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. 2000 Jan;83(1):122–126. doi: 10.1136/heart.83.1.122

Acute myocardial infarction: thrombolysis

E Topol 1
PMCID: PMC1729274  PMID: 10618353

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Figure 1:  .

Figure 1:  

(A) Mortality curves in GUSTO 1 by thrombolytic strategy assignment. For streptokinase (SK) the parentheses indicate the heparin strategy, intravenous (iv) or subcutaneous (sc). (B) Patency of the infarct vessel at 90 minutes of treatment in the GUSTO 1 angiographic trial evaluating the four thrombolytic strategies.

Figure 2:  .

Figure 2:  

(A) Patency of the infarct vessel in two angiographic comparative trials. (B) Mortality at 30 days for each thrombolytic strategy.

Figure 3:  .

Figure 3:  

Prothrombotic effects of fibrinolytic treatment. Coronary thrombus is composed of a platelet core with fibrin-thrombin admixture ("white" and "red" clot). After fibrinolytic treatment, there is exposure of free thrombin, which autocatalytically begets more thrombin and strongly promotes platelet aggregation (note more platelet mass). Platelets themselves are resistant to fibrinolytic treatment and furthermore secrete large amounts of plasminogen activator inhibitor (PAI-1), which is a potent antagonist to fibrinolysis. Reproduced from Topol EJ. Circulation 1998;97:211-18, with permission.

Figure 4:  .

Figure 4:  

Angiographic patency (TIMI 3) of the infarct vessel in four sets of patients using the same core angiographic laboratory t-PA is compared with three trials of combined half dose fibrinolysis and full dose glycoprotein IIb/IIIa inhibition.

Figure 5:  .

Figure 5:  

Odds ratio and 95% confidence intervals (CI) for 30 day composite of death, myocardial infarction, and urgent revascularisation in three trials of catheter based reperfusion with abciximab or placebo.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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