Introduction:
Everolimus (EVL) has been shown to reduce the severity of CAV in de novo heart transplant (HTx) recipients. However, there is still little knowledge about the effects of conversion from mycophenolate mofetil (MMF) to EVL with reducing calcineurin inhibitor (CNI) dose on cardiac allograft vasculopathy (CAV) in maintenance HTx recipients. To evaluate this hypothesis, we performed a retrospective study.
Methods:
We examined 63 consecutive HTx recipients who were investigated with three-dimensional intravascular ultrasound (3D-IVUS) analysis every year. 24 recipients were converted to EVL with low-dose CNI from MMF with standard-dose CNI (EVL group) while the others maintained on MMF with standard-dose CNI (MMF group). 3D-IVUS analyses in a year after conversions to EVL with low-dose CNI was compared with those just before the conversions in EVL group, while recent two 3D-IVUS analyses at one year interval were compared in the control group.
Results:
At the former analyses, plaque volume (PVI) and %plaque volume (%PVI, PVI/vessel volume percent) were significantly greater and lumen volume (LVI) was smaller in the EVL group in comparison with those in the MMF group. %PVI increased (10.37±7.53 versus 12.95±9.83, P=0.008) and LVI (10.57±2.63 versus 9.52±2.42 mm
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/mm, P<0.001) reduced significantly in the control group but not in the EVL group. The increase in %PVI during one year was suppressed and the decrease in LVI preserved in the EVL group compared with the control group (2.60±0.92 vs -0.66±1.14 %, p=0.031, -1.05±0.26 vs 0.05±0.19 mm
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/mm, p=0.007, respectively). These effects were sustained at 2 years (p=0.042 and p=0.005).
Conclusions:
Compared with persistent MMF therapy, EVL conversion with low-dose CNI significantly reduce the severity of luminal narrowing in maintenance HTx recipients.
Differential Expression of the IFN-γ-Inducible CXCR3-Binding Chemokines, IFN-Inducible Protein 10, Monokine Induced by IFN, and IFN-Inducible T Cell α Chemoattractant in Human Cardiac Allografts: Association with Cardiac Allograft Vasculopathy and Acute Rejection