Liberation of vessel-adherent myeloperoxidase reflects plaque burden in patients with stable coronary artery disease

ObjectiveMyeloperoxidase (MPO) has emerged as an important pathophysiological determinant of inflammatory vascular artery disease. It is appreciated that vessel immobilized, rather than circulating, MPO is critical for the progression of atherosclerotic lesions. The objective of this study was to investigate whether vessel-immobilized MPO is associated with the extent of coronary plaque burden.MethodsMPO plasma levels were determined by ELISA before and after heparin-release of vessel-bound MPO, to study the relation between vascular MPO deposition and densitometrically assessed coronary plaque burden in 77 patients with stable coronary artery disease.ResultsPatients with a low increase in MPO plasma levels upon heparinization had a significantly smaller total plaque area and volume (12.1[IR:6.2-19.4]mm2 vs. 19.8[IR:11.3-31.5]mm2, p < 0.01; 27.8[IR:12.3-44.8]mm3 vs. 55.2[IR:24.2-87.5]mm3, p < 0.05). Multivariable linear regression revealed that ΔMPO was independently associated with plaque area, and that ΔMPO increased with the number of affected vessels. Selective sampling confirmed the predominant role of coronary MPO deposition.ConclusionOur data demonstrate that heparin-induced mobilization of vessel-bound MPO is closely linked to coronary plaque burden and thus further corroborate the evidence for the intimate involvement of this enzyme in vascular pathophysiology, as well as the importance of inflammation in atherosclerosis.