We are grateful to Fiol Sala et al for their comments regarding our publication.1 In their experience, “the De Winter ECG pattern” could be explained by incomplete occlusion of the left anterior descending artery, which would explain the absence of ST elevation. This affirmation is in contrast to the observations of the De Winter group,2 who highlighted the invariability of the ECG pattern from first medical contact until arrival in the catheterization laboratory, as most patients (86%) had TIMI flow 0 or 1 on coronary angiography. The presence or absence of collaterals does not appear to be a determinant either, given that only 28% of cases in that series had collaterals (Rentrop 2-3) in the territory of the left anterior descending artery. The role of ischemic preconditioning in this context is unknown. The above series did not mention the existence of angina prior to the episode that could have indicated intermittent occlusion of the artery before complete thrombosis. None of our patients had previous angina symptoms. In contrast to the case described by Dressler et al,3 in which presumably there was complete occlusion of the proximal left anterior descending artery despite the absence of angiographic confirmation, coronary reperfusion prevented observation of further ECG evolution. Therefore, we concur with Fiol Sala et al that ST-elevation is possible in the absence of coronary flow restoration.
In the case presented by Fiol Sala et al, Figure B does not show the characteristic “De Winter pattern” of ST-depression at the J-point, by which we mean that it is not a valid example to illustrate the previously presented concept.
We appreciate the proposed pathophysiological mechanism, which is added to those previously suggested.2,4 However, the characteristic large infarct extension and subsequent ECG evolution after angioplasty indicate involvement beyond the subendocardium. This is in contrast to previous observations that related ST-segment-depression with prominent positive T waves to localized subendocardial ischemia.4