Key result
Reperfusion therapy for acute myocardial infarction altered soluble adhesion molecules, with tPA persistently depressing sL-selectin and elevating sPECAM-1 compared to streptokinase, PTCA, and controls.
Why the study?
Leukocyte endothelial interactions mediated by adhesion molecules after ischemia and reperfusion in acute myocardial infarction and their variation by reperfusion treatment are not fully characterized.
Does the type of reperfusion therapy (tPA, SK, or PTCA) alter the time course of soluble adhesion molecules in patients with acute myocardial infarction?
Observational (n=44)
No
Does the type of reperfusion therapy (tPA, SK, or PTCA) alter the time course of soluble adhesion molecules in patients with acute myocardial infarction?
Different reperfusion strategies for acute myocardial infarction elicit distinct patterns of soluble adhesion molecule release, suggesting varying effects on leukocyte-endothelial interactions.
Answers are grounded in this paper and cite their sources.
tPA-linked adhesion molecule shifts in AMI should not alter practice; hypothesis-generating for differential inflammatory effects across reperfusion strategies.
BACKGROUND: Tissue damage after ischemia and reperfusion involves leukocyte endothelial interactions mediated by cell adhesion molecules. This study was designed to determine the time course of soluble adhesion molecules in patients with acute myocardial infarction after attempted reperfusion by thrombolysis with tissue plasminogen activator (tPA) or streptokinase (SK), or percutaneous transluminal coronary angioplasty (PTCA). METHODS: In 3 x 10 randomly selected patients with acute myocardial infarction undergoing thrombolysis with tPA or SK, or treated with PTCA, plasma concentrations of soluble L-selectin, P-selectin, E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) were measured by enzyme-linked immunosorbent assay, 30 min and 1, 2, 4, 8, 12 and 24 hours after intervention. RESULTS: After thrombolysis with tPA, soluble L-selectin concentrations were persistently depressed and soluble PECAM-1 concentrations were elevated, compared with controls, SK and PTCA. While soluble VCAM-1 concentrations did not differ within the first hours after interventions between the three groups, soluble VCAM-1 rose by 24 hours after tPA thrombolysis but did not increase after SK and PTCA treatment. Soluble ICAM-1 concentrations were consistently elevated after PTCA compared with controls and thrombolysed patients. Soluble E-selectin was depressed after tPA thrombolysis and PTCA in comparison with controls, while the SK group showed an increase throughout the observation period. Soluble P-selectin was increased after PTCA and SK lysis up to 8 hours after treatment compared with controls, but no significant differences could be found between treatment groups. CONCLUSION: Adhesion molecules mediating leukocyte endothelial interactions are altered subsequent to postischemic reperfusion and by treatment with thrombolytic agents and angioplasty. The clinical relevance of these biological changes remains to be determined.
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Kerner et al. (2001) conducted an observational in Acute myocardial infarction (n=44). Reperfusion therapy (tPA, streptokinase, or PTCA) vs. Healthy controls was evaluated on Plasma concentrations of soluble adhesion molecules over 24 hours. Reperfusion therapy for acute myocardial infarction altered soluble adhesion molecules, with tPA persistently depressing sL-selectin and elevating sPECAM-1 compared to streptokinase, PTCA, and controls.
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