Abstract 13516: Serum Levels of Soluble Hemoglobin Scavenger Receptor are a Novel Biomarker of Plaque Instability in Coronary Atherosclerotic Lesions
Background: Atherosclerotic progression is linked to intraplaque hemorrhage. Erythrocyte extravasation releases free hemoglobin (Hb). The heme-containing iron in Hb generates free radicals that induce lipid peroxidation, which may be related to plaque instability. Therefore, effective clearance of free Hb after intraplaque hemorrhage is a relevant pathway to reduce plaque instability. In atherosclerotic plaques, the only route for clearance of the haptoglobin-Hb complex is via macrophages, which is mediated by the hemoglobin scavenger receptor (CD163). The soluble form of CD163 (sCD163) is a normal constituent of blood and is generated by proteolytic cleavage of CD 163 at the cell surface.
Methods: To elucidate whether increased blood levels of sCD163 are a marker of plaque stability, we measured serum sCD163 levels in 50 control subjects and 446 patients with either acute myocardial infarction (AMI, n=172), unstable angina pectoris (UAP) (n=131), or stable angina pectoris (SAP) (n=143) using an enzyme-linked immunosorbent assay.
Results: Serum sCD163 levels were significantly higher in AMI or UAP patients compared with SAP patients (P< 0.01) or control subjects (P<0.0001) (AMI, 799±305 ng/mL; UAP, 712±265 ng/mL; SAP, 660±201 ng/mL; controls, 507±146 ng/mL). Serum sCD163 levels in ST-elevation MI (STEMI) patients were significantly higher than those in non-STEMI patients (P<0.05). In addition, serum sCD163 levels in Q-MI patients were significantly higher compared with non-Q MI patients (P<0.05). In UAP patients, serum sCD163 levels were significantly higher in hypertension or diabetes mellitus patients (P<0.05). In addition, serum sCD163 levels in UAP patients with Braunwald class III were significantly higher than in patients with Braunwald class I (P<0.05).
Conclusions: These findings suggest that increased serum sCD163 levels are a novel biomarker of plaque instability in coronary atherosclerotic lesions.
- © 2013 by American Heart Association, Inc.