To the Editor:

We have read with great interest the article of Núñez Gil et al1 recently published in this Journal. The authors report on a retrospective series of patients with transient midventricular dyskinesias (TMVD).

As they point out, the incidence of this new variant seems to be lower than that of the apical forms (TAD),1 although some authors report that they might be underestimated and that they constitute 30% to 40% of all such cases.2

We find it interesting to compare the series published by those authors with ours involving 14 patients, reviewed retrospectively, who were diagnosed over a period between October 2004 and December 20073; 13 patients had TAD and 1 had TMVD. The TMVD patients studied by Núñez Gil et al were younger than the TAD group in our center (59 [11] years vs 71 [8] years) and the most frequent finding at presentation was the presence of negative T waves (60%), in contrast to our group, in which ST segment elevation was the most common electrocardiographic abnormality (78%). In an exhaustive review of the literature, we have found 7 series of patients with TMVD. The majority also coincides in associating younger ages with the forms of TMVD, and there are no significant differences in terms of the remaining clinical and analytical variables. However, the authors of one of these reports conclude that TMVD, as compared to TAD, occurs in patients: of younger age (58 years vs 70 years; P=.02); with fewer cardiovascular risk factors (38% vs 77%; P=.01), especially a lower incidence of hypertension; with less frequent presence of negative T waves (69% vs 97%; P=.01) and a tendency to develop fewer complications during the acute phase (cardiogenic shock, arrhythmias, and left ventricular failure).4 These findings agree with those of Núñez Gil et al, who recorded no episodes of ventricular failure or shock.

It proves difficult to understand the localization of the changes in contractility, and it is curious that the new variants, like TMVD and the more recent basal forms,5 are being documented more than 10 years after the first reports of TAD. The widespread use of imaging techniques during the acute phase probably explains this fact. We coincide with Núñez Gil et al in that TMVD could be an incomplete or attenuated form in younger patients, triggered by less stressful events that, together with a particular distribution of adrenoceptors and sympathetic terminals, would provoke a peculiar form of ventricular dysynergy. Myocardial stunning is the most widely accepted pathophysiological basis. Along this line and based on previous studies,6,7 we demonstrated, using thrombolysis in myocardial infarction (TIMI) frame counts (TFC), in cases of TAD and of TMVD, the existence of microvascular dysfunction in the left coronary territory as compared to a control group of patients with normal coronary arteries3: TFC in anterior descending artery, 26 (4) versus 19 (1) (P=.0004) and TFC in circumflex artery, 23 (4) versus 18.5 (2.6) (P=.008). We found no significant differences in the TFC in the right coronary territory. We do not know whether or not these findings are in some way related to the high prevalence of recurrent anterior descending artery in our series (57%, similar to that observed by Núñez Gil et al in their TMVD group), which has not been reported for other series. This raises the question as to whether the microvascular dysfunction could be a cause or a consequence of myocardial toxicity induced by catecholamines.

Future studies will surely resolve this enigma, which persists 18 years after the initial report of the syndrome. Until then, we should keep an open mind to the close relationship between brain and heart and consider TMVD to be a particular form within the spectrum of stress cardiomyopathy.