CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Teruo Inoue, MD, FACC*,
Toru Kato, MD,
Toshihiko Uchida, MD,
Masashi Sakuma, MD,
Atsuko Nakajima, BSc,
Mitsuei Shibazaki, BSc,
Yoshitaka Imoto, BSc,
Masahiko Saito, MD,
Shigemasa Hashimoto, MD,
Yutaka Hikichi, MD and
Koichi Node, MD
* Department of Cardiovascular and Renal Medicine, Saga University Faculty of Medicine, 5-1-1 Nabeshima, Saga 849-8501, Japan (Email: inouete{at}med.saga-u.ac.jp).
We thank Drs. Tiong and Brieger for their interest in our work and their suggestion that shear-induced down-regulation of Mac-1 (CD11b/CD18) on the surface of neutrophils, depending upon the experimental work by Fukuda et al. (1), might limit our study. We evaluated the trans-cardiac gradient of neutrophil Mac-1 expression by sampling both coronary sinus and peripheral blood in the study (2) cited by Drs. Tiong and Brieger as well as in our previous ones (3–7). Although in this study we did not precisely address the sampling method for peripheral blood, the sampling site for peripheral blood was the femoral vein and was consistent at each sampling point in our study series. The method was based on the sampling via 6-F femoral venous sheath that was left for access for 5-F coronary sinus catheterization during 48-h post-percutaneous coronary intervention (PCI) course, also consistent at each sampling point. As Drs. Tiong and Brieger observed, the most reliable determination of trans-cardiac gradient requires strict sampling of both coronary sinus and peripheral blood with the same catheter sizes. Using our technique, however, we can envision that shear stress might be quite less, compared with the technique with a 21-gauge needle puncture. Formerly, we evaluated the Mac-1 expression at different sampling sites by the same method and by different methods at the same site. As a result, we confirmed that the values were identical between samples via 6-F sheath under 5-F catheter insertion and those via 5-F catheter (T. Inoue et al., unpublished data, 1996). In addition to this evidence, we believe that the consistency of the methods at each point provides our results with a significant value.
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1. Fukuda S, Schmid-Schonbein GW. Regulation of CD18 expression on neutrophils in response to fluid shear stress Proc Natl Acad Sci U S A 2003;100:13152-13157.[Abstract/Free Full Text]2. Inoue T, Kato T, Uchida T, et al. Local release of C-reactive protein from vulnerable plaque or coronary artery wall injured by stenting J Am Coll Cardiol 2005;46:239-245.[Abstract/Free Full Text] 3. Inoue T, Sakai Y, Fujito T, et al. Clinical significance of neutrophil adhesion molecule expression after coronary angioplasty on the development of restenosis Thromb Haemost 1998;79:54-58.[Web of Science][Medline] 4. Inoue T, Sakai Y, Hoshi K, et al. Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty Circulation 1998;97:2511-2518.[Abstract/Free Full Text] 5. Inoue T, Sohma R, Miyazaki T, et al. Activation process of platelets and neutrophils after coronary stent implantationcomparison with balloon angioplasty. Am J Cardiol 2000;86:1057-1062.[CrossRef][Web of Science][Medline] 6. Inoue T, Uchida T, Yaguchi I, et al. Stent-induced expression and activation of the leukocyte integrin Mac-1 is associated with neointimal thickening and restenosis Circulation 2003;107:1757-1763.[Abstract/Free Full Text] 7. Inoue T, Uchida T, Sakuma M, et al. Cilostazol inhibits leukocyte integrin Mac-1, leading to a potential reduction in restenosis after coronary stent implantation J Am Coll Cardiol 2004;44:1408-1414.[Abstract/Free Full Text]
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