Shams Y-Hassan

Acute cardiac sympathetic disruption in the pathogenesis of the takotsubo syndrome: A systematic review of the literature to date☆

Takotsubo syndrome (TS), also known as broken heart syndrome and neurogenic stunned myocardium, is an acute cardiac disease entity characterized by a clinical picture mimicking that of an acute coronary syndrome. The pathogenesis of TS has not been established yet. Among the most often debated pathologic mechanisms of TS are as follows: first, multi-vessel coronary spasm; second, myocardial microvascular dysfunction; third, aborted myocardial infarction caused by transient thrombotic occlusion of a long wrap-around left anterior descending artery; fourth, left ventricular outflow tract obstruction; fifth, blood-borne catecholamine cardiac toxicity; and sixth, cardiac sympathetic disruption and norepinephrine seethe and spillover. The aim of this review is to provide a thorough analysis of the literature data coming mainly from the neurological literature and dealing with the pathogenesis of TS. Substantial evidence challenging the first five hypotheses and arguing in favor of the hypothesis that acute cardiac sympathetic eruption and norepinephrine seethe and spillover is causing TS in predisposed patients is presented.

Capecitabine caused cardiogenic shock through induction of global takotsubo syndrome

5-Fluorouracil (5-FU) and its oral pro-drug capecitabine are widely used in oncology for the treatment of various solid tumours, including colorectal cancers. Cardiotoxicity to these drugs is not an uncommon adverse effect and has been reported in 1%-18% of patients. Capecitabine has been reported to trigger mid-apical Takotsubo syndrome (TS). We describe here the case of a 55-year-old man who presented with cardiogenic shock and ECG signs of ST-elevation myocardial infarction. The symptoms began 28 h after the commencement of capecitabine adjuvant therapy, following a radical right-sided hemicolectomy for low-differentiated adenocarcinoma of the caecum. Echocardiography showed severe global left ventricular dysfunction. Cardiac magnetic resonance imaging showed no signs of late gadolinium enhancement. These clinical, cardiac image study findings and the course of the disease with full recovery within one week were consistent with global TS triggered by the adjuvant therapy capecitabine and presenting with a life-threatening cardiogenic shock. Moreover, we have demonstrated the speedy dynamic of the left ventricular wall motion abnormality with global TS at presentation and basal (inverted) TS findings 4 days later on.

Sepsis-induced myocardial depression and takotsubo syndrome

Abstract Background and objectives: Myocardial depression in the setting of sepsis and septic shock is common and has been recognized for a long time. The aim of this study is to find out an association and causal link between sepsis and takotsubo syndrome (TS). Methods: Fifteen cases of TS were studied. Critical review of the literature dealing with sepsis and myocardial depression was done Results: Fifteen cases of sepsis-induced TS are described. Fifty-three per cent of the patients were men. The ages ranged from 39 to 76 years (mean age 60 years). Two-thirds of the patients had ST-elevation myocardial infarction ECG changes. Complications occurred in 80% of the patients. No specific types of sepsis or micro-organisms were associated with the development of TS. Critical review of the sepsis-induced myocardial depression shows that the left ventricular dysfunction, which is reversible within one-to-two weeks, is characterized by segmental ventricular dysfunction, and involvement of the right ventricle in one fourth of cases. These features are also consistent with TS. Conclusions: Sepsis triggers TS, which may be the cause of the majority of cases of sepsis-induced myocardial depression. Acute cardiac sympathetic disruption with noradrenaline spill-over may be the cause of sepsis-induced TS.

Bromocriptine-Induced Coronary Spasm Caused Acute Coronary Syndrome, Which Triggered Its Own Clinical Twin – Takotsubo Syndrome

Bromocriptine-induced coronary spasm (BICS) causing myocardial infarction has been reported. Association between BICS and Takotsubo syndrome (TS) has not been described. We report on a 37-year-old woman presenting with a clinical picture of acute coronary syndrome 1 day after initiation of treatment with bromocriptine for ablactation 3 weeks after a full-term spontaneous vaginal delivery. Coronary angiography showed diffuse narrowing of a large diagonal branch. Left ventriculography showed widespread hypokinesia extending beyond the diagonal branch supply region. There was a slight elevation of myocardial infarction biomarkers that was disproportional to the degree of left ventricular dysfunction. Follow-up coronary angiography, intravascular ultrasound and left ventriculography showed normal coronary arteries including the diagonal branch and complete normalization of the left ventricular function. Cardiac magnetic resonance examination showed no signs of late myocardial gadolinium enhancement. The clinical picture and course of the disease was consistent with TS. Consequently, we describe for the first time a case of TS triggered by myocardial ischemia caused by BICS. Furthermore, our case and sufficient supporting data from the literature demonstrate that acute coronary syndrome is an important and frequent but up till now missed trigger factor for TS.

Insights into the pathogenesis of takotsubo syndrome, which with persuasive reasons should be regarded as an acute cardiac sympathetic disease entity.

