QT interval prolongation in end-stage liver disease cannot be explained by nonhepatic factors.

Introduction: QT interval prolongation in patients with end-stage liver disease (ESLD) is common. However, electrolyte abnormalities, renal insufficiency, treatment with QT-prolonging drugs, and other factors known to prolong QT interval independently of liver disease occur frequently in ESLD. Moreover, elevated heart rate may be present in ESLD and result in spurious QTc prolongation if the Bazett formula is used for rate correction. It thus remains unclear whether QT prolongation in ESLD is directly caused by liver failure, or indirectly by these confounding factors.

Methods: Medical records of all patients (n = 437) who received orthotopic liver transplantation (OLTx) at our institution between 2008 and 2011 were reviewed. Data from 51 patients with available pre-OLTx dobutamine stress echo (DSE), post-OLTx ECG and without nonhepatic factors affecting QT interval duration were analyzed. For each patient, QT versus RR regression line was calculated from ECG tracings obtained during DSE. The QT interval on post-OLTx ECG was compared with the pre-OLTx QT predicted by the regression line for the same RR interval.

Results: QT interval shortened significantly post-OLTx (from 394 ± 47 to 364 ± 45 ms at RR interval 750 ± 144 ms; P < 0.002) when compared using the regression method. Corrected QT intervals calculated by Bazett and Fridericia formulas also shortened. Patients with prolonged QT pre-OLTx had significantly higher INR and lower serum albumin.

Conclusion: ESLD impairs ventricular repolarization even in the absence of other known factors affecting repolarization. QT prolongation in ESLD is associated with impaired synthetic liver function.