Mast cell infiltration in acute coronary syndromes: implications for plaque rupture
Maija Kaartinen, MD*
,
Allard C. van der Wal, MD
,
Chris M. van der Loos, PhD
,
Jan J. Piek, MD
,
Karel T. Koch, MD
,
Anton E. Becker, MD, FACC
and
Petri T. Kovanen, MD*
* Wihuri Research Institute, Helsinki, Finland
Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland
Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands

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Figure 1 a, Frozen section of part of an atherectomy specimen obtained from a patient with unstable angina (group 2). The section is immunodouble-stained for macrophages (anti-CD68) in red and for smooth muscle cells (anti-alpha actin) in blue. The boxed area is enlarged in b through d. Original magnification x30. b, Inflammatory area containing closely packed macrophages (red) and sparse smooth muscle cells (blue). c, Adjacent section stained for mast cells (antitryptase). d, Adjacent serial section stained for T lymphocytes (anti-CD3). Original magnification b through d, x90.
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Figure 2 Graphs showing the numbers per square millimeter of mast cells and T lymphocytes (upper panel) and the percentages of immunostained macrophage and smooth muscle cell areas (lower panel) in the atherectomy specimens of each group (group 1: chronic stable angina; group 2: unstable angina, Braunwalds classes I and II; and group 3: unstable angina pectoris in patients requiring intravenous treatment with nitrates and heparin, Braunwalds class III). Individual data points, means and p values are shown.
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Figure 3 Graph showing the numbers per square millimeter of TNF- -positive mast cells and of MMP-9-positive macrophages in atherectomy specimens for each patient group (see Fig. 2). Individual data points, means and p values are shown.
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Copyright © 1998 by the American College of Cardiology Foundation.