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J Am Coll Cardiol, 2004; 44:936-937, doi:10.1016/j.jacc.2004.05.039
© 2004 by the American College of Cardiology Foundation
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LETTER TO THE EDITOR

Circulating monocytes and late in-stent restenosis: Reply

Daiju Fukuda, MD

The Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City, University Medical School, Osaka, Japan, 1-4-3, Asahimachi, Abenoku, Osaka 545-8585, Japan

Kenei Shimada, MD, Atsushi Tanaka, MD, Takahiko Kawarabayashi, MD, Minoru Yoshiyama, MD and Junichi Yoshikawa, MD, FACC

(Email: daiju{at}qg7.so-net.ne.jp).

We greatly appreciate the interest and thoughtful comments of Bauriedel et al. on our report (1) concerning the relationship between circulating monocytes and late in-stent restenosis. As Bauriedel et al. commented, we consider that our results are supported by several experimental studies (2). Furthermore, we believe that our report raised an issue on the contribution of monocytes, including smooth muscle progenitor cells, to neointimal formation in human stented lesions. There is increasing evidence that smooth muscle progenitors play an important roll in neointimal hyperplasia. Sata et al. (3) have demonstrated that circulating smooth muscle progenitor cells significantly contribute to neointimal hyperplasia in several models of atherosclerosis. Consistently, it was reported that smooth muscle-like cells with specific growth, adhesion, and integrin profiles could outgrow from human peripheral mononuclear cells (4). In humans, it is difficult to precisely investigate the cellularity of in-stent plaque and its origin. A number of studies have attempted to elucidate the lineage of progenitors; however, they remain unidentified. In addition, these cells are thought to contain a lot of lineages and be heterogeneous.

In-stent restenosis is different from typical atherosclerosis because of its plaque composition and rapid progression. As Bauriedel et al. (5,6) described in their work, there is the possibility that innate immunity cells relate to neointimal formation. In addition, these data are useful for understanding the mechanism of in-stent restenosis. Furthermore, several inflammatory agents have been demonstrated to relate to in-stent restenosis. We have demonstrated that not only plasma C-reactive protein levels but also in-stent restenosis are associated with ruptured plaques that may closely associate with inflammatory cells like monocytes (7,8). Therefore, there is possibility that these agents may have influences on mobilization and differentiation of smooth muscle progenitors.

At any rate, it is plausible that circulating monocytes contribute to in-stent restenosis. Identifying neointima-associated cells is important to know the mechanism of in-stent restenosis, and we think that further investigations are needed.


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  1. 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]
  2. Colombo A, Sangirogi G. The monocyte: the key in the lock to reduce stent hyperplasia? J Am Coll Cardiol 2004;43:24-26.[Free Full Text]
  3. Sata M, Saiura A, Kunisato A, et al. Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis Nat Med 2002;8:403-409.[CrossRef][Medline]
  4. Simper D, Stalboerger PG, Panetta CJ, Wang S, Caplice NM. Smooth muscle progenitor cells in human blood Circulation 2002;106:1199-1204.[Abstract/Free Full Text]
  5. 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]
  6. Skowsch D, Jabs A, Andrie R, Dinkelbach S, Luderitz 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]
  7. Sano T, Tanaka A, Namba M, et al. C-reactive protein and lesion morphology in patients with acute myocardial infarction Circulation 2003;108:282-285.[Abstract/Free Full Text]
  8. Tanaka A, Kawarabayashi T, Nishibori Y, et al. In-stent restenosis and lesion morphology in patients with acute myocardial infarction Am J Cardiol 2003;92:1208-1211.[Medline]

Related Article

Circulating monocytes and late in-stent restenosis
Gerhard Bauriedel, Dirk Skowasch, Alexander Jabs, Stefan Krämer, René Andrié, and Berndt Lüderitz
J. Am. Coll. Cardiol. 2004 44: 936. [Full Text] [PDF]




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