Cardiac allograft vasculopathy prevention

Cardiac allograft vasculopathy Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2] Raviteja Guddeti, M.B.B.S. [3]

Prevention

As the pathogenesis of CAV consists of both immunological and non-immunological insults, it has been suggested that preventative strategies should consist of control of risk factors for CAV and optimal immunosuppressive therapy. However, the best preventative strategy to delay development of CAV is yet to be determined.

Optimization of Immunosuppressive Therapy

Options for immunosuppressive therapy for prevention of CAV include :

• Sirolimus (Rapamycin)
• Everolimus, a Rapamycin derivative
• Corticosteroids
• Mycophenolate mofetil

Everolimus and Sirolimus

• Act by inhibiting mTOR (mammalian target), thereby having anti-proliferative effects in response to allo-antigens.
• Everolimus is not currently FDA approved for clinical use in the United States.

• Associated with significantly reduced incidence of graft rejection.
• Serial IVUS studies to evaluate intimal proliferation demonstrated smaller increase in maximal intimal thickness and intimal index in patients taking everolimus. Similar results were found in trials that studied sirolimus.
• Side effect profile:
  • Everolimus: increase in serum creatinine levels, hyperlipidemia, anemia, thrombocytopenia, peripheral edema, hypertension. However, opportunistic viral infections less often seen.
  • Sirolimus: Similar to everolimus, however recent reports of impaired wound healing have been reported in renal transplant patients.

Mycophenolate mofetil

• Studies have shown trend towards a lower maximal intimal thickness on IVUS, lower incidence of retransplantation and death with mycophenolate when compared to azathioprine.

Calcineurin inhibitors

• The use of calcineurin inhibitors i.e cyclosporin and tacrolimus have not been shown to lower the risk of developing CAV.
• This suggests that other immunological pathways may exists that play a role in the pathogenesis of CAV. Moreover, side effects from use of these drugs leads to a high incidence of not only chronic renal disease but also hypertension and hyperlipidemia which in turn may accelerate the process of CAV.