Early and midterm risk of coronary allograft vasculopathy in patients bridged to orthotopic heart transplantation with ventricular assist devices.


Journal Article

BACKGROUND: Coronary transplant vasculopathy (CAV) has been associated with both immunologic and nonimmunologic factors. The impact of preoperative ventricular assist device (VAD) support on the development of CAV has not been studied. To examine this, we obtained posttransplant coronary angiograms from a group of patients bridged with VAD and compared them to post transplant coronary angiograms of a non-VAD cohort. METHODS: Adult patients undergoing orthotopic heart transplant between 1996-2000 were retrospectively studied and divided into VAD and non-VAD patients. Coronary angiograms were retrospectively reviewed and severity of coronary vasculopathy was categorized as trivial, mild, moderate, or severe. Other variables studied included recipient and donor demographics, cytotoxic panel reactive antibodies (PRA) against T-cell targets and flow cytometric crossmatching against donor T lymphocytes. RESULTS: There was no significant difference between groups regarding demographics. However, VAD patients had a sixfold greater chance of having a T-cell PRA >10% at the time of transplant (p < 0.05), and a fourfold greater chance of having a positive cross match when compared to non-VAD patients (p < 0.05). There was no significant difference in the degree of CAV between groups. Normal coronary anatomy was present in 76% of VAD patients and 64% of non-VAD patients (p = 0.37). These results were similar at 2- and 3-year follow-up (76 vs. 74% and 80 vs. 62%, respectively). CONCLUSION: Preoperative VAD use is associated with increased sensitization; however, these patients develop CAV at the same rate as those not bridged with a VAD.

Full Text

Cited Authors

  • Gonzalez-Stawinski, GV; Cook, DJ; Chang, ASY; Atik, F; Navia, JL; Banbury, M; Roselli, E; Young, JB; Starling, RA; Smedira, NG

Published Date

  • May 15, 2005

Published In

Volume / Issue

  • 79 / 9

Start / End Page

  • 1175 - 1179

PubMed ID

  • 15880065

Pubmed Central ID

  • 15880065

International Standard Serial Number (ISSN)

  • 0041-1337

Digital Object Identifier (DOI)

  • 10.1097/00007890-200505150-00041


  • eng

Conference Location

  • United States