To the Editor:
We have read the interesting article from Gadaleta et al1 on prolongation of the corrected QT interval as an independent predictor of risk in acute coronary syndrome without ST elevation.
We present our study's data. It included 40 patients with demonstrated ischaemic cardiopathy, who had an echocardiography stress test taken with dobutamine, with the intention of studying the presence of viable myocardium, which was considered as improved basal contractility in 2 or more segments and in at least 1 point. The protocol consisted of 3 min phases with increasing dosages of dobutamine (5.10 and 20 µg/kg/min). An ECG of 12 derivations was recorded basally and at the end of each phase. The maximum and minimum QT intervals were evaluated; the dispersion (QTD) is the difference between the 2. The QT intervals were corrected according to Bazett's formula (QTDc). Patients with viable myocardium showed a greater QTD at low dobutamine dosages (10 µg) than ischaemic patients without viable myocardium, and differences were statistically significant (71.5 [21.5] and 56.3 [17.4] ms for patients with and without viable myocardium respectively; P=.021), and greater QTDc (86.1 [30.8] and 60 [20.1] ms respectively; P=.013). The ROC curve analysis showed an area below the curve of 0.76 (95% of confidence interval, 0.60-0.93; P=.008) (Figure). As a result, a QTDc >59 ms predicted myocardial viability with a sensitivity of 76.9% and specificity of 55.6%. However, the increase of QTD disappeared with higher dosages of dobutamine.
Figure 1. The ROC curve of QTD, where it shows that 59ms is the value which combines the best sensitivity and specificity for diagnosing myocardial viability.
Our data coincide with others who have observed that myocardial viability associates with lower QTD at rest and an increase with infusion of low dosages of dobutamine (10 µg).2,3 Although an even greater increase of QTD has been described with high dosages of dobutamine (20 µg), it seems to be related with inducible ischaemia. Consequently, those with persistent akinesia did not show changes in QTD.4
Myocardial viability after an AMI is associated with a heterogeneous myocardial repolarization, and therefore, seems to associate with a greater QTD. These patients present a greater arrhythmic risk with exercise and an increased incidence of recurring ischaemic events.2 It has been observed that changes in duration and QTD induced by exercise allow for identification of patients with a high risk of sudden death after an AMI.5
As a result, the measurement of QTD after an infusion of low dosages of dobutamine (10 µg) or during the completion of a stress test could help identify patients with viable myocardium after an AMI, with the resulting effects for the prognosis and procedure of these patients. The importance of this fact lies in the low cost and universal availability of ECG.