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All rights reserved. doi:10.1016/j.ijcard.2009.10.055 Transient left ventricular dysfunction and stroke: An intriguing mystery still far from being fully elucidated Cesare de Gregorio ⁎, Giuseppe Andò, Concetta Lentini, Scipione Carerj Clinical and Experimental Department of Medicine and Pharmacology, Cardiology Unit, Messina University Medical School, Messina, Italy article info Article history: Received 30 April 2009 Accepted 1 May 2009 Available online 23 May 2009 Keywords: Apical ballooning Echocardiography Stroke Stress-related cardiomyopathy Takotsubo cardiomyopathy Left ventricular dysfunction Dear Editor, We read with great interest the article about Stroke and Takotsubo Cardiomyopathy (TC) recently published by Will Lee et al. [1] on the International Journal of Cardiology. The authors deal with the case of a 43-year-old woman in whom these two clinical entities were found at the same time, but with no evidence of cardioembolic sources. They also emphasize the intricate relationship between acute brain injuries and stress cardiomyopathy. We strongly agree with them about the likelihood of a common catecholamine-mediated pathway underlying both TC and various acute brain diseases [2,3]. It cannot be denied that the complexity of heart–brain relationship dates back to five decades ago, when evolving ECG changes apparently ⁎ Corresponding author. Dipartimento Clinico-Sperimentale di Medicina e Farm- acologia, Unità Operativa di Cardiologia, Azienda Ospedaliera Universitaria di Messina, Via Consolare Valeria, 98125, Messina, Italy. Tel./fax: +39 090 2213531. E-mail address: cesaredegregorio@tiscali.it (C. de Gregorio). consistent with myocardial ischemia were described in subarachnoid haemorrhage (SAH) [4]. Fig. 1 depicts such typical ECG anomalies in a SAH patient with apical ballooning. More recently, a great body of literature on this subject, but also on the relationship between LV dysfunction and other brain injuries, has been generated. Early autopsy-based studies had already shown that in most patients these anomalies are not related with coronary artery disease or with gross myocardial damage, despite the release of circulating biomarkers [5,6]. Clinicians are now aware about the fact that transient LV dys- function usually occurs in the lack of significant coronary artery disease, even though microvascular impairment and/or coronary artery stenoses have also been described in some cases [7–9]. Mayo Clinic diagnostic criteria for stress-related cardiomyopathy ruled out the occurrence of this phenomenon in patients presenting with head trauma or intracranial bleeding, mainly because the distribution of wall-motion abnormalities varied significantly in early studies [10]. On the contrary, their ultimate review likely offers a gleam on a common pathophysiological mechanism for both neurogenic stress and TC [11]. Nonetheless, questions about the relationship between acute ischemic stroke and TC are still open. In fact, whereas apical ballooning (neurogenic cardiomyopathy) and SAH are likely to share a common stress-catecholaminergic disorder, without any cause/effect relation- ship, this latter may be claimed with ischemic stroke patients [12]. In this context, timing between the two events becomes such an important issue in order to confirm the cardiomyopathy as a con- sequence of the ischemic brain injury. This pathogenesis was hypo- thesized by Yoshimura et al. [13] in a series of 7 patients. However, in 3 out of them a cardioembolic source was found. Therefore, when brain attack is subsequent (or simultaneous) to TC, like in the case presented by Lee et al. [1], it seems appropriate to rule out a cardioembolic pathogenesis. Unfortunately, the recognition of LV thrombus formation may be overtaken during emergency echocardiography [12], when to confirm (or to exclude) myocardial infarction is the primary clinical step.