Takotsubo Cardiomyopathy Following Acute Cerebral Events

Abstract

Objective: Takotsubo cardiomyopathy (TCM) is characterized by transient apical ventricular dysfunction typically induced by acute stress. Acute cerebral events including ischemic stroke (IS) or epileptic events (EEs) may be associated with massive catecholamine release. We aimed to identify the characteristics and outcomes of patients who experienced the Takotsubo syndrome complicated by IS or EE. Methods: Between 2008 and 2013, 87 patients were admitted to our intensive care unit for TCM. Of these, 6 had previously experienced acute cerebral symptoms within 2 days of experiencing either IS or EE. Takotsubo syndrome was diagnosed on cardiac MRI, echocardiography, electrocardiography (ECG), biology and coronary angiography data. Results: Five women and 1 man were included in the study. The mean age was 63.7 ± 20.1 years (range 44-84). Four of them (67%) initially presented an acute IS and 2 (33%) had EE. The suspected brain injury was found in the insular cortex for 4 patients and the posterior fossa for 2 patients. Hemiparesis, aphasia and cerebellar symptoms were the main neurological signs. Abnormal ECG findings including ST-segment elevation (33%) or T-wave inversion (50%) developed between a few hours and 48 h after the onset of the IS or EE. Peak troponin was 1.8 (0.79-14.11) µg/l. A transient reduction in the left ventricular ejection fraction (46 ± 12%) with apical hypokinesis was found using echocardiography. Two (33%) patients went on to develop acute heart failure. Coronary angiography confirmed the lack of significant coronary stenosis for all 6 patients. Conclusion: TCM can develop within the first few days after an acute cerebral event. It occurs predominantly in women with insular or posterior fossa lesions and is possibly induced by vegetative reactions.

Myocardial function at the early phase of traumatic brain injury: a prospective controlled study

“…Accordingly, in a recent retrospective study, conventional cardiac ultrasonography was mostly performed on day one, revealing an acute myocardial depression after TBI [10]. Nevertheless, we cannot exclude a delayed myocardial dysfunction occurring within the first post-traumatic days [24]. In our study, slight systolic and diastolic STE changes might be undermined by the early ultrasound assessment and might be significant in later examinations.…”

Authors' Reply to the Letter by Madias Entitled ‘Stroke or Seizures, and Takotsubo Syndrome: A Possibly Underdiagnosed Association'

“…In this disease, stroke could be either the cause or the consequence of TTS. In our study published in European Neurology [2] , we assumed that ischemic stroke or epileptic events affecting specific brain regions could induce a massive catecholamine release, as suggested by other authors [3] . We acknowledge that we did not investigated blood catecholamine levels because of the retrospective nature of the study.…”

Strokes or Seizures, and Takotsubo Syndrome: A Possibly Underdiagnosed Association

“…Considering the brain-heart pathophysiological link in Takotsubo syndrome (TTS) [1,2] , the need for a Neurocardiology field seems inevitable. These thoughts are prompted by the very interesting contribution of Blanc et al [3] , published in this journal, about 6 patients who suffered TTS in the setting of acute cerebral events (ACE), 4 following an ischemic stroke (IS) and 2 after epileptic events (EEs). As the authors state that ACE 'may be associated with massive catecholamine release' [3] , it would have been contributory to have catecholamine ders whether monitoring of patients with ACE (IS, EE and SH) should have routine continuous electrocardiographic monitoring (arrhythmias, repolarization and depolarization abnormalities), an ECHO assessment and testing for a rise of troponins and brain natriuretic peptides, irrespective of their hemodynamic status.…”

“…These thoughts are prompted by the very interesting contribution of Blanc et al [3] , published in this journal, about 6 patients who suffered TTS in the setting of acute cerebral events (ACE), 4 following an ischemic stroke (IS) and 2 after epileptic events (EEs). As the authors state that ACE 'may be associated with massive catecholamine release' [3] , it would have been contributory to have catecholamine ders whether monitoring of patients with ACE (IS, EE and SH) should have routine continuous electrocardiographic monitoring (arrhythmias, repolarization and depolarization abnormalities), an ECHO assessment and testing for a rise of troponins and brain natriuretic peptides, irrespective of their hemodynamic status. Such an undertaking will require not only mere implementation and ordering of the above modalities and diagnostic tests, but close collaboration of neurologists and cardiologists under the auspices of a hybrid field of Neurocardiology.…”

“…Of interest is that TTS was triggered by lesions in the insular cortex or posterior fossa [3] , brain regions previously associated with brain-triggered injury to the heart [1,2] . The prevalence of TTS triggered by IS, EE or subarachnoid hemorrhage (SH) must be higher than currently appreciated, considering that a large number of patients with TTS were detected in patients with SE who were prospectively and proactively evaluated with serial sophisticated echocardiography (ECHO) techniques [4,5] , particularly if one subscribes to the notion that TTS could present in atypical and/or milder forms [6] .…”