A Sinkovic1. 1. Department of Internal Intensive Medicine, Teaching Hospital Maribor, Slovenia.
Abstract
BACKGROUND: The antifibrinolytic effect of plasminogen-activator-inhibitor type 1 (PAI-1) may be responsible for delays in reperfusion and/or reinfarctions after streptokinase (STK) therapy in patients with acute myocardial infarction (AMI). HYPOTHESIS: This study aimed to demonstrate the prognostic role of pretreatment PAI-1 levels for the outcome of STK therapy in patients with AMI, depending on reperfusion and/ or reinfarction. METHODS: The mean pretreatment PAI-1 level of 104 patients with AMI, treated with STK, determined by chromogenic method, was 5.8 +/- 8.6 U/ml, range 0.3-66.2 U/ml. Streptokinase therapy was successful when reperfusion was achieved, as assessed noninvasively, without subsequent reinfarction; it failed when reperfusion was delayed and/or reinfarction developed. RESULTS: Fibrinolysis with STK failed significantly in patients with elevated pretreatment PAI-1 levels (p < 0.05), especially with levels >4.0 U/ml (p< 0.01). The mean pretreatment PAI-1 level was significantly higher in unsuccessfully treated patients. Multivariate statistical testing demonstrated that among pretreatment variables, elevated PAI-1 activity was the most significant independent risk factor of failed fibrinolysis with STK. CONCLUSIONS: Among pretreatment variables, elevated pretreatment PAI-1 activity in patients with AMI was the most significant independent risk factor of failed fibrinolysis with STK, especially at levels > 4.0 U/ml.
BACKGROUND: The antifibrinolytic effect of plasminogen-activator-inhibitor type 1 (PAI-1) may be responsible for delays in reperfusion and/or reinfarctions after streptokinase (STK) therapy in patients with acute myocardial infarction (AMI). HYPOTHESIS: This study aimed to demonstrate the prognostic role of pretreatment PAI-1 levels for the outcome of STK therapy in patients with AMI, depending on reperfusion and/ or reinfarction. METHODS: The mean pretreatment PAI-1 level of 104 patients with AMI, treated with STK, determined by chromogenic method, was 5.8 +/- 8.6 U/ml, range 0.3-66.2 U/ml. Streptokinase therapy was successful when reperfusion was achieved, as assessed noninvasively, without subsequent reinfarction; it failed when reperfusion was delayed and/or reinfarction developed. RESULTS: Fibrinolysis with STK failed significantly in patients with elevated pretreatment PAI-1 levels (p < 0.05), especially with levels >4.0 U/ml (p< 0.01). The mean pretreatment PAI-1 level was significantly higher in unsuccessfully treated patients. Multivariate statistical testing demonstrated that among pretreatment variables, elevated PAI-1 activity was the most significant independent risk factor of failed fibrinolysis with STK. CONCLUSIONS: Among pretreatment variables, elevated pretreatment PAI-1 activity in patients with AMI was the most significant independent risk factor of failed fibrinolysis with STK, especially at levels > 4.0 U/ml.
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