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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:2105-a.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Periprocedural Kinetics in Serum Levels of Cytokines and Adhesion Molecules in Elective PTCA and Stent Implantation: Impact on Restenosis

P. Christian Schulze^*; Eyleen Kluge^*; Gerhard Schuler; Bernward Lauer

University of Leipzig, Heart Center (P.C.S., E.K., G.S.), Department of Cardiology, Strümpellstrasse 39, 04289 Leipzig, Germany; Cardiovascular Division (P.C.S.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; and Zentralklinik Bad Berka (B.L.), Department of Cardiology, Bad Berka, Germany

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Coronary restenosis after percutaneous transluminal coronary angioplasty (PTCA) remains a significant clinical problem occurring in 30% of patients even after wide accessibility and application of intraluminal stent implantation. Recent developments in stent design have made new techniques such as brachytherapy and drug-eluting stents available for clinical approaches; nonetheless, restenosis with its complex multifactorial genesis will continue to be an important problem with a major impact on long-term outcome of patients after coronary interventions. Several factors have been suggested to serve as predictors of the later occurrence of restenosis, but no serum parameter with predictive value has been clinically established so far.

The pathophysiology of coronary restenosis has not been fully elucidated; however, an initial vascular injury is supposed to initiate a local inflammatory response that induces the recruitment of circulating immune-competent cells through an increased expression and translocation of several adhesion molecules such as P-selectin, E-selectin, and monocyte chemoattractant molecule-1 (MCP-1).^1,2 Migration of leukocytes, release of cytokines, and growth factors result in the induction of local inflammatory reactions and vascular remodeling.³ Patients with angina pectoris and acute myocardial infarction show a systemic inflammatory activation and elevated serum levels of vascular adhesion molecules.^1,2 Therefore, the local vascular inflammation seems to be accompanied by alterations of serum parameters exhibiting a systemic inflammatory response toward local tissue damage.

We investigated periprocedural serum kinetics of cytokines (TNF and IL-1ß) and adhesion molecules (ICAM-1, VCAM-1, E-selectin and P-selectin) from baseline to 48 hours after elective PTCA and intracoronary stent implantation in patients with stable angina . . . [Full Text of this Article]

Oliver Hofnagel; Horst Robenek

Institute for Arteriosclerosis Research, University of Muenster, Germany

Noriaki Kume; Manabu Minami; Takeshi Shimaoka; Shin Yonehara; Toru Kita

Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University, Japan

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