title: Widespread coronary inflammation in unstable angina.
abstract: BACKGROUND
  Inflammation within vulnerable coronary plaques may cause unstable angina by promoting rupture and erosion. In unstable angina, activated leukocytes may be 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 content neutrophil myeloperoxidase content in the cardiac and femoral circulations in five groups of patients: two groups with unstable angina and stenosis in either the left anterior descending coronary artery (24 patients) or the right coronary artery (9 patients); 13 with chronic stable angina; 13 with variant angina and recurrent ischemia; and 6 controls. Blood samples were taken from the aorta, the femoral vein, and the great cardiac vein, which selectively drains blood from the left but not the right coronary artery.
  
  
  RESULTS
  The neutrophil myeloperoxidase content of aortic blood was similar in both groups of patients with unstable angina (-3.9 and -5.5, with negative values representing depletion of the enzyme due to neutrophil activation) and significantly lower than in the other three groups (P<0.05). Independently of the site of the stenosis, the neutrophil myeloperoxidase content in blood from the great cardiac vein was significantly decreased in both groups of patients with unstable angina (-6.4 in those with a left coronary lesion and -6.6 in those with a right coronary lesion), but not in patients with stable angina and multiple stenoses, patients with variant angina and recurrent ischemia, or controls. There was also a significant transcoronary reduction in myeloperoxidase content in both groups with unstable angina.
  
  
  CONCLUSIONS
  The widespread activation of neutrophils across the coronary vascular bed in patients with unstable angina, regardless of the location of the culprit stenosis, challenges the concept of a single vulnerable plaque in unstable coronary syndromes.
authors.affiliation: Institute of Cardiology, Catholic University, Rome.
authors.forename: Antonino
authors.initials: A
authors.lastname: Buffon
authors.forename: Luigi M
authors.initials: LM
authors.lastname: Biasucci
authors.forename: Giovanna
authors.initials: G
authors.lastname: Liuzzo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: D'Onofrio
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
authors.forename: Attilio
authors.initials: A
authors.lastname: Maseri
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000276:immunology; D000789:Angina, Unstable / Q000097:blood / Q000276:immunology*; D001011:Aorta / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002405:Catheterization, Central Venous; D002406:Catheterization, Peripheral; D003326:Coronary Circulation / Q000276:immunology*; D023921:Coronary Stenosis / Q000097:blood / Q000276:immunology*; D005260:Female; D005268:Femoral Vein / Q000276:immunology; D006801:Humans; D007249:Inflammation; D007548:Isosorbide Dinitrate / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000276:immunology; D018375:Neutrophil Activation; D009504:Neutrophils / Q000201:enzymology; D009195:Peroxidase / Q000097:blood; D018709:Statistics, Nonparametric; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D015415:Biomarkers; D014665:Vasodilator Agents; D002097:C-Reactive Protein; D009195:Peroxidase; D007548:Isosorbide Dinitrate