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Vol. 62. Issue 4.
Pages 462-463 (April 2009)
Vol. 62. Issue 4.
Pages 462-463 (April 2009)
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Francisco L Gadaletaa
a H.I.G.A. Eva Perón, Buenos Aires, Argentina
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To the Editor:

Since 2003, when we published our first series of 102 patients, the objective was to call attention to a new application for measuring the QTc interval in patients with acute coronary syndrome without ST elevation. We showed that it was capable of predicting future ischaemic events and not arrhythmic ones.1 The interesting work of Moreno et al is of the same indication. They were able to find out viable myocardial presence by dobutamine infusion and by using QT dispersion (QTd). By employing low dosages of dobutamine (10 µg), they found significant differences (71.5 [21.5] and 56.3 [17.4] ms) in patients with viable and non-viable myocardium, respectively (P=.021) and even greater QTdc (86.1 [30.8] and 60.0 [20.1] ms respectively; P=.013). Finally, they concluded that a QTdc >59 ms predicted myocardial viability. In 1979 Greeberg et al were the first to discuss QTc variations in the stress test.2 Some years later, Sporton et al3 induced myocardial ischaemia with atrial stimulation in 24 patients and observed a clear increase of QTd in coronary patients compared to normal ones. In synchrony, by applying QTd to the stress test, Roukema et al4 showed for the first time that this is greater in coronary patients than in non-coronary controls (74 [7] compared to 40 [4]; P<.003). Recently, Carluccio et al5 studied the development of contraction anomalies evaluated by bidimensional echocardiograms and those induced by dipyridamole infusion. They observed 2 interesting facts; the first was the prolongation of maximum QT in patients who developed contractility alterations. The second was the increase of QTd in those with significant coronary lesions and in those where alteration of contractility was produced. However, in coronary patients with a negative dipyridamole test, the QTd had no variation. Some received a second dosage of dipyridamole for contractile anomaly to appear, and in those, the QTd increase was at 162 % (64%). Finally, the use of aminophylline to resolve ischaemia not only reversed motility changes, but also normalized the QTd.

Finally, I believe the work of Moreno et al offers an important contribution to the application of QT and QTd intervals as predictors of ischaemic events, and as they say, given the low cost and universal availability, they should be sufficiently studied in the future.

Gadaleta FL, Llois SC, Lapuente AR, Batchvarov VN, Kaski JC..
Prognostic value of corrected QT-interval prolongation in patients with unstable angina pectoris.
Am J Cardiol, 92 (2003), pp. 203-5
Greeberg PS, Friscia DA, Ellstead MH..
Predictive accuracy of QX/QT ratio, QTc interval, ST depression and R wave amplitude during stress testing.
Am J Cardiol, 44 (1979), pp. 18-23
Sporton SC, Taggart P, Sutton PM, Walker JM, Hardman SM..
Acute ischaemia: a dynamic influence on QT dispersion.
Roukema G, Singh JP, Meijs M, Carvalho C, Hart G..
Effect of exercise-induced ischemia on QT interval dispersion.
Am Heart J, 135 (1998), pp. 88-92
Carluccio E, Biagioli P, Bentivoglio M, Mariotti M, Politano M, Savino K, et al..
Effects of acute myocardial ischemia on QT dispersion by dipyridamole stress echocardiography.
Am J Cardiol, 91 (2003), pp. 385-90
Revista Española de Cardiología (English Edition)

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