Q-T interval (QTC) in patients with cirrhosis: relation to vasoactive peptides and heart rate

• Published in: Scandinavian journal of clinical and laboratory investigation Vol. 67; no. 6; pp. 643 - 653
• Main Authors: Henriksen, J. H., Gülberg, V., Fuglsang, S., Schifter, S., Bendtsen, F., Gerbes, A. L., Møller, S.
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.01.2007; Taylor & Francis
• Subjects: Adult; Aged; Bazett correction; Blood Pressure; Calcitonin Gene-Related Peptide - blood; calcitonin gene-related peptides; Cardiac Pacing, Artificial; Catecholamines - blood; cirrhotic cardiomyopathy; Electrocardiography; Endothelin-1 - blood; Endothelin-3 - blood; endothelins; Endothelins - blood; Female; Fridericia correction; heart frequency correction of Q-T interval; Heart Rate; Hemodynamics; Humans; Hypertension, Portal - complications; Liver Cirrhosis - complications; liver dysfunction; Long QT Syndrome - blood; Long QT Syndrome - diagnosis; Long QT Syndrome - etiology; Male; Middle Aged; portal hypertension; Reference Values; sympathoadrenal activity; vasoactive peptides
• ISSN: 0036-5513; 1502-7686
• DOI: 10.1080/00365510601182634

Objective. Prolonged Q-T interval (QT) has been reported in patients with cirrhosis who also exhibit profound abnormalities in vasoactive peptides and often present with elevated heart rate (HR). The aim of this study was to relate QT to the circulating level of endothelins (ET-1 and ET-3) and calcitonin gene-related peptide (CGRP) in patients with cirrhosis. In addition, we studied problems with HR correction of QT. Material and methods. Forty-eight patients with cirrhosis and portal hypertension were studied during a haemodynamic investigation. Circulating levels of ETs and CGRP were determined by radioimmunoassays. Correction of QT for HR above 60 beats per min was performed using the methods described by Bazett (QTC) and Fridericia (QTF). Results. Prolonged QTC (above 440 ms), found in 56 % of the patients, was related to the presence of significant portal hypertension and liver dysfunction (p<0.05 to 0.001), but not to elevated ET-1, ET-3 or CGRP. When corrected according to Bazett, QTC showed no significant relation to differences in HR between patients (r = 0.07, ns). QTF showed some undercorrection of HR (r = −0.36; p<0.02). During HR variation in the individual patient, QTC revealed a small but significant overcorrection (2.6 ms per heartbeat per min; p<0.001). This value was significantly (p<0.02) smaller with QTF (1.2 ms per heartbeat per min). Conclusions. The prolonged QTC in cirrhosis is related to liver dysfunction and the presence of portal hypertension, but not to the elevated powerful vasoconstrictor (ET-1) or vasodilator (CGRP, ET-3) peptides. The problems with correction of the QT for elevated HR in cirrhosis are complex, and the lowest HR should be applied for determination of the QT.