title: Prevention and treatment of coronary artery vasculopathy.
abstract: OBJECTIVE
  Cardiac allograft vasculopathy (CAV) is still one of the major causes of death following heart transplantation. Here, we review the recent advances in its prevention and treatment.
  
  
  RESULTS
  Preventive measures comprise control of classical risk factors, prophylaxis against cytomegalovirus, avoidance of graft endothelial damage during heart transplantation, and prevention of acute rejection. These measures can be effective if begun early. The treatment options for established CAV are limited, percutaneous revascularization and coronary artery bypass graft only being viable for a minority of patients because of the diffuse nature of CAV. Retransplantation is the only definitive therapy for CAV and may be considered for suitable patients with advanced CAV and allograft dysfunction. One of the most promising developments in the recent years is the use of mTOR inhibitors, which can now be regarded as effective in preventing CAV in de novo patients; their role in the treatment of established CAV is still uncertain despite some encouraging recent findings.
  
  
  CONCLUSIONS
  The implementation of measures and lifestyles that help prevent CAV should be a priority of postheart transplantation management. Research should urgently evaluate mTOR inhibitors for the treatment of established CAV.
authors.affiliation: Advanced Heart Failure and Heart Transplant Unit, Hospital Universitario A Coruña, Corunna, Spain. anne.dipchand@sickkids.ca
authors.forename: Maria G
authors.initials: MG
authors.lastname: Crespo-Leiro
authors.forename: Raquel
authors.initials: R
authors.lastname: Marzoa-Rivas
authors.forename: Eduardo
authors.initials: E
authors.lastname: Barge-Caballero
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Paniagua-Martín
mesh_terms: D003324:Coronary Artery Disease / Q000209:etiology* / Q000517:prevention & control / Q000628:therapy*; D016027:Heart Transplantation / Q000009:adverse effects* / Q000379:methods*; D006801:Humans