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

Abstract

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 (QT_C) and Fridericia (QT_F). Results. Prolonged QT_C (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, QT_C showed no significant relation to differences in HR between patients (r = 0.07, ns). QT_F showed some undercorrection of HR (r = −0.36; p<0.02). During HR variation in the individual patient, QT_C 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 QT_F (1.2 ms per heartbeat per min). Conclusions. The prolonged QT_C 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.

• Bazett correction
• calcitonin gene‐related peptides
• cirrhotic cardiomyopathy
• endothelins
• Fridericia correction
• heart frequency correction of Q‐T interval
• liver dysfunction
• portal hypertension
• sympathoadrenal activity
• vasoactive peptides

Acknowledgements

We express our gratitude to Alice Rudbøl (technician), Georgina Narvaez (secretary), Hanne B. Hansen, MSc and Rosemary Sørensen for skilful assistance. The work was supported by a grant from Savværksejer Jeppe Juhl og Hustru Ovita Juhl's Mindefond.