The pathogenesis of takotsubo syndrome (TS) has not been established yet. The literature data dealing with the pathogenesis of TS are abundant but scattered among different medical specialities. Subarachnoid hemorrhage and other acute intracranial diseases and injuries are among the important and currently well-recognized trigger factors for TS. In both induced and spontaneous subarachnoid hemorrhages, signs suggestive of increased cardiac sympathetic overactivity have been documented. Surgical and pharmacological sympathectomy has shown to have protective cardiac effects in both animal and human studies. Increase in local release of norepinephrine from the heart of patients with TS has been measured. Signs of both cardiac sympathetic denervation and myocardial lesions adjacent to the cardiac nerve terminals have been seen. Furthermore, the systematized and typically circumferential pattern of ventricular wall motion abnormality is incongruent with the coronary artery supply region and appears most likely to follow the cardiac sympathetic nerve distribution. In conclusion, compelling literature data support the hypothesis that acute cardiac sympathetic disruption and norepinephrine seethe and spillover is causing TS in predisposed patients. TS is most probably an acute cardiac sympathetic disease entity causing myocardial stunning in which takotsubo is one among other cardiac image study findings.

Post-ischemic myocardial stunning was the starting point of takotsubo syndrome: Restitution is justified after falling down on

I readwith great interest the article by Messas et al. [1] in the recent issue of International Journal of Cardiology in which a case of acute coronary syndrome (ACS) and findings consistent with takotsubo syndrome (TS) is described. I cordially congratulate the authors for the well-examined and properly investigated case reportwithmany crucial clinical findings. The authors have demonstrated important findings, verified by advanced invasive, cardiac image and scintigraphic assessments, whichmay clarify the relation of ACS to TS and its pathogenesis. This assertion is not based only on the findings of the present case but also on substantial literature evidence supporting what this case has showed. This case had undoubtedly ACS (most probably aborted myocardial infarction) documented by electrocardiographic changes, cardiac biomarker elevation and atherothrombotic changes verified by optical coherence tomography. At the same time, the left ventriculography revealed typical mid apical ballooning; there was mild elevation of cardiac biomarkers; cardiac magnetic resonance imaging revealed the absence of any late gadolinium enhancement in the akinetic/hypokinetic regions; and the left ventricular wall motion abnormality (LVWMA) recovered completely after 6 days. These features, as the authors of the case report have appropriately mentioned, are typical for TS. There was no history of any antecedent stress factor apart from resuscitation and ACS. It will be justifiable to deem the case as TS triggered by ACS. However, in case of strict application of

The pathogenesis of reversible T-wave inversions or large upright peaked T-waves: Sympathetic T-waves

Reversible electrocardiographic (ECG) repolarization changes including T-wave inversions (TWI), large upright peaked T-waves (LUPTW) and prolongation of the corrected QT interval (P-QTc) have been reported in association with myriads of acute cardiac and non-cardiac diseases. Through the last 70 years, the TWIs have been described under different terms as; cerebral, giant, global, canyon, Wellens or coronary and cardiac memory T waves. During the last 15 years, the reversible TWI and LUPTW in association with P-QTc have been described as characteristic ECG features in takotsubo syndrome (TS), which also may be triggered by the same aforementioned acute cardiac and non-cardiac disease entities. The pathogenesis of these reversible T-wave changes is not clear-cut. In this manuscript, substantial evidences for a causal link between the local cardiac sympathetic disruption and the development of the reversible TWI and LUPTW are presented. As a result, a pathogenetic term for the reversible TWI or LUPTW, which is sympathetic T waves (sympathetic TWI or sympathetic LUPTW), would be the most appropriate term.

Contemporary review on the pathogenesis of takotsubo syndrome: The heart shedding tears: Norepinephrine churn and foam at the cardiac sympathetic nerve terminals

Takotsubo syndrome (TS), an increasingly recognized acute cardiac disease entity, is characterized by a unique pattern of circumferential and typically regional left ventricular wall motion abnormality resulting in a conspicuous transient ballooning of the left ventricle during systole. The mechanism of the disease remains elusive. However, the sudden onset of acute myocardial stunning in a systematic pattern extending beyond a coronary artery territory; the history of a preceding emotional or physical stress factor in two thirds of cases; the signs of sympathetic denervation at the regions of left ventricular dysfunction on sympathetic scintigraphy; the finding of myocardial edema and other signs consistent with (catecholamine-induced) myocarditis shown by cardiac magnetic resonance imaging; and the contraction band necrosis on histopathological examination all argue strongly for the involvement of the cardiac sympathetic nervous system in the pathogenesis of TS. In this narrative review, extensive evidence in support of local cardiac sympathetic nerve hyperactivation, disruption and norepinephrine spillover causing TS in predisposed patients is provided.

Cerebellar haemorrhage triggered Takotsubo-like left ventricular dysfunction syndrome

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Epidemiology, pathogenesis, and management of takotsubo syndrome

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