HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: j.jacc.2007.02.070v1 50/1/25    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lepper, P. M. Articles by von Eynatten, M. Search for Related Content PubMed Articles by Lepper, P. M. Articles by von Eynatten, M.

CLINICAL RESEARCH

Association of Lipopolysaccharide-Binding Protein and Coronary Artery Disease in Men

Philipp M. Lepper, MD^_*,,_*, Christian Schumann, MD, Kathy Triantafilou, PhD, F. Maximilian Rasche, MD, Tibor Schuster, MS, Hedwig Frank, E. Marion Schneider, PhD^||, Martha Triantafilou, PhD and Maximilian von Eynatten, MD^#

^_* Department of Intensive Care Medicine, University Hospital of Bern (Inselspital), Bern, Switzerland
Department of Internal Medicine II, University of Ulm, Ulm, Germany
Infection and Immunity Group, University of Sussex, Brighton, United Kingdom
Institute of Medical Statistics and Epidemiology, Technical University of Munich, Munich, Germany
^|| Section of Experimental Anaesthesiology, University of Ulm, Ulm, Germany
^# Department of Nephrology, Technical University of Munich, Munich, Germany

Manuscript received November 27, 2006; revised manuscript received January 11, 2007, accepted February 5, 2007.

^_* Reprint requests and correspondence: Dr. Philipp M. Lepper, Department of Intensive Care Medicine, Inselspital, University of Bern, CH-3010 Bern, Switzerland. (Email: philipp.lepper{at}insel.ch).

Objectives: In this study we tested the hypothesis that lipopolysaccharide-binding protein (LBP) might be able to be used as a biomarker for coronary artery disease (CAD).

Background: The mechanisms by which the innate immune recognition of pathogens could lead to atherosclerosis remain unclear. Lipopolysaccharide-binding protein is the first protein to encounter lipopolysaccharide and to deliver it to its cellular targets, toll-like receptors; therefore, its presence might be a reliable biomarker that indicates activation of innate immune responses.

Methods: A total of 247 men undergoing elective coronary angiography were studied, and the extent of coronary atherosclerosis was assessed by 2 established scores: "extent score" and "severity score." Levels of LBP, markers of inflammation, and traditional risk factors for CAD were assessed.

Results: Serum LBP concentration was significantly increased in 172 patients with angiographically confirmed CAD compared with 75 individuals without coronary atherosclerosis (20.6 ± 8.7 pg/ml vs. 17.1 ± 6.0 pg/ml, respectively; p = 0.002). Moreover in multivariable logistic regression analyses, adjusted for established cardiovascular risk factors and markers of systemic inflammation, LBP was a significant and independent predictor of prevalent CAD (p < 0.05 in all models).

Conclusions: Lipopolysaccharide-binding protein might serve as a novel marker for CAD in men. The present results underlie the potential importance of innate immune mechanisms for CAD. Further studies are warranted to bolster the data and to identify pathogenetic links between innate immune system activation and atherosclerosis.

Abbreviations and Acronyms   BMI = body mass index   ES = extent score   FPG = fasting plasma glucose   HDL = high-density lipoprotein   HOMA = homeostasis model assessment   LBP = lipopolysaccharide-binding protein   LDL = low-density lipoprotein   LPS = lipopolysaccharide   TLR = toll-like receptor   VLDL = very low-density lipoprotein

This article has been cited by other articles:

				A. N. DeMaria, J. J. Bax, O. Ben-Yehuda, P. Clopton, G. K. Feld, G. S. Ginsburg, B. H. Greenberg, J. D. Knoke, W. Y.W. Lew, J. A.C. Lima, et al. Highlights of the year in JACC 2007. J. Am. Coll. Cardiol., January 29, 2008; 51(4): 490 - 512. [Full Text] [PDF]