QT prolongation in end-stage liver disease: A result of altered sex hormone metabolism?

✍ Scribed by M H Lehmann

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 115 KB
• Volume: 26
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.510260137

✦ Synopsis

To the Editor: diac interaction would not constitute definitive proof of the I read with great interest the paper by Mohamed et al. 1 hypothesis, nor would possible parallel mechanisms (e.g., documenting a prolonged QT cmax in patients with end-stage autonomic) necessarily be excluded. liver disease that shortens after liver transplantation. The

The findings of Mohamed et al. 1 raise the intriguing possiauthors were able to exclude alterations in serum electrolyte bility that end-stage liver disease may serve as an unanticilevels as etiologic and suggested, instead, an autonomic pated natural experimental model for probing the recently mechanism on the basis of evidence of changes in indices appreciated relationship between sex hormones and cardiac of sympathetic and parasympathetic tone in many of the repolarization. patients.

An alternative explanation for the described QT-interval MICHAEL H. LEHMANN, M.D. changes worthy of consideration involves the well-known Sinai Hospital/Arrhythmia Center disturbances in sex hormone metabolism found in advanced 14800 West McNichols, Suite 410 liver disease. 2 A consistent sex disparity in the pathophysiol-Detroit, MI ogy of cardiac repolarization has recently emerged: women