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Rescue thrombolysis: alteplase as adjuvant treatment after streptokinase in acute myocardial infarction
J P Mounsey1, J S Skinner, T Hawkins
1Northern Regional Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne.
Insights
Further thrombolysis with alteplase improved outcomes for acute myocardial infarction patients who did not achieve reperfusion after initial streptokinase treatment. This intervention reduced infarct size and improved left ventricular function in this high-risk group.
Area of Science:
- Cardiology
- Thrombolytic Therapy
- Myocardial Infarction Management
Background:
- Acute myocardial infarction (AMI) patients failing reperfusion after thrombolysis face high morbidity and mortality.
- Management is challenging, particularly in centers lacking interventional cardiology.
- Additional thrombolysis may improve reperfusion and left ventricular function.
Purpose of the Study:
- To evaluate the efficacy of secondary thrombolysis with alteplase in AMI patients with failed reperfusion after streptokinase.
- To assess the impact on infarct size and left ventricular ejection fraction.
Main Methods:
- 37 AMI patients with failed reperfusion (ST elevation reduction <25%) after streptokinase were randomized to alteplase or placebo.
- Control group (43 patients) showed reperfusion after streptokinase.
- Outcomes assessed via electrocardiogram (Selvester Q wave score) and nuclear gated scan for left ventricular ejection fraction (LVEF).
Main Results:
- Alteplase significantly reduced electrocardiographic infarct size (14% vs 20%, P=0.03) and improved LVEF (44% vs 34%, P=0.04) compared to placebo in non-reperfused patients.
- Benefits were observed in patients with failed fibrinogenolysis (fibrinogen > 1 g/l).
- No significant differences in infarct size or LVEF were found in patients who reperfused after streptokinase.
Conclusions:
- Patients with acute myocardial infarction and failed reperfusion after streptokinase may benefit from additional thrombolysis with alteplase.
- This strategy can reduce infarct size and improve left ventricular function.
Background:
In acute myocardial infarction patients who do not reperfuse their infarct arteries shortly after thrombolytic treatment have a high morbidity and mortality. Management of this high risk group remains problematic, especially in centres without access to interventional cardiology. Additional thrombolytic treatment may result in reperfusion and improved left ventricular function.
Methods:
Failure of reperfusion was assessed non-invasively as less than 25% reduction of ST elevation in the electrocardiographic lead with maximum ST shift on a pretreatment electrocardiogram. 37 patients with acute myocardial infarction who showed electrocardiographic evidence of failed reperfusion 30 minutes after 1.5 MU streptokinase over 60 minutes were randomly allocated to receive either alteplase (tissue type plasminogen activator (rt-PA) 100 mg over three hours) (19 patients) or placebo (18 patients). 43 patients with electrocardiographic evidence of reperfusion after streptokinase acted as controls. Outcome was assessed from the Selvester Q wave score of a predischarge electrocardiogram and a nuclear gated scan for left ventricular ejection fraction 4-6 weeks after discharge.
Results:
Among patients in whom ST segment elevation was not reduced after streptokinase, alteplase treatment resulted in a significantly smaller electrocardiographic infarct size (14% (8%) v 20% (9%), P = 0.03) and improved left ventricular ejection fraction (44 (10%) v 34% (16%), P = 0.04) compared with placebo. This benefit was confined to patients who failed fibrinogenolysis after streptokinase (fibrinogen > 1 g/l). In patients in whom ST segment elevation was reduced after streptokinase, infarct size and left ventricular ejection fraction were not significantly different from those in patients treated with additional alteplase.
Conclusion:
Patients without electrocardiographic evidence of reperfusion after streptokinase may benefit from further thrombolysis with alteplase.