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J Thorac Cardiovasc Surg 2005;130:1175
© 2005 The American Association for Thoracic Surgery

Cardiothoracic Transplantation

Persistently increased systemic, but not cardiac-specific, adhesion molecule expression and coronary endothelial dysfunction in human cardiac allografts

^a Department of Cardiovascular Surgery, German Heart Center Munich, Technical University of Munich, Munich, Germany.
^b Department of Cardiac Surgery, University of Munich, Munich, Germany.
^c Department of Cardiology, University of Munich, Munich, Germany.

Received for publication January 28, 2005; revisions received May 11, 2005; accepted for publication May 18, 2005.

^_* Address for reprints: Stephen M. Wildhirt, MD, PhD, Department of Cardiovascular Surgery, German Heart Center Munich, Technical University of Munich, Lazarettstr. 46 of Munich, Lazarettstr. 36, 80636 Munich, Germany (Email: wildhirt{at}gmx.net).

BACKGROUND: Adhesion molecules are involved in inflammatory processes that alter endothelial function and lead to impairment of coronary vasomotor function. We studied a possible relationship between systemic expression, cardiac-specific expression, or both of P-selectin and intercellular adhesion molecule 1 and coronary vasomotor function both 1 and 12 months after heart transplantation in human subjects.

METHODS: The expression of endomyocardial and soluble forms of P-selectin and intercellular adhesion molecule 1, as well as levels of tumor necrosis factor , were determined in aortic and coronary sinus blood samples 1, 6, and 12 months after heart transplantation in 42 transplant recipients and 20 age-matched, nontransplanted control subjects. In addition, both endothelium-dependent (acetylcholine) and endothelium-independent (adenosine) coronary vasomotor function were assessed by using a Doppler flow wire and quantitative coronary angiography 1 and 12 months after heart transplantation.

RESULTS: Adhesion molecules were highly expressed 1 month after heart transplantation and remained at high levels 12 months after heart transplantation when compared with levels in nontransplanted control subjects. No cardiac-specific expression or release of P-selectin or intercellular adhesion molecule 1 was observed. There was a significant inverse correlation between coronary vasomotor function and soluble adhesion molecule expression both 1 and 12 months after heart transplantation.

CONCLUSION: Persistently high levels of circulating adhesion molecules are of systemic, but not cardiac-specific, origin and reflect a chronic inflammatory state throughout the first year after heart transplantation. This is associated with impairment of coronary vasomotor function, an early and potentially reversible step in the process of atherothrombosis and transplant coronary artery disease.