TY - JOUR
T1 - Importance of hepatitis C coinfection in the development of QT prolongation in HIV-infected patients
AU - Nordin, Charles
AU - Kohli, Amit
AU - Beca, Sorin
AU - Zaharia, Valentin
AU - Grant, Taneisha
AU - Leider, Jason
AU - Marantz, Paul
PY - 2006/4
Y1 - 2006/4
N2 - 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.
AB - 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.
KW - Albumin
KW - Cardiomyopathy
KW - HIV disease
KW - Hepatitis C
KW - QT prolongation
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U2 - 10.1016/j.jelectrocard.2005.09.001
DO - 10.1016/j.jelectrocard.2005.09.001
M3 - Article
C2 - 16580420
AN - SCOPUS:33645405364
SN - 0022-0736
VL - 39
SP - 199
EP - 205
JO - Journal of Electrocardiology
JF - Journal of Electrocardiology
IS - 2
ER -