Parfrey P S, Harnett J D, Foley R N, Kent G M, Murray D C, Barre P E, Guttmann R D
Division of Nephrology, Health Sciences Centre, Newfoundland, Montreal, Canada.
Transplantation. 1995 Nov 15;60(9):908-14.
In chronic uremia, cardiomyopathy manifests itself as systolic dysfunction, concentric left ventricular (LV) hypertrophy, or LV dilatation. To determine the impact of renal transplantation on uremic cardiomyopathy, all dialysis patients participating in a long-term cohort study who received a successful renal transplant were followed with echocardiography. The transplanted group comprised 102 of 433 (24%) endstage renal disease (ESRD) patients. They were significantly younger and, on starting ESRD therapy, had significantly less ischemic heart disease and cardiac failure than the overall ESRD cohort. During followup, ischemic heart disease developed in only 1 patient and none experienced cardiac failure. In the 12% (n = 12) of patients with systolic dysfunction before renal transplant, fractional shortening normalized in all patients, increasing from 21.5 +/- 4.6% to 33.5 +/- 5.6% after transplantation. In the 41% (n = 41) with concentric LV hypertrophy before transplantation, the LV mass index improved from 158 +/- 39 g/m2 to 132 +/- 39 g/m2. LV dilatation was present in 32% (n = 32) of patients before transplantation. After transplantation, LV volume fell from 116 +/- 3.1 ml/m2 to 89 +/- 21 ml/m2, and LV mass index in this group fell from 166 +/- 55 g/m2 to 135 +/- 37 g/m2. It was not possible to associate risk factors characteristic of the uremic state with the improvement in cardiac structure and function, although the fall in LV mass was significantly associated with fall in blood pressure. We conclude that correction of the uremic state by renal transplantation leads to normalization of LV contractility in systolic dysfunction, regression of hypertrophy in concentric LV hypertrophy, and improvement of cavity volume in LV dilatation. The degree of improvement suggests that dialysis patients with uremic cardiomyopathy would benefit from renal transplantation.
在慢性尿毒症中,心肌病表现为收缩功能障碍、左心室(LV)向心性肥厚或LV扩张。为了确定肾移植对尿毒症心肌病的影响,对参与一项长期队列研究且肾移植成功的所有透析患者进行了超声心动图随访。移植组包括433例终末期肾病(ESRD)患者中的102例(24%)。他们明显更年轻,并且在开始ESRD治疗时,与整个ESRD队列相比,缺血性心脏病和心力衰竭的发生率明显更低。在随访期间,仅1例患者发生缺血性心脏病,无患者发生心力衰竭。在肾移植前有收缩功能障碍的患者中,12%(n = 12)的患者缩短分数均恢复正常,移植后从21.5±4.6%增加到33.5±5.6%。在移植前有LV向心性肥厚的患者中,41%(n = 41)的患者LV质量指数从158±39 g/m²改善至132±39 g/m²。移植前32%(n = 32)的患者存在LV扩张。移植后,LV容积从116±3.1 ml/m²降至89±21 ml/m²,该组LV质量指数从166±55 g/m²降至135±37 g/m²。虽然LV质量的下降与血压下降显著相关,但无法将尿毒症状态的危险因素与心脏结构和功能的改善联系起来。我们得出结论,通过肾移植纠正尿毒症状态可使收缩功能障碍患者的LV收缩力恢复正常,使LV向心性肥厚患者的肥厚消退,并改善LV扩张患者的腔容积。改善程度表明,患有尿毒症心肌病的透析患者将从肾移植中获益。