Abstract
Although interferon (IFN) shows cardiotoxicity and arrhythmogenesis, the influence of IFN on signal-averaged electrocardiography remains to be clarified. The aim of this study was to test a clinical hypothesis that IFN therapy for hepatitis C virus may induce ventricular late potentials (LPs) and related arrhythmias in patients with chronic active hepatitis. Signal-averaged and ambulatory electrocardiograms were recorded sequentially in patients with chronic active hepatitis C (n = 22) throughout the entire period of IFN therapy. The filtered QRS duration (fQRS) and low amplitude (< 40 μV) signal duration (LAS40) were significantly increased (95.5 ± 8.5 to 99.6 ± 9.4 msec, P < 0.0001, and 32.8 ± 3.1 to 36.3 ± 3.0 msec, P < 0.0001, respectively), whereas the root mean square voltage in the terminal 40 msec of the fQRS (RMS40) was significantly decreased (25.5 ± 5.4 to 22.3 ± 5.2 μV, P < 0.005) 1 month after starting the IFN therapy. The ventricular LP was negative in all subjects before starting therapy, but became positive in 7 patients after the therapy commenced. There were no differences in clinical baseline characteristics between the LP-positive (n = 7) and LP-negative (n = 15) groups. Significant increases in mean heart rate, fQRS, and LAS40 were observed after starting the therapy, irrespective of the appearance of the ventricular LP, whereas a decrease in RMS40 was observed only in the LP-positive group. No sustained ventricular arrhythmias were documented in the ambulatory electrocardiography and no cardiac events were encountered in the follow-up period. Therefore, the results indicate a reversible and subclinical risk of IFN-induced arrhythmogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 1033-1040 |
| Number of pages | 8 |
| Journal | International heart journal |
| Volume | 46 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Dec 1 2005 |
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All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
Cite this
Influence of interferon therapy on signal-averaged and ambulatory electrocardiograms in patients with chronic active hepatitis. / Hiramatsu, Shin Ichi; Maruyama, Toru; Ito, Hiroyuki; Shimoda, Shinji; Kaji, Yoshikazu; Harada, Mine.
In: International heart journal, Vol. 46, No. 6, 01.12.2005, p. 1033-1040.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Influence of interferon therapy on signal-averaged and ambulatory electrocardiograms in patients with chronic active hepatitis
AU - Hiramatsu, Shin Ichi
AU - Maruyama, Toru
AU - Ito, Hiroyuki
AU - Shimoda, Shinji
AU - Kaji, Yoshikazu
AU - Harada, Mine
PY - 2005/12/1
Y1 - 2005/12/1
N2 - Although interferon (IFN) shows cardiotoxicity and arrhythmogenesis, the influence of IFN on signal-averaged electrocardiography remains to be clarified. The aim of this study was to test a clinical hypothesis that IFN therapy for hepatitis C virus may induce ventricular late potentials (LPs) and related arrhythmias in patients with chronic active hepatitis. Signal-averaged and ambulatory electrocardiograms were recorded sequentially in patients with chronic active hepatitis C (n = 22) throughout the entire period of IFN therapy. The filtered QRS duration (fQRS) and low amplitude (< 40 μV) signal duration (LAS40) were significantly increased (95.5 ± 8.5 to 99.6 ± 9.4 msec, P < 0.0001, and 32.8 ± 3.1 to 36.3 ± 3.0 msec, P < 0.0001, respectively), whereas the root mean square voltage in the terminal 40 msec of the fQRS (RMS40) was significantly decreased (25.5 ± 5.4 to 22.3 ± 5.2 μV, P < 0.005) 1 month after starting the IFN therapy. The ventricular LP was negative in all subjects before starting therapy, but became positive in 7 patients after the therapy commenced. There were no differences in clinical baseline characteristics between the LP-positive (n = 7) and LP-negative (n = 15) groups. Significant increases in mean heart rate, fQRS, and LAS40 were observed after starting the therapy, irrespective of the appearance of the ventricular LP, whereas a decrease in RMS40 was observed only in the LP-positive group. No sustained ventricular arrhythmias were documented in the ambulatory electrocardiography and no cardiac events were encountered in the follow-up period. Therefore, the results indicate a reversible and subclinical risk of IFN-induced arrhythmogenesis.
AB - Although interferon (IFN) shows cardiotoxicity and arrhythmogenesis, the influence of IFN on signal-averaged electrocardiography remains to be clarified. The aim of this study was to test a clinical hypothesis that IFN therapy for hepatitis C virus may induce ventricular late potentials (LPs) and related arrhythmias in patients with chronic active hepatitis. Signal-averaged and ambulatory electrocardiograms were recorded sequentially in patients with chronic active hepatitis C (n = 22) throughout the entire period of IFN therapy. The filtered QRS duration (fQRS) and low amplitude (< 40 μV) signal duration (LAS40) were significantly increased (95.5 ± 8.5 to 99.6 ± 9.4 msec, P < 0.0001, and 32.8 ± 3.1 to 36.3 ± 3.0 msec, P < 0.0001, respectively), whereas the root mean square voltage in the terminal 40 msec of the fQRS (RMS40) was significantly decreased (25.5 ± 5.4 to 22.3 ± 5.2 μV, P < 0.005) 1 month after starting the IFN therapy. The ventricular LP was negative in all subjects before starting therapy, but became positive in 7 patients after the therapy commenced. There were no differences in clinical baseline characteristics between the LP-positive (n = 7) and LP-negative (n = 15) groups. Significant increases in mean heart rate, fQRS, and LAS40 were observed after starting the therapy, irrespective of the appearance of the ventricular LP, whereas a decrease in RMS40 was observed only in the LP-positive group. No sustained ventricular arrhythmias were documented in the ambulatory electrocardiography and no cardiac events were encountered in the follow-up period. Therefore, the results indicate a reversible and subclinical risk of IFN-induced arrhythmogenesis.
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U2 - 10.1536/ihj.46.1033
DO - 10.1536/ihj.46.1033
M3 - Article
VL - 46
SP - 1033
EP - 1040
JO - International Heart Journal
JF - International Heart Journal
SN - 1349-2365
IS - 6
ER -