852-2 Widespread Coronary Inflammation In Patients With Unstable Angina

Background: Inflammation may cause unstable angina (UA) by favoring coronary plaque rupture and erosion, In UA activated leukocytes were found in peripheral and coronary sinus blood, but it is unclear whether they are selectively activated in the vascular bed of the culprit stenosis, Methods: We measured the difference in neutrophil myeloperoxidase content (MPXI) across the cardiac and femoral circulation in 5 groups of patients: 33 with UA and single stenosis either in left descending (LAD) artery (UA-L, 24 patients) or right coronary artery (UA-R, 9 patients), 13 with stable angina, 13 with variant angina and 6 controls. Blood samples were taken simultaneously from aorta, femoral vein and great cardiac vein (GCV) which selectively drains LAD but not right coronary blood (as we confirmed by the presence or absence of evidence of vasodilation in the GCV following nitrates injection into left and right coronaries respectively), Plasma levels of C-reactive protein (CRP) were also measured. Results: Aortic MPXI was similar in UA-L and UA-R (-3.9 and -5.5), but significantly lower than in the other three groups (all P<O.05). A significant negative correlation was found between aortic MPXI and CRP values (r=-0.45, P=0,025), MPXI significantly decreased in GCV both in UA-L (-6.4, P<0.O01) and UA-R (-6.6, P=0.003), but not in stable angina with LAD stanosis, variant angina with LAD ischemia, or controls. No MPXI decrease was observed in any group in the femoral vein, The GCV-aorta gradient was also significantly correlated with CRP levels (r=-0.41, P=0,011 ). Conclusions: The widespread inflammatory activation of neutrophils across the COronary vascular bed, independent of culprit stenosis location and of ischemia, carries important pathophysiologicel implications and challenges the concept of a single coronary vulnerable plaque in unstable coronary syndromes.