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心脏移植受者死亡或再次移植相关的临床病理相关性

Clinicopathological correlations in heart transplantation recipients complicated by death or re-transplantation.

作者信息

McDonald Michelle M, Mihalj Maks, Zhao Bihong, Nathan Sriram, Matejin Stanislava, Ottaviani Giulia, Jezovnik Mateja K, Radovancevic Rajko, Kar Biswajit, Gregoric Igor D, Buja L Maximilian

机构信息

Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at Houston, Houston, TX, United States.

Department of Advanced Cardiopulmonary Therapies and Transplantation, University of Texas Health Science Center at Houston, Houston, TX, United States.

出版信息

Front Cardiovasc Med. 2022 Nov 3;9:1014796. doi: 10.3389/fcvm.2022.1014796. eCollection 2022.

DOI:10.3389/fcvm.2022.1014796
PMID:36407445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9669710/
Abstract

PURPOSE

This study aimed to identify and correlate pathological findings with clinical outcomes in patients after orthotopic heart transplantation (OHT) who either died or underwent a re-transplantation.

METHODOLOGY AND STUDY DESIGN

Single-center retrospective analysis of primary OHT patients who died or were re-transplanted between October 2012 and July 2021. Clinical data were matched with corresponding pathological findings from endomyocardial biopsies on antibody-mediated rejection, cellular rejection, and cardiac allograft vasculopathy. Re-assessment of available tissue samples was performed to investigate acute myocardial injury (AMI) as a distinct phenomenon. These were correlated with clinical outcomes, which included severe primary graft dysfunction. Patients were grouped according to the presence of AMI and compared.

RESULTS

We identified 47 patients with truncated outcomes after the first OHT. The median age was 59 years, 36 patients (76%) were male, 25 patients (53%) had a prior history of cardiac operation, and 21 patients (45%) were supported with a durable assist device before OHT. Of those, AMI was identified in 22 (47%) patients (AMI group), and 25 patients had no AMI (non-AMI group). Groups were comparable in baseline and perioperative data. Histopathological observations in AMI group included a non-significant higher incidence of antibody-mediated rejection Grade 1 or higher (pAMR ≥ 1) (32% vs. 12%, = 0.154), and non-significant lower incidence of severe acute cellular rejection (ACR ≥ 2R) (32% vs. 40%, = 0.762). Clinical observations in the AMI group found a significantly higher occurrence of severe primary graft dysfunction (68% vs. 20%, = 0.001) and a highly significant shorter duration from transplantation to death or re-transplantation (42 days [IQR 26, 120] vs. 1,133 days [711-1,664], < 0.0001). Those patients had a significantly higher occurrence of cardiac-related deaths (64% vs. 24%, = 0.020). No difference was observed in other outcomes.

CONCLUSION

In heart transplant recipients with a truncated postoperative course leading to either death or re-transplantation, AMI in endomyocardial biopsies was a common pathological phenomenon, which correlated with the clinical occurrence of severe primary graft dysfunction. Those patients had significantly shorter survival times and higher cardiac-related deaths. The presence of AMI suggests a truncated course after OHT.

摘要

目的

本研究旨在确定原位心脏移植(OHT)后死亡或接受再次移植患者的病理结果,并将其与临床结局相关联。

方法和研究设计

对2012年10月至2021年7月期间死亡或接受再次移植的原发性OHT患者进行单中心回顾性分析。将临床数据与心内膜心肌活检中关于抗体介导的排斥反应、细胞排斥反应和心脏移植血管病变的相应病理结果进行匹配。对可用组织样本进行重新评估,以研究急性心肌损伤(AMI)这一独特现象。将这些结果与临床结局相关联,临床结局包括严重原发性移植物功能障碍。根据是否存在AMI对患者进行分组并比较。

结果

我们确定了47例首次OHT后结局不佳的患者。中位年龄为59岁,36例(76%)为男性,25例(53%)有心脏手术史,21例(45%)在OHT前使用了耐用辅助装置。其中,22例(47%)患者被确定为发生AMI(AMI组),25例患者未发生AMI(非AMI组)。两组在基线和围手术期数据方面具有可比性。AMI组的组织病理学观察结果包括抗体介导的排斥反应1级或更高(pAMR≥1)的发生率略高但无统计学意义(32%对12%,P = 0.154),以及严重急性细胞排斥反应(ACR≥2R)的发生率略低但无统计学意义(32%对40%,P = 0.762)。AMI组的临床观察发现,严重原发性移植物功能障碍的发生率显著更高(68%对20%,P = 0.001),从移植到死亡或再次移植的持续时间显著更短(42天[IQR 26,120]对1133天[711 - 1664],P < 0.0001)。这些患者心脏相关死亡的发生率显著更高(64%对24%,P = 0.020)。在其他结局方面未观察到差异。

结论

在术后病程不佳导致死亡或再次移植的心脏移植受者中,心内膜心肌活检中的AMI是一种常见的病理现象,与严重原发性移植物功能障碍的临床发生相关。这些患者的生存时间显著更短,心脏相关死亡发生率更高。AMI的存在提示OHT后病程不佳。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/7898d771f0ec/fcvm-09-1014796-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/18bc10b98915/fcvm-09-1014796-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/f860bc74e7c8/fcvm-09-1014796-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/7898d771f0ec/fcvm-09-1014796-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/18bc10b98915/fcvm-09-1014796-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/f860bc74e7c8/fcvm-09-1014796-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70c4/9669710/7898d771f0ec/fcvm-09-1014796-g003.jpg

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