Paoletti E, Cannella G
Divisione di Nefrologia, Dialisi e Trapianto, Azienda Ospedaliera Universitaria San Martino, Genova, Italy.
Transplant Proc. 2010 Nov;42(9 Suppl):S41-3. doi: 10.1016/j.transproceed.2010.07.007.
Left ventricular hypertrophy (LVH) contributes to elevated cardiac mortality with graft function in renal transplant recipients. Antihypertensive therapy, and especially angiotensin-converting enzyme (ACE) inhibitors, proved to be effective in regressing the LVH of renal transplant recipients, at least in part by interacting with immunosuppressive agents, thus raising the possibility that immunosuppressive therapy might affect changes in the left ventricular mass (LVM) of recipients. This review mainly focuses on the potential role of mammalian target of rapamycin (mTOR) inhibition to regress cardiac hypertrophy in both experimental models and in the clinical setting. We comment on the results of experimental studies conducted on animal models, which showed regression of cardiac hypertrophy by sirolimus (SRL). We also discuss clinical studies that show that conversion from calcineurin inhibitors to SRL is effective to achieve regression of LVH in both kidney and cardiac transplant recipients, mainly by reducing the true left ventricular wall hypertrophy.
左心室肥厚（LVH）会导致肾移植受者心脏死亡率随移植肾功能升高。抗高血压治疗，尤其是血管紧张素转换酶（ACE）抑制剂，已被证明对肾移植受者的LVH消退有效，至少部分是通过与免疫抑制剂相互作用，从而增加了免疫抑制治疗可能影响受者左心室质量（LVM）变化的可能性。本综述主要关注雷帕霉素靶蛋白（mTOR）抑制在实验模型和临床环境中使心脏肥厚消退的潜在作用。我们对在动物模型上进行的实验研究结果进行了评论，这些研究表明西罗莫司（SRL）可使心脏肥厚消退。我们还讨论了临床研究，这些研究表明，将钙调神经磷酸酶抑制剂转换为SRL对肾移植和心脏移植受者的LVH消退有效，主要是通过减少真正的左心室壁肥厚。
