title: Platelet and leukocyte adhesion and activation in unstable angina and post-PTCA.
abstract: BACKGROUND
  Unstable atherosclerotic plaques activate blood cells which may adhere to the coronary endothelium causing vessel occlusion. However, it is unknown if different clinical syndromes associated with plaque rupture induce similar blood cell activation and adhesion to the endothelium.
  
  
  METHODS
  We studied changes in adhesion molecule expression of platelets (GPIIb/IIIa), neutrophils--CD18, CD11b and L-selectin--and monocytes (CD14) after interaction with active lesions of patients with stable angina subjected to PTCA and patients with unstable angina (UA). Generation of superoxide (SO) radicals from PMNs and PMN sequestration in the coronary circulation were also assessed. Blood samples were collected from the aorta (Ao) and coronary sinus (CS) before and 15 min after PTCA (n=13) and within the first 48 h of UA (n=12).
  
  
  RESULTS
  PTCA induced a marked up-regulation of CD18, CD11b, CD14 and GPIIb/IIIa with L-selectin shedding and reduced SO formation, whereas only minor L-selectin down-regulation and decreased SO production indicated activation in UA. However, a significant decrease in neutrophil count in the CS compared to the Ao was only observed in UA.
  
  
  CONCLUSIONS
  The magnitude of cellular activation depends on the underlying clinical setting and just partially contributes to cell adhesion to the endothelium which might be modulated by different extent of vascular occlusion and shear forces.
authors.affiliation: Heart Institute (InCor)-University of São Paulo Medical School, São Paulo, SP-05403-000, Brazil. Carlos.serrano@incor.usp.br
authors.forename: Carlos V
authors.initials: CV
authors.lastname: Serrano
authors.forename: Roberto
authors.initials: R
authors.lastname: Rocha Giraldez
authors.forename: Juliano de Lara
authors.initials: JL
authors.lastname: Fernandes
authors.forename: José Carlos
authors.initials: JC
authors.lastname: Nicolau
authors.forename: Jay L
authors.initials: JL
authors.lastname: Zweier
authors.forename: José Antonio F
authors.initials: JA
authors.lastname: Ramires
mesh_terms: D000789:Angina, Unstable / Q000503:physiopathology* / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D039481:CD11b Antigen / Q000502:physiology; D018821:CD18 Antigens / Q000502:physiology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D006801:Humans; D019041:L-Selectin / Q000502:physiology; D018950:Lipopolysaccharide Receptors / Q000502:physiology; D008297:Male; D018375:Neutrophil Activation / Q000502:physiology; D018384:Oxidative Stress; D010973:Platelet Adhesiveness; D015854:Up-Regulation
chemical_list: D039481:CD11b Antigen; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D018950:Lipopolysaccharide Receptors; D019041:L-Selectin