Cardiac allograft vasculopathy--a changing perspective.
Together, recent clinical and basic studies show that Cardiac allograft vasculopathy (CAV) is multifactorial and regulated by interacting forces at different stages. Data show that at least three forms of vasculopathy (fibrosis, arteritis, atheroma) contribute to the thickening of graft vascular disease. Current therapy to prevent or treat CAV should focus on control of both alloantigen dependent and independent forces. In the future, therapies will be targeted at manipulation of the donor (to reduce antigenicity and ischemic injury) as well as manipulation of the recipient to attenuate or permanently interrupt the immune responses in a donor specific manner.
Russell
M E
ME
Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215, USA.
D000367:Age Factors; D000818:Animals; D001167:Arteritis / Q000209:etiology / Q000276:immunology; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000517:prevention & control; D004195:Disease Models, Animal; D005544:Forecasting; D017353:Gene Deletion; D006084:Graft Rejection / Q000276:immunology / Q000517:prevention & control; D016027:Heart Transplantation / Q000009:adverse effects* / Q000276:immunology; D006801:Humans; D007519:Isoantigens / Q000276:immunology; D051379:Mice; D018345:Mice, Knockout; D012307:Risk Factors; D014019:Tissue Donors; D016042:Transplantation, Heterotopic; D014184:Transplantation, Homologous; D018084:Ultrasonography, Interventional
D007519:Isoantigens