Abstract

To the Editor: We read with interest the report by Kia et al 1 in a recent issue of American Journal of Transplantation. In this study, tricuspid regurgitation (TR) on pretransplant transthoracic echocardiography (TTE) was an independent predictor of reduced survival after liver transplantation. The authors hypothesized that back pressure with hepatic congestion, or poor cardiac reserve, could explain the association between TR and worse outcome. However, the increased mortality of the TR group was primarily beyond the perioperative period making it difficult to link TR with the causes of death. Furthermore, only 20% of TR was graded as being more severe than mild. Mild TR is common in the general population where it has not been linked with mortality 2, 3. In the hyperdynamic state of cirrhosis, a relatively high prevalence of mild but functionally insignificant TR might be expected 4. TTE is performed routinely in our unit during the transplant assessment process. An elevated estimated pulmonary artery systolic pressure or right ventricle dilatation precipitates further investigation with right heart catheterization. To validate Kia et al's 1 findings, we repeated their study in 236 patients transplanted for chronic liver disease between January 2007 and March 2010. Exclusion criteria were combined liver–kidney transplant, regraft and diagnosis of hepatopulmonary syndrome or portopulmonary hypertension. Data were obtained from a prospectively collected database and retrospective case-note review. Sixty-eight patients (28.8%) had TR (mild, 65 patients; moderate, 3 patients). Baseline characteristics are shown in Table 1. During the immediate postoperative period, TR and non-TR patients had a comparable frequency of renal replacement therapy (TR, 23.5%; non-TR, 19.0%, p = 0.439), length of stay in intensive care (TR, 3 days; non-TR, 2 days, median, p = 0.404) and hospital (TR, 13 days; non-TR, 11 days, median, p = 0.190). The estimated 1- and 3-year posttransplant survival was 91.9% and 85.1%, respectively for TR patients, and 88.3% and 82.0% for non-TR patients (log-rank, p = 0.509). No patient with moderate TR died during follow-up. The causes of death within 1 year of transplantation were sepsis (n = 8), hepatic artery thrombosis (n = 4), primary nonfunction (n = 2), cardiac (n = 2), hepatocellular carcinoma (n = 2) and others (n = 6). Five patients with TR (7.4%) and 19 patients without TR (11.3%) died by 1 year posttransplant (p = 0.362). After adjusting for age, Model for End-State Liver Disease (MELD) and donor risk index, there was no association between TR and 1-year mortality (odds ratio [OR] 0.61; 95% confidence interval [CI] 0.21–1.72, p = 0.349). Similarly, there was no association between TR and 1-year graft loss (death/retransplantation) (adjusted OR 0.95; 95% CI 0.40–2.28, p = 0.905). The pretransplant characteristics of our cohort differ from those reported by Kia et al (Table 2). It is possible that TR has greater prognostic relevance in patients with a higher MELD and more hyperdynamic state. Kia et al 1 did not report the impact of grade of TR on outcome, and moderate-to-severe TR may be more significant than mild. Moreover, their inclusion of patients with mild portopulmonary hypertension may be of importance. We conclude that in patients with a lower MELD score and without portopulmonary hypertension, mild TR on TTE may not be a useful indicator of worse outcome after liver transplantation. The observations of Kia et al 1 should be interpreted with caution. J. A. Leithead1,2*, K. Kandiah1, H. Steed1, B. K. Gunson1,2, R. P. Steeds3, and J. W. Ferguson1 1Liver Unit, Queen Elizabeth Hospital, Birmingham, UK 2NIHR Biomedical Research Unit and Centre for Liver Research, University of Birmingham, Birmingham, UK 3Department of Cardiology, Queen Elizabeth Hospital, Birmingham, UK *Corresponding author: Joanna Agnes Leithead, j.a.leithead@bham.ac.uk The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation.

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