(Circulation. 2000;101:e33.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Angiotensin-Converting Enzyme Tissue Activity in the Diffuse In-Stent Restenotic Plaque
From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy.
Correspondence to Flavio Ribichini, MD, Laboratorio di Emodinamica, Ospedale Santa Croce, Via Michele Copino 26, 12100 Cuneo, Italy. E-mail emodinamica{at}scroce.sanitacn.it
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Introduction |
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We present the 6-month anatomic, histological, and immunohistochemical (IHC) images of a diffuse and aggressive type of in-stent restenosis of a popliteal artery of a patient homozygous for the D (deletion) allele of the ACE gene (Figures 1
, 2, and 3).
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A detailed description of the histological changes of
the arterial wall with time after coronary stenting
in humans was published recently.1 These findings have
confirmed that the ultrasound-detected "neointima"
observed >1 month after implantation is composed primarily of smooth
muscle cells (SMCs) and a proteoglycan-rich matrix. In the first weeks
after stenting, the metallic struts associate with inflammatory
cells, local thrombus formation, and "dedifferentiated"
-actin–negative spindle-shaped cells. Later,
multinucleated giant cells and -actin–positive spindle-shaped cells
are observed in a more differentiated fibrocellular
lesion.1 2 ACE increases up to 100-fold during the
transformation of monocytes to macrophages, and most of the
dedifferentiated SMCs (-actin–negative cells) stain for
ACE.3 However, ACE activity is thought to be limited only
to the first 2 months of the reparative process that follows
postballoon injury.
Our samples reproduce the histological findings
reported in 2 previous studies,1 2 but in contrast to the
results of Ohishi et al3 obtained from postballoon
restenotic samples, IHC staining for ACE was seen even 6 months
after stent implantation. In fact, the spindle-shaped cells observed in
the most external part of the restenotic plaque (close to the
wire) stained for ACE in our sample (Figure 3A
).
The data presented suggest that the transition of the stent-induced inflammatory process, rich in ACE-positive cells, into a fibrocellular lesion composed of differentiated SMCs is not a time-determined sequence. Rather, it might be an ongoing process, evolving from peripheral areas (close to the wire) to central areas and ultimately leading to progressive lumen occlusion in patients with enhanced ACE activity. This is consistent with clinical studies that advocate a role of ACE in restenosis of coronary stents.4
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Footnotes |
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The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke’s Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
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References |
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TopIntroductionReferences |
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1. Farb A, Sangiorgi G, Carter AJ, Walley VM, Edwards WD, Schwartz RS, Virmani R. Pathology of acute and chronic coronary stenting in humans. Circulation. 1999;99:44–52.
2.
Komatsu R, Ueda M, Naruko T, Kojima A, Becker AE.
Neointimal tissue response at sites of coronary
stenting in humans. Circulation. 1998;98:224–233.
3.
Ohishi M, Ueda M, Rakugi H, Okamura A, Naruko T,
Becker AE, Hiwada K, Kamitani A, Kamide K, Higaki J, Ogihara Y.
Upregulation of angiotensin-converting enzyme during the
healing process after injury at the site of
percutaneous transluminal coronary angioplasty
in humans. Circulation. 1997;96:3328–3337.
4.
Ribichini F, Steffenino G, Dellavalle A, Matullo G,
Colajanni E, Camilla T, Vado A, Benetton G, Uslenghi E, Piazza A.
Plasma activity and insertion/deletion polymorphism of
angiotensin I–converting enzyme: a major risk factor and a
marker of risk for coronary stent restenosis.
Circulation. 1998;97:147–154.
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