Importance of hepatitis C coinfection in the development of QT prolongation in HIV-infected patients

Charles Nordin, Amit Kohli, Sorin Beca, Valentin Zaharia, Taneisha Grant, Jason Leider, Paul Marantz

Research output: Contribution to journalArticlepeer-review

44 Scopus citations


Background: Case reports and unblinded studies suggest that human immunodeficiency virus (HIV) disease is associated with QT prolongation and torsade de pointes ventricular tachycardia. Hepatitis C coinfection is common in patients with HIV disease, and cirrhosis is also associated with QT prolongation. We therefore undertook a systematic analysis of the role of liver injury, nutritional state, and coinfection with hepatitis C in the etiology of QT prolongation in HIV disease. Methods: We performed a blinded, controlled retrospective cohort study of 1648 patients over a 3-year period at a university-affiliated municipal hospital. All electrocardiograms were included if patients with HIV disease had measurements of CD4 count and viral load within 3 months and serum electrolytes within 30 days (n = 816). Control subjects were chosen randomly from the general medicine service (n = 832). QT interval was measured in lead II and corrected for heart rate by Bazett's formula (QTc). Results: QTc was slightly but significantly longer in patients with HIV disease than in controls (443 ± 37 vs 436 ± 36 milliseconds, P < .001). Patients with hepatitis C had more pronounced QTc prolongation (452 ± 41 vs 437 ± 35 milliseconds, P < .001). CD4 count, HIV viral load, and HIV medications had no effect on QTc. When patients with hepatitis C were excluded from the analysis, there was no statistical difference between patients with HIV disease and controls (438 ± 34 vs 436 ± 36 milliseconds, P = .336). Multiple linear regression revealed that both HIV and hepatitis C infection predicted QTc prolongation, as did age, female sex, history of hypertension, use of opiates, low serum K+ and albumin, and high AST. Hepatitis C coinfection nearly doubled the risk of QTc of 470 milliseconds or greater in patients with HIV disease (29.6% vs 15.8%, P < .001). Conclusions: Human immunodeficiency virus and hepatitis C infections both independently prolong QTc. Coinfection with hepatitis C greatly increases the likelihood of clinically significant QTc prolongation in patients with HIV disease.

Original languageEnglish (US)
Pages (from-to)199-205
Number of pages7
JournalJournal of Electrocardiology
Issue number2
StatePublished - Apr 2006
Externally publishedYes


  • Albumin
  • Cardiomyopathy
  • HIV disease
  • Hepatitis C
  • QT prolongation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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