Diltiazem in the Prevention of Coronary Artery Disease in Heart-Transplant Recipients

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Abstract
Schroeder et al. (Jan. 21 issue)1 present preliminary evidence to suggest that the calcium-channel blocker diltiazem prevents the accelerated coronary artery disease observed in heart-transplant recipients. They attempt to explain their findings by citing previously published work on the antiatherogenic properties of calcium-channel blockers. However, coronary artery narrowing after heart transplantation is likely to be multifactorial in its genesis, with immune-mediated endothelial injury playing a prominent part2. In addition, calcium-channel blockers may possess immunosuppressive activity, and diltiazem, nifedipine, and verapamil have been shown to reduce the number of rejection episodes and improve graft outcome in renal-transplant recipients3. This immunosuppressive effect has been ascribed to the ability of calcium-channel blockers to modulate levels of intracellular calcium in alloreactive T cells, inhibiting alloproliferative T-cell responses in vitro4. Thus, despite the fact that there were similar numbers of rejection episodes in the two groups described by Schroeder et al., the addition of diltiazem to the post-transplantation regimen may have provided a level of immunosuppression over and above that provided by its purported antiatherogenic properties that was ultimately reflected in the reduced narrowing of the coronary arteries. Indeed, the absence of donor alloreactivity in vitro in a cell-mediated lymphocytotoxicity assay has been associated with better graft survival in heart-transplant recipients followed for up to three years5. Perhaps the authors have some evidence to suggest that the same might be true for the heart-transplant recipients who received diltiazem.