ABC | Volume 112, Nº1, January 2019

Original Article Dotta et al Regional QT dispersion as predictor of reperfusion Arq Bras Cardiol. 2019; 112(1):20-29 Figure 3 – Behavior of the regional QT interval, corrected for heart rate, in subgroups of patients with failed reperfusion or failed rescue; data expressed as median and interquartile range (m,IQR); QTcD: dispersion of the QTc interval; TNK: tenecteplase; T3B3 (+): patients with TIMI 3 and Blush grade 3 in the culprit artery; T3B3 (-): patients with TIMI 3 and Blush grade < 3 in the culprit artery; Wilcoxon test. *Failed rescue: patients without ST-segment resolution and with optimal coronary and tissue perfusion [T3B3 (+)]; †failed reperfusion: patients with ST-segment resolution, without optimal coronary and tissue perfusion [T3B3 (-)]. Without ST-segment resolution With ST-segment resolution 33 4* 49 18† T3B3(+) T3B3(–) Failed reperfusion n = 18 p-value Failed rescue n = 4 p-value dQTcR (ms) Pre-TNKase 0.46 Pre-TNKase 0.06 42.5 (23.0-69.5) 8.0 (3.7-10.0) Post-TNKase Post-TNKase 31.0 (17.7-56.2) 35.0 (22.7-64.0) and Blush grades 3), especially in anterior wall infarction. On the other hand, different from previous reports on streptokinase and alteplase, 31,32 we used TNK, a fibrin-specific, recombinant tissue plasminogen activator, which has been shown better results regarding coronary reperfusion. Besides, we included a larger number of patients compared with previous studies. Regional QTcD in anterior wall infarction significantly increased in ECG obtained 60 minutes after thrombolysis in patients with adequate reperfusion (TIMI 3 and Blush grade 3), reinforcing the idea that QTcD following AMI depends on permeability of the culprit artery, as well on dimension and localization of the ventricular wall involved. One possible mechanism for our results is based on the effect of cardiac stunning caused by reperfusion injury. Besides, there is evidence that vascular, metabolic, mitochondrial, neuronal, thermal and electric processes contribute to post-reperfusion dysfunction. 33-35 Nevertheless, the exactmechanism, the adequate prevention of the ischemia-reperfusion lesion, and above all, the correlation of reperfusion injury with electrocardiographic findings have not been elucidated in the literature. 36 Considering the correlation between ECG leads and the infarcted area, it is possible to analyze the repolarization of the injured area. Calculation of the regional QTcD estimates heterogeneity of ventricular repolarization in the area at risk. Thereby, the need for a decision-making tool for fibrinolytic therapy emphasizes the importance of post-thrombolysis electrocardiographic reperfusion markers. ECG plays a crucial and more important role in PIS than in primary PCI. The identification of patients that meet reperfusion criteria and of those who should be referred for rescue PCI should be promptly and fast performed. A crucial point is the cost‑benefit of the system and the delay in the ideal time between fibrinolysis and PCI. Despite the large variation in this time window in the clinical trials, a time interval of 2‑24 hours after successful fibrinolysis. 37 The classical electrocardiographic criterion for reperfusion has a sensitivity and specificity of 60% and 80%, respectively. 38 We showed that both sensitivity and specificity increased when regional QTcD was added to ST-segment resolution, suggesting that this method may help to stratify patients in a more accurate way. Analysis of subgroups did not show significant differences in regional QTcD between patients with at least 50% ST‑segment resolution and inadequate flow by angiography [T3B3(-)], i.e ., patients with failed reperfusion, and patients without ST‑segment resolution but who showed angiographic reperfusion [T3B3 (+)]. Our study showed an increase in QTcD and regional QTcD in anterior wall infarction particularly in patients T3B3(+). In agreement with a previous study, 39 QTcD depends on the localization of AMI, and higher QTcD was observed in the anterior wall as compared with inferior wall acute myocardial infarction. The large area of infarction in this subgroup should have greater influence on repolarization vectors than on non- anterior wall infarction. This study indicates a possible step forward in the analysis of electrocardiographic variables, in light of current controversies of angiographic data, T3B3(-) showed worse ejection fraction and higher QTcD compared with the T3B3(+) subgroup, which may also have prognostic implications. Although QTcD is still a matter of controversy in electrocardiology, 40 some questions remain unanswered in the specialized literature. Studies on electrocardiographic variables using better estimation methods may yield interesting information in many medical scenarios. 26