Changes in ventricular repolarization during percutaneous transluminal coronary angioplasty in humans assessed by QT...

Based on clinical, epidemiological, and experimental data, transient cardiac ischaemia is one of the major triggering factors of malignant ventricular arrhythmia. According to animal studies, increased dispersion of repolarization is of pathophysiological relevance in this context. Therefore we explored the impact of myocardial ischaemia during single vessel coronary angioplasty on the change in ventricular repolarization, measured by QT and JT intervals and their dispersion in the 12-lead electrocardiogram. We also assessed a novel method, the 3-dimensional T vector loop, to find out whether it was sensitive to changes in ventricular repolarization during ischaemia, and whether there was any correlation with changes in the dispersion of the QT and/or JT intervals.

This study was prospective with consecutive patients. Only patients in sinus rhythm and without bundle branch block were included.

All coronary angioplasties were performed at Norrlands University Hospital, Umeå. The analysis of the material was performed at the Karolinska Hospital, Stockholm.

Twenty-nine consecutive patients went through 30 elective one-vessel percutaneous transluminal coronary angioplasty (PTCA) procedures. PTCA was performed in 10 stenoses of the left anterior descending, 10 of the left circumflex, and 10 of the right coronary artery.

A 12-lead electrocardiogram was recorded continuously as part of routine monitoring of the patient during PTCA and the T vector loop was calculated from the simultaneously recorded. X, Y, Z leads.

Repolarization was assessed by the QRS, QT and JT intervals as well as by the T vector loop parameters (Tarea, Tavplan, and Teigenv) before and at the end of the first occlusion during PTCA.

PTCA, with an average occlusion time of 171 +/- 60 s (mean +/- SD), induced ischaemia on the 12-lead electrocardiogram in 73% of cases. The overall response for the 30 procedures was a significantly increased dispersion of ventricular repolarization, both corrected and uncorrected for heart rate. QT dispersion increased by, on average, 19% from 74 +/- 35 to 88 +/- 36 ms, QTc dispersion by 27% from 71 +/- 39 to 90 +/- 42 ms, and JTc dispersion by 19% from 78 +/- 32 to 94 +/- 43 ms (P < 0.05). The T vector loop became more circular and bulgy during occlusion (all three parameters changed by between 33% and 59%). There was a significant correlation between changes in one of the T vector loop parameters (Teigenv), and changes in JT and QT dispersion in the left anterior descending group.

Transient ischaemia during PTCA induced significant changes in ventricular repolarization, especially during occlusion of the left anterior descending artery and resulted in a significant increase in both QT and QTc dispersion. The degree of QT dispersion was such that several patients were at risk of ventricular arrhythmia, if a proper triggering extrasystole had occurred. In addition, and as an original observation, the 3-dimensional T vector loop morphology seemed even more sensitive to coronary occlusion than QT dispersion.