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Abstract
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). 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. 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. 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.
Highlights
Coronary artery reperfusion is the only intervention that has been shown to reduce the size of myocardial infarction.Thrombolysis and percutaneous transluminal coronary angioplasty (PTCA) are established methods to achieve reopening of an occluded vessel in patients with acute myocardial infarction [1,2,3]
While soluble vascular cell adhesion molecule-1 (VCAM-1) concentrations did not differ within the first hours after interventions between the three groups, soluble VCAM-1 rose by 24 hours after tissue plasminogen activator (tPA) thrombolysis but did not increase after SK and PTCA treatment
The first contact between leukocytes and the vessel wall is established by members of the selectin family of adhesion molecules: L-selectin (CD62L), which is exclusively expressed by leukocytes; P-selectin (CD62P), which can be found in platelets and Weibel–Palade bodies of endothelial cells; and E-selectin (CD62E), a transcriptionally regulated glycoprotein exclusively expressed by endothelial cells
Summary
Thrombolysis and PTCA are established methods to achieve reopening of an occluded vessel in patients with acute myocardial infarction [1,2,3] Despite this observation, ICAM-1 = intercellular adhesion molecule-1; PECAM-1 = platelet endothelial cell adhesion molecule-1; PTCA = percutaneous transluminal coronary angioplasty; SK = streptokinase; tPA = tissue plasminogen activator; VCAM-1 = vascular cell adhesion molecule-1. Methods: In 3 × 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 enzymelinked immunosorbent assay, 30 min and 1, 2, 4, 8, 12 and 24 hours after intervention. The clinical relevance of these biological changes remains to be determined
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