Impact of cytokine release on ventricular function after hepatic reperfusion: a prospective observational echocardiographic study with tissue Doppler imaging

Marco P Zalunardo, Martin Schläpfer, Beatrice Beck-Schimmer, Burkhardt Seifert, Donat R Spahn, Dominique Bettex, Marco P Zalunardo, Martin Schläpfer, Beatrice Beck-Schimmer, Burkhardt Seifert, Donat R Spahn, Dominique Bettex

Abstract

Background: Postreperfusion syndrome and haemodynamic instability are predictors for poor outcome after liver transplantation. Cytokine release has been claimed to be responsible for postreperfusion syndrome. However, the underlying pathophysiologic mechanism is not clarified. The aim of this prospective observational study was to correlate cardiac performance (measured by transoesophageal echocardiography (TEE), Doppler and Tissue Doppler Imaging (TDI)) to plasmatic cytokines: IL-6, IL-8, CXCL1, TGF-β and CD40L at 5 different time points during liver transplantation.

Methods: Seventeen consecutive patients scheduled for orthotopic liver transplantation, age 18 to 75 years without contraindication for transoesophageal echocardiography were included. Patients were monitored with TEE and TDI. Systolic and diastolic cardiac function, MAP, MPAP, CVP, PCWP, CO and blood samples for cytokine assays were recorded or collected after induction, 15 min after vena cava inferior clamping, 2 to 5 min after reperfusion, 60 min after reperfusion and at the end of surgery.

Results: Mean arterial pressure and catecholamine requirements remained unchanged, MPAP, CVP and CO increased, SVR decreased after unclamping. Postreperfusion syndrome did not develop. The haemodynamic parameters and the variations of TEE parameters were consistent with the volume load changes during clamping and declamping and did not reveal systolic or diastolic cardiac dysfunction. All cytokines, except TGF-β, increased.

Conclusion: These findings suggest, that significant cytokine release during liver transplantation is not necessarily coincident with haemodynamic instability and impaired cardiac function.

Trial registration: ClinicalTrials.gov: NCT00547924.

Figures

Fig. 1
Fig. 1
Haemodynamic parameters. Mean arterial pressure (a), cardiac output (b) and systemic vascular resistance (c) at the different time points of the study. ¶ increase of cardiac output from a baseline to c immediate reperfusion (p < 0,001). § increase of cardiac output from b clamping the vena cava inferior to c immediate reperfusion (p < 0,001). + increase of systemic vascular resistance from a baseline to b clamping the vena cava inferior (p = 0,004). # decrease of systemic vascular resistance from a baseline to c immediate reperfusion (p = 0,002). ‡ decrease of systemic vascular resistance from b clamping the vena cava inferior to c immediate reperfusion (p < 0,001)

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Source: PubMed

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