Increased plasma soluble intercellular adhesion molecule-1 levels in patients with acute myocardial infarction
Insights
Plasma soluble intercellular adhesion molecule-1 (sICAM-1) is elevated in acute myocardial infarction (AMI) and unstable angina (UA). Increased sICAM-1 suggests a role in repeated ischemia and reperfusion injury, highlighting its inflammatory role in ischemic heart disease.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biomarkers
Background:
- Intercellular adhesion molecule-1 (ICAM-1) mediates leukocyte adhesion to endothelial cells.
- Soluble ICAM-1 (sICAM-1) is a marker of endothelial activation and inflammation.
Purpose of the Study:
- To investigate plasma sICAM-1 levels in patients with acute myocardial infarction (AMI), unstable angina (UA), and stable exertional angina (SEA).
- To assess the association of sICAM-1 levels with myocardial ischemia and reperfusion.
Main Methods:
- Plasma sICAM-1 levels were measured in 30 AMI patients, 21 UA patients, 35 SEA patients, and 21 controls.
- Measurements were taken at various time points for AMI and UA patients.
Main Results:
- Plasma sICAM-1 levels were significantly higher in AMI (acute and chronic phases) and UA groups compared to SEA and control groups (p < 0.01).
- AMI patients with a history of UA showed significantly higher sICAM-1 levels compared to those without UA.
- Elevated sICAM-1 correlated with repeated episodes of myocardial ischemia and reperfusion not resulting in necrosis.
Conclusions:
- Increased plasma sICAM-1 is associated with acute and chronic phases of AMI and unstable angina.
- Elevated sICAM-1 may indicate repeated myocardial ischemia/reperfusion events and play a role in the inflammatory pathogenesis of ischemic myocardium.
Abstract:
Intercellular adhesion molecule-1 (ICAM-1) is a major ligand for 2 members of the CD18 family of leukocyte integrin adhesion molecules and mediates adhesion between leukocytes and stimulated endothelial cells. We examined plasma soluble ICAM-1 (sICAM-1) levels in 30 patients with acute myocardial infarction (AMI) within 6 h of symptom onset, 21 patients with unstable angina (UA), 35 patients with stable exertional angina (SEA) and 21 control subjects. Plasma sICAM-1 levels (ng/ml) were significantly higher in both the acute and chronic phases of AMI and in the UA group than in the SEA and the control groups (195 +/- 14, 198 +/- 16 in the acute and chronic phases of AMI, 188 +/- 11 in the UA group vs 142 +/- 7 in the SEA group, 141 +/- 10 in the control group, p < 0.01). Plasma sICAM-1 levels were significantly higher in AMI patients when preceded by unstable angina than when not preceded by unstable angina at any point over the time course except 1 week after admission (p < 0.01 vs admission, 12 h, 2 days, 3 days, 5 days, 2 weeks, 3 weeks. p < 0.05 vs 24 h). These results suggest that the increase in sICAM-1 is associated with repeated episodes of myocardial ischemia and reperfusion not leading to myocardial necrosis. The increase in sICAM-1 may play an important role as an inflammatory component in the pathogenesis of the ischemic myocardium.
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