• Annual incidence rate of 5% to 10%.
• CAV is 40% by 17 years after HTx (vary by age)
• Risks factors: older donor age, older recipient age, transplant era, no induction therapy, retransplantation, black race, rejection in the first year postTx and repeated episodes of cellular rejection
• Severe CAV is positively correlated with persistent inflammation and a higher degree of HLA mismatch.
• In contrast with eccentric lesions seen in atheromatous disease, CAV results a generalized process from neointimal proliferation
• Characterized by concentric narrowing that affects the entire length of the coronary tree, from the epicardial to the intramyocardial segments, leading to rapid tapering, pruning, and obliteration of third-order branch vessels.

Intravascular Ultrasound (IVUS) is more sensitive tool for the diagnosis of CAV than coronarography (See Image below); others as MRI and Optical coherence tomography are still not widespread application in pediatrics but it is related with early diagnosis and allows changes in the treatment

Therapeutic Options

1. Statins
2. Vasodilators
3. Endothelial Protection (aspirin + clopidogrel)
4. Infection and CAV (control CMV INFECTION)
5. Immunosuppression: mTOR inhibitors (Sirolimus or Everolimus)
6. Emerging New Strategies for the Prevention or Treatment of CAV

• • Three different strategies for CAV are emerging: inhibitio of growth factors, cytokines, and circulating antibodies; cell therapy or tolerance induction
  • Sensitive methods for detecting circulating antibodies and improved therapeutic strategies (eg: photopheresis)