801-4 Prognostic Implications of QT and QU Interval Measures in Acute Myocardial Infarction

Abstract

Prolongation of the QT interval corrected using Bazett's formula (QTc) has been reported as a marker for increased risk of arrhythmic events after acute myocardial infarction (AMI). However, the QU interval changes have not been examined. At the same time, QU interval may be of clinical significance, especially in the light of recent experimental evidence linking the U wave with the subpopulation of the so-called M cells within myocardial wall. To evaluate prognostic significance of QT and QU interval measures in AMI, we studied 512 survivors of acute phase of their first myocardial infarction. Patients with conduction defects and drugs likely to affect QT measures were noT included into the analysis. The following intervals were estimated in all the measurable leads on a standard predischarge 12-lead ECG (25 mm/sec paper speed) using a digitizing pad — mean RR, mean and max QT, and mean QU. All QT and QU intervals were subsequently corrected for heart rate using Bazett's formula. At one year follow-up, 23 patients (Group I. 19 male. mean age 58.7 ± 8.9 years) suffered arrhythmic events (VT/VF or sudden cardiac death). This subset of patients was compared with arrhythmia-free group of 489 subjects (Group II, 385 male, mean age 56.1 ± 9.2 years). Statistical analysis was performed using unpaired t-test and ANOVA, results are expressed as mean ± SD. Group QT mean QTc mean QT max QTc max QU mean QUc mean I 358.7 ± 31.5 426.6 ± 30.7 396.5 ± 38.5 472.8 ± 40.3 459.5 ± 58.7 535.2 ± 41.3 II 387.3 ± 44.1 423.9 ± 24 421.7 ± 51.5 467.9 ± 79.1 552.0 ± 73.9 585.7 ± 55.1 p < 0.002 NS 0.02 NS 0.001 0.01 The significant difference in QU and QUc, but not in QT intervals persisted even after elimination of the effect of heart rate (ANOVA: p < 0.007 and 0.011, respectively). The differences in the QT but not QU interval measures in the 2 groups can be explained by differing heart rates. Shorter QU interval seemed to identify patients at risk of arrhythmic events after AMI. The pathophysiological basis for this finding is not clear, but could be related to differences in the subpopulation of M cells within myocardial wall.