Evaluation of Tp-e interval and Tp-e/QT ratio in patients with chronic hepatitis B

C Demir1, M Demir2

  • 1Department of Infectious Disease, Şevket Yılmaz Education and Research Hospital, Bursa, Turkey.

Prague Medical Report
|February 4, 2014
PubMed

Insights

Chronic hepatitis B (CHB) patients show increased ventricular repolarization abnormalities, indicated by elevated Tp-e interval and Tp-e/QT ratio. These findings suggest a potential link between CHB, inflammation, and cardiac arrhythmia risk.

Area of Science:

  • Cardiology
  • Hepatology
  • Electrophysiology

Background:

  • Chronic hepatitis B (CHB) is a viral inflammatory liver disease.
  • Altered ventricular repolarization and impaired autonomic function are noted in CHB.
  • The Tp-e interval and Tp-e/QT ratio may reflect transmural dispersion of repolarization and arrhythmia risk.

Purpose of the Study:

  • To evaluate ventricular repolarization using Tp-e interval and Tp-e/QT ratio in CHB patients.
  • To assess the relationship between these repolarization parameters and inflammation in CHB.
  • To compare cardiac repolarization metrics between CHB patients and healthy controls.

Main Methods:

  • Fifty-five CHB patients and 50 controls were enrolled.
  • 12-lead electrocardiograms were used to measure Tp-e interval, corrected Tp-e (cTp-e), Tp-e/QT ratio, QT dispersion (QTd), and corrected QTd.
  • Statistical analysis compared these parameters between the CHB group and the control group.

Main Results:

  • CHB patients exhibited significantly increased QTd and corrected QTd compared to controls.
  • The cTp-e interval and Tp-e/QT ratio were significantly higher in CHB patients.
  • These findings indicate prolonged ventricular repolarization and increased dispersion in CHB patients.

Conclusions:

  • Ventricular repolarization is impaired in patients with chronic hepatitis B.
  • Elevated Tp-e interval and Tp-e/QT ratio in CHB patients suggest increased risk for ventricular arrhythmias.
  • Further research is warranted to explore the link between CHB, inflammation, and cardiac electrophysiological changes.

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