Discussion of Questions

Question A. Takotsubo cardiomyopathy refers to a reversible syndrome characterized by an LV systolic dysfunction with no coronary obstructive cause^[1]. The singular TTS characteristics are the LV apical ballooning (Takotsubo format), LV akinetic apical region, and hyperkinetic base (compensatory stimulation)^[2-4]. This syndrome is related to an episode of physical or emotional stress (trigger) that can induce a high peak of catecholamines on the patient’s blood^[5].

Question B. The most accepted physiopathological theory for TTS proposes that an autonomic response for a high-stress episode induces an overload of cortisol and catecholamines in the patient’s blood. Also, there is a differential response for the peak of epinephrine in the beta-2 adrenergic receptors (negative response to high levels of epinephrine) and G-protein (beta-1) coupled receptors (positive response to high levels of epinephrine), and a differential aggrupation of those different receptors in specific areas of the ventricles (high presence of beta-1 receptors in the apical area with low beta-2, and high beta-2 receptors in a basal area with low beta-1)^[6]. Those characteristics produce the apical-basal gradient of hypocontractility and hypercontractility, converging in the Takotsubo format of the heart^[7]. Along with that, there is a vasospasm response of the epicardium and microvascular tissues which contributes to the ischemia and the similar aspect of the disease to myocardial infarction^[5,8].

Question C. There are no specific clinical signs suggestive of TTS. Most patients are admitted to the ER with typical precordial pain and short breathing, ECG with inverted, symmetric, and peaked T wave in one wall derivations added to ST-segment alterations^[9], and echo with a reduced ejection fraction, which are signs that make any doctor suspects of myocardial infarction (acute coronary syndrome [ACS])^[7,10]. In 2004, scientists proposed the Mayo Clinic diagnostic criteria to help doctors diagnosing TTS. This criteria scores transient LV dysfunction with wall motion abnormalities extended beyond a single epicardial vascular distribution, absence of obstructive coronary disease, ECG with ST-elevation and T-wave inversion, and absence of pheochromocytoma or myocarditis as a base for diagnosing TTS^[11].

Question D. That is the most problematic issue of this disease, just an urgent CATH, that shows no obstructive alterations, is able to differentiate a myocardial infarction from a TTS, which changes completely the clinical trial.

Question E. Analyzing data from the international Takotsubo Registry, it clearly stays that TTS is more frequently caused by a physical than an emotional trigger (36% physical, 27.7% emotional, 7.8% both, and 28% with no triggering event). Added to that, surgery, as physical stress, is one of the most recurrent triggers for high peaks of catecholamines in patients, being TTS a major complicator in the postoperative period of general surgery operations. TTS was already reported in open gastrectomy, in complications of liver transplant, and even in a caesarean section^[1,11-13]. Afonso et al. showed, in a systematic review, that TTS can be an early complication of cardiac surgery originating from the administration of inotropic drugs, postoperative anxiety, hypoperfusion during cardiopulmonary bypass, and pain^[12]. It is noteworthy, from the surgical point of view, the description of isolated cases of TTS in the postoperative period of cardiac surgeries, especially those associated with mitral valve disease. This detail cannot fail to be considered in cases that present a picture suggestive of acute myocardial infarction with normal coronary arteries. Suspicion is important because the use of amines is still indicated, and beta-blockers should be used. The suspicion of obstructive hypertrophic cardiomyopathy may lead to the indication of surgical treatment, a fact that is countersense since the hypertrophy of TTS is reversible.