LETTER TO THE EDITOR
Circulating monocytes and late in-stent restenosis
Gerhard Bauriedel, MD, FACC
University of Bonn, Department of Cardiology, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany
Dirk Skowasch, MD,
Alexander Jabs, MD,
Stefan Krämer, BS,
René Andrié, MD and
Berndt Lüderitz, MD, FACC
(Email: Gerhard.Bauriedel{at}ukb.uni-bonn.de).
We read with great interest the study by Fukuda et al. (1) that evaluated the relationship between white blood cells in peripheral blood and in-stent neointimal volume at six-month follow-up. The investigators demonstrated increased circulating monocyte numbers after coronary stent implantation and found the peak monocyte count related to in-stent neointimal hyperplasia. These exciting findings are strongly supported by several experimental studies, as outlined in the corresponding editorial (2), and add another piece of evidence to the concept that apparently not mural smooth muscle cells but other cell types play a more central role in neointima formation.
Given the diversity of peripheral blood leucocyte subpopulations, the exact identity of neointima-associated leukocytes deserves careful consideration. In this context, we recently identified dendritic cells as novel neointimal cell type and demonstrated their maximal presence during early neointima formation after rat carotid balloon injury (3. In another study, we also showed bone marrow-derived and neural crest-derived cells within human in-stent restenosis atherectomy samples. Herein, dendritic cells constituted the major mononuclear lesional cell type, whereas monocytes/macrophages were confined to areas adjacent to stent struts (4). It is tempting to speculate that dendritic cells of the peripheral blood, possibly included in the monocyte fraction, may have been the key player in lesion formation in the study of Fukuda et al. (1). Because C-reactive protein (CRP) had been shown to have chemotactic effects on monocytes/macrophages (5) and to increase neointimal formation (6), we also would like to suggest that further studies on in-stent restenosis should elucidate specific subpopulations of the monocyte/macrophage lineage and the role of CRP.
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- Fukuda D, Shimada K, Tanaka A, Kawarabayashi T, Yoshiyama M, Yoshikawa J. Circulating monocytes and in-stent neointima after coronary stent implantation J Am Coll Cardiol 2004;43:18-23.[Abstract/Free Full Text]
- Colombo A, Sangiorgi G. The monocyte: the key in the lock to reduce stent hyperplasia? J Am Coll Cardiol 2004;43:24-26.[Free Full Text]
- Bauriedel G, Jabs A, Skowasch D, et al. Dendritic cells in neointima formation after rat carotid balloon injury J Am Coll Cardiol 2003;42:930-938.[Abstract/Free Full Text]
- Skowasch D, Jabs A, Andrié R, Dinkelbach S, Lüderitz B, Bauriedel G. Presence of bone-marrow- and neural-crest-derived cells in intimal hyperplasia at the time of clinical in-stent restenosis Cardiovasc Res 2003;60:684-691.[Abstract/Free Full Text]
- Torzewski M, Rist C, Mortensen RF, et al. C-reactive protein in the arterial intima. Role of C-reactive protein receptor-dependent monocyte recruitment in atherogenesis Arterioscler Thromb Vasc Biol 2000;20:2094-2099.[Abstract/Free Full Text]
- Wang CH, Li SH, Weisel RD, et al. C-reactive protein upregulates angiotensin type 1 receptors in vascular smooth muscle Circulation 2003;107:1783-1790.[Abstract/Free Full Text]
Related Article
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Circulating monocytes and late in-stent restenosis: Reply
- Daiju Fukuda, Kenei Shimada, Atsushi Tanaka, Takahiko Kawarabayashi, Minoru Yoshiyama, and Junichi Yoshikawa
J. Am. Coll. Cardiol. 2004 44: 936-937.
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