a population of acute myocardial infarctions varies with time. Depending on the thrombolytic agent and the rate of administration, the patency increases at a variable rate attaining a plateau at the 4th-6th hour, the maximal patency being obtained between the 24th to the 48th hour. Therefore, assessing patency at the 90th minute of thrombolytic therapy is an approximate and relatively inaccurate method of assessing the efficacy of a given thrombolytic agent. When evaluating a thrombolytic drug administered at a certain dosage, the rate of reperfusion and the value and precocity of the plateau phase must be taken into account. The respective performances of different thrombolytics in terms of arterial patency are comparable. Nevertheless, the rate of reperfusion with Streptokinase given at the dose of 1.5 million i.v. in 60 minutes is lower than that obtained with more recent thrombolytic drugs. Streptokinase also appears to be less active on chronic thrombi. The late patency rate after the 24th hour is over 90% with nearly all thrombolytic drugs but it would seem to be less with rt-PA because of a higher reocclusion rate associated with this particular agent. The study of reocclusion requires control coronary angiography between the 24th and 72nd hour (7th day in some studies). The prevalence of this complication is influenced by several factors, especially the severity of residual stenosis after thrombolysis and the grade of perfusion obtained after the treatment: secondary reocclusion is significantly lower with long-acting and non-fibrin specific thrombolytic agents. It is approximately 2 to 5% with APSAC, Streptokinase and pro-urokinase, and two to three times greater with rt-PA. Finally, the use of more powerful antiplatelet drugs than those currently available and of specific anti-thrombin agents could reduce the rate of secondary reocclusion. Associations of thrombolytic agents, the development of thrombolytic chimera and new thrombolytic molecules could improve the efficacy of thrombolytic therapy in terms of capacity of reperfusion and tolerance, especially with respect to haemorrhagic complications.
Bassand
J P
JP
Service de cardiologie, CHU Saint-Jacques, Besançon.
Schiele
F
F
Bernard
Y
Y
Anguenot
T
T
D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy*; D015425:Myocardial Reperfusion / Q000379:methods*; D010960:Plasminogen Activators / Q000627:therapeutic use; D012008:Recurrence; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy; D014654:Vascular Patency / Q000187:drug effects
D013300:Streptokinase; D010960:Plasminogen Activators
La perméabilité artérielle, objectif du traitement thrombolytique.