Key result
Tissue-type plasminogen activator did not directly reduce myocardial infarct size compared to saline in a canine model (44% vs 46% of risk zone in the high-dose study).
Why the study?
Does tissue-type plasminogen activator directly reduce infarct size or improve no-reflow independently of lysing coronary thrombi in a canine model of ischemia-reperfusion?
Population
Canine model of 2 hours of occlusion of the left anterior descending coronary artery followed by 4 hours of…
Comparison
Tissue-type plasminogen activator administered… vs Saline
Design
Preclinical
Follow-up
4 hours of reperfusion
Authors
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t-PA lacks direct cardioprotection in canine ischemia-reperfusion; leaves open whether clinical benefits are exclusively thrombolytic.
Does tissue-type plasminogen activator directly reduce infarct size or improve no-reflow independently of lysing coronary thrombi in a canine model of ischemia-reperfusion?
Absolute Event Rate: 44% vs 46%
In a canine model, t-PA did not directly reduce infarct size or improve no-reflow independent of its thrombolytic effects, suggesting its clinical benefits are solely due to lysing thrombi.
Kloner et al. (1989) studied Acute myocardial infarction. Tissue-type plasminogen activator (t-PA) vs. Saline was evaluated on Myocardial infarct size as a percentage of the risk zone. Tissue-type plasminogen activator did not directly reduce myocardial infarct size compared to saline in a canine model (44% vs 46% of risk zone in the high-dose study).
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