American Journal of Cardiology
Volume 79, Issue 10 , Pages 1339-1342, 15 May 1997

Effect of coronary angioplasty on precordial QT dispersion

From The Division of Cardiology, Foothills Hospital & The University of Calgary, Calgary, Alberta, Canada

Received 19 September 1996; received in revised form 3 February 1997; accepted 4 February 1997.

Abstract 

Dispersion of the QT interval is a measure of inhomogeneity of ventricular repolarization. Because ischemia is associated with regional abnormalities of conduction and repolarization, we hypothesized that the surface electrocardiographic interval dispersion would increase in patients with symptomatic coronary artery disease in the absence of myocardial infarction and that successful revascularization would reduce QT interval dispersion. Thirty-seven consecutive patients with ischemia due to 1-vessel coronary artery disease without prior myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA) were evaluated. Standard 12-lead electrocardiograms were performed 24 hours before, 24 hours after, and late (>2 months) after PTCA. Precordial QT interval dispersions were determined from differences in the maximum and minimum corrected QT intervals. Mean QT interval dispersion before PTCA was 60 ± 9 ms, immediately after PTCA 23 ± 14 ms (p < 0.001), and late after PTCA 29 ± 18 ms (p < 0.001 vs before PTCA). The shortest precordial QT interval increased immediately after PTCA (367 ± 40 vs 391 ± 39 ms; p < 0.02) and then remained stable late after PTCA (376 ± 36 ms, p = NS vs immedately after PTCA). Symptomatic recurrent ischemia in 8 patients with documented restenosis increased QT interval dispersion (56 ± 15 ms [p < 0.01] vs 25 ± 14 ms immediately after PTCA), which decreased again after successful repeat PTCA (22 ± 13 ms [p < 0.01] vs before the second PTCA). QT interval dispersion decreases after successful coronary artery revascularization and increases with restenosis. Therefore, QT interval dispersion may be a marker of recurrent ischemia due to restenosis after PTCA.

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 This study was supported by the Heart and Stroke Foundation of Alberta.

PII: S0002-9149(97)00136-7

American Journal of Cardiology
Volume 79, Issue 10 , Pages 1339-1342, 15 May 1997