title: Macrophage infiltration predicts restenosis after coronary intervention in patients with unstable angina.
abstract: BACKGROUND
  Restenosis remains the major limitation of percutaneous coronary revascularization. Macrophages release cytokines, metalloproteinases, and growth factors that may induce smooth muscle cell migration and proliferation. We tested the hypothesis that primary lesions that develop restenosis after coronary atherectomy have more macrophages and smooth muscle cells than primary lesions that do not develop restenosis.
  
  
  RESULTS
  Fifty patients with unstable angina were identified. Total and segmental areas were quantified on trichrome-stained sections of coronary atherectomy tissue. Macrophages and smooth muscle cells were identified by immunohistochemical staining. Restenosis, defined as > 50% stenosis diameter by quantitative cineangiography, was present in 30 patients. The other 20 patients (< 50% stenosis) constitute the "no restenosis" group. The percentages of smooth muscle cell areas were similar in specimens from patients with and without restenosis (57 +/- 5% and 52 +/- 6%) (P = NS). However, macrophage-rich areas were larger in plaque tissue from patients with restenosis (20.4 +/- 2%) than in tissue from patients without restenosis (9.3 +/- 2%) (P = .0007). Multiple stepwise logistic regression analysis identified macrophages as the only independent predictor for restenosis (P = .006).
  
  
  CONCLUSIONS
  Macrophages are increased in coronary atherectomy tissue from primary lesions that develop restenosis, suggesting a possible role for macrophages in the restenotic process after percutaneous coronary intervention.
authors.affiliation: Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston, USA. prmoreno@bics.bwh.harvard.edu
authors.forename: P R
authors.initials: PR
authors.lastname: Moreno
authors.forename: V H
authors.initials: VH
authors.lastname: Bernardi
authors.forename: J
authors.initials: J
authors.lastname: López-Cuéllar
authors.forename: J B
authors.initials: JB
authors.lastname: Newell
authors.forename: C
authors.initials: C
authors.lastname: McMellon
authors.forename: H K
authors.initials: HK
authors.lastname: Gold
authors.forename: I F
authors.initials: IF
authors.lastname: Palacios
authors.forename: V
authors.initials: V
authors.lastname: Fuster
authors.forename: J T
authors.initials: JT
authors.lastname: Fallon
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery*; D017225:Atherectomy, Coronary; D006328:Cardiac Catheterization; D002784:Cholesterol / Q000097:blood; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery*; D003920:Diabetes Mellitus; D005260:Female; D006801:Humans; D006973:Hypertension; D008075:Lipoproteins, HDL / Q000097:blood; D008264:Macrophages / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012008:Recurrence; D012044:Regression Analysis; D012307:Risk Factors; D012907:Smoking
chemical_list: D008075:Lipoproteins, HDL; D002784:Cholesterol