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Pretransplant dyslipidaemia influences primary graft dysfunction after lung transplantation

Cottini, Silvia R. ; Ehlers, Ulrike E. ; Pagnamenta, Alberto ; Brandi, Giovanna ; Weder, Walter ; Schuepbach, Reto A. ; Béchir, Markus ; Benden, Christian

In: Interactive CardioVascular and Thoracic Surgery, 2016, vol. 22, no. 4, p. 402-405

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    Title
    • Pretransplant dyslipidaemia influences primary graft dysfunction after lung transplantation
    Author
    • Cottini, Silvia R.. Surgical Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland
    • Ehlers, Ulrike E.. Surgical Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland
    • Pagnamenta, Alberto. Department of Intensive Care Medicine of the Ente Ospedaliero Cantonale (EOC), Intensive Care Unit of Regional Hospital of Mendrisio, Mendrisio, Switzerland
    • Brandi, Giovanna. Surgical Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland
    • Weder, Walter. Division of Thoracic Surgery, University Hospital Zurich, Zurich, Switzerland
    • Schuepbach, Reto A.. Surgical Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland
    • Béchir, Markus. Surgical Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland
    • Benden, Christian. Division of Pulmonary Medicine, University Hospital Zurich, Zurich, Switzerland
    Document Type
    • Postprint
    Language
    • English
    Published in
    • Interactive CardioVascular and Thoracic Surgery, 2016, vol. 22, no. 4, p. 402-405. Oxford University Press
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:332913
    Summary
    Abstract OBJECTIVES Primary graft dysfunction (PGD) is a major cause of mortality within the first year following lung transplantation. Pulmonary hypertension, elevated body mass index (BMI), prolonged ischaemic time of the graft, intraoperative blood transfusions >1000 ml and the use of cardiopulmonary bypass or extracorporeal membrane oxygenation increase the risk for PGD. We aimed to evaluate whether dyslipidaemia is an additional risk factor for the development of PGD. METHODS We retrospectively analysed demographic and clinical data of 264 patients who received their first bilateral lung transplantation between March 2000 and October 2013 at our institution. The endpoint was PGD grade 3 at any time, defined according to the International Society for Heart and Lung Transplantation (ISHLT) criteria. Fasting lipid profiles at listing time or just before transplantation (baseline) were documented and dyslipidaemia was defined as any of the parameters being out of range. Comparisons of continuous variables between patients with PGD grade 3 and patients without were performed with the Mann-Whitney U-test, whereas proportions were compared with the χ2 test. Continuous variables were presented as arithmetic means with standard deviation for ease of comparison, but levels of statistical significance were computed using the appropriate non-parametric statistical test. To identify PGD risk factors, a forward stepwise logistic regression model was used. RESULTS PGD occurred in 63 recipients (24%). Pretransplant dyslipidaemia was documented in 153 recipients (58%) and was significantly more prevalent among recipients developing PGD (45 vs 108, P < 0.013). Despite various underlying pulmonary pathologies, higher triglyceride (TG) levels (1.41 ± 0.78 vs 1.16 ± 0.78, P < 0.012), lower high-density lipoprotein-cholesterol (HDL-C) concentrations (1.24 ± 0.55 vs 1.57 ± 0.71, P < 0.0005) and higher cholesterol/HDL-C values (3.80 ± 2.02 vs 3.00 ± 0.92, P < 0.0005) were associated with a lower incidence of PGD. Patients with PGD had significantly longer ischaemic time (350 ± 89 vs 322 ± 91, P = 0.017) and higher BMI (23 ± 5 vs 21 ± 4.4, P < 0.007). CONCLUSIONS Dyslipidaemia seems to be an independent risk factor for PGD after lung transplantation: low circulating levels of HDL-C and hypertriglyceridaemia increase the incidence of PGD. Even if HDL-C levels are difficult to alter today, triglyceride and cholesterol levels can be addressed therapeutically and may have a positive influence on the development of PGD.