(Circulation. 1996;94:3098-3102.)
© 1996 American Heart Association, Inc.
Articles |
Macrophage Infiltration Predicts Restenosis After Coronary Intervention in Patients With Unstable Angina
the Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston, and the Cardiovascular Institute (V.F., J.T.F.), Mount Sinai School of Medicine, New York, NY.
Correspondence to Pedro R. Moreno, MD, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail prmoreno@bics.bwh.harvard.edu.
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.
Methods and 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.
Key Words: atherosclerosis • angioplasty • coronary disease • leukocytes
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