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Updated: Aug 15, 2026
An Immunological Model for Heterotopic Heart and Cardiac Muscle Cell Transplantation in Rats
Published on: May 8, 2020
Persistently increased systemic, but not cardiac-specific, adhesion molecule expression and coronary endothelial
Stephen M Wildhirt1, Costas Schulze, Nicole Conrad
1Department of Cardiovascular Surgery, German Heart Center Munich, Technical University of Munich, Munich, Germany. wildhirt@gmx.net
Insights
Persistently high systemic levels of adhesion molecules after heart transplantation are linked to impaired coronary vasomotor function. This suggests a chronic inflammatory state impacting transplant recipients within the first year.
Area of Science:
- Cardiology
- Immunology
- Transplantation Medicine
Background:
- Adhesion molecules (P-selectin, intercellular adhesion molecule 1) play roles in inflammation and endothelial dysfunction.
- Impaired coronary vasomotor function is a concern after heart transplantation.
Purpose of the Study:
- To investigate the relationship between systemic and cardiac-specific expression of adhesion molecules and coronary vasomotor function post-heart transplantation.
- To assess these markers and function at 1 and 12 months after transplantation.
Main Methods:
- Measured soluble and endomyocardial P-selectin and intercellular adhesion molecule 1, and TNF-alpha in blood samples from 42 transplant recipients and 20 controls.
- Assessed endothelium-dependent (acetylcholine) and independent (adenosine) coronary vasomotor function using Doppler wire and angiography at 1 and 12 months.
Main Results:
- High expression of adhesion molecules observed 1 and 12 months post-transplant compared to controls.
- No evidence of cardiac-specific expression or release of these adhesion molecules.
- Significant inverse correlation found between soluble adhesion molecule levels and coronary vasomotor function.
Conclusions:
- Elevated circulating adhesion molecules post-transplant are systemic, not cardiac-specific, indicating chronic inflammation.
- This chronic inflammation is associated with impaired coronary vasomotor function.
- Impaired vasomotor function may represent an early, potentially reversible stage of transplant coronary artery disease and atherothrombosis.
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 alpha, 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.
