Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2000;102:1549-1555

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Labarrere, C. A.
Right arrow Articles by Halbrook, H. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Labarrere, C. A.
Right arrow Articles by Halbrook, H. G.
Related Collections
Right arrow Chronic ischemic heart disease
Right arrow Other Vascular biology
Right arrow CV surgery: transplantation, ventricular assistance, cardiomyopathy
Right arrow Risk Factors
Right arrow Other arteriosclerosis
Right arrow Transplantation

(Circulation. 2000;102:1549.)
© 2000 American Heart Association, Inc.


Clinical Investigation and Reports

Value of Serum-Soluble Intercellular Adhesion Molecule-1 for the Noninvasive Risk Assessment of Transplant Coronary Artery Disease, Posttransplant Ischemic Events, and Cardiac Graft Failure

Carlos A. Labarrere, MD; David R. Nelson, MS; Steven J. Miller, PhD; Jennifer M. Nieto, BS; Jennifer A. Conner, BS; Douglas E. Pitts, MD; Philip C. Kirlin, MD; Harold G. Halbrook, MD

From the Methodist Research Institute (C.A.L., S.J.M., J.M.N., J.A.C.) and Department of Transplantation (D.E.P., P.C.K., H.G.H.), Clarian Health Partners (Methodist, Indiana University, Riley Hospitals), Indianapolis, Ind, and Department of Biostatistics and Epidemiology (D.R.N.), Cleveland Clinic Foundation, Cleveland, Ohio.

Background—Adhesion molecules on arterial endothelium have been implicated in spontaneous atherosclerosis and transplant coronary artery disease (CAD). We studied whether elevated serum-soluble intercellular adhesion molecule-1 (sICAM-1) during the immediate posttransplant period was a risk factor for CAD, posttransplant ischemic events, or cardiac graft failure.

Methods and Results—We initially studied serum sICAM-1 in a subset of 16 cardiac allograft recipients (5.5±0.7 samples per patient) to determine a cutoff point that best correlated with presence of arterial and arteriolar endothelial ICAM-1 in matching endomyocardial biopsies. The cutoff value was 308 ng/mL. Subsequently, we prospectively evaluated serum sICAM-1 in serial samples (5.3±0.1 per patient) obtained during the first 3 months after transplantation in a validation subset of 130 recipients and correlated early sICAM-1 levels with long-term outcome. Serum sICAM-1 >308 ng/mL correlated significantly with ICAM-1 on arterial and arteriolar endothelium (P=0.02). Cardiac allograft recipients with serum sICAM-1 >308 ng/mL had 2.67 (95% CI, 1.28 to 5.59, P=0.009) times greater risk of CAD and 3.63 (95% CI, 1.05 to 12.5, P=0.04) times greater risk of graft failure. Recipients with sICAM-1 >308 ng/mL also developed more severe CAD (P=0.009) and more ischemic events (P=0.03) after transplantation.

Conclusions—Serum sICAM-1 levels can be used to noninvasively assess risk of transplant CAD, posttransplant ischemic events, and cardiac graft failure.


Key Words: cell adhesion molecules • coronary disease • heart failure • risk factors • transplantation




This article has been cited by other articles:


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
M. P. Mendez, S. B. Morris, S. Wilcoxen, M. Du, Y. K. Monroy, H. Remmer, H. Murphy, P. J. Christensen, and R. Paine III
Disparate mechanisms of sICAM-1 production in the peripheral lung: contrast between alveolar epithelial cells and pulmonary microvascular endothelial cells
Am J Physiol Lung Cell Mol Physiol, April 1, 2008; 294(4): L807 - L814.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
M. P. Mendez, S. B. Morris, S. Wilcoxen, E. Greeson, B. Moore, and R. Paine III
Shedding of soluble ICAM-1 into the alveolar space in murine models of acute lung injury
Am J Physiol Lung Cell Mol Physiol, May 1, 2006; 290(5): L962 - L970.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
K. Kaneko, Y. Yonemitsu, T. Fujii, M. Onimaru, C.-H. Jin, M. Inoue, M. Hasegawa, T. Onohara, Y. Maehara, and K. Sueishi
A free radical scavenger but not FGF-2-mediated angiogenic therapy rescues myonephropathic metabolic syndrome in severe hindlimb ischemia
Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1484 - H1492.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
N. L. Tsakadze, S. D. Sithu, U. Sen, W. R. English, G. Murphy, and S. E. D'Souza
Tumor Necrosis Factor-{alpha}-converting Enzyme (TACE/ADAM-17) Mediates the Ectodomain Cleavage of Intercellular Adhesion Molecule-1 (ICAM-1)
J. Biol. Chem., February 10, 2006; 281(6): 3157 - 3164.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
S. M. Wildhirt, C. Schulze, N. Conrad, R. Bauernschmitt, R. Lange, and W. von Scheidt
Persistently increased systemic, but not cardiac-specific, adhesion molecule expression and coronary endothelial dysfunction in human cardiac allografts
J. Thorac. Cardiovasc. Surg., October 1, 2005; 130(4): 1175 - 1175.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
N. L. Tsakadze, U. Sen, Z. Zhao, S. D. Sithu, W. R. English, and S. E. D'Souza
Signals mediating cleavage of intercellular adhesion molecule-1
Am J Physiol Cell Physiol, July 1, 2004; 287(1): C55 - C63.
[Abstract] [Full Text] [PDF]