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A Rare Cause of Takotsubo Cardiomyopathy Related Left Ventricular Apical Thrombus Requiring Surgery

https://doi.org/10.1016/j.hlc.2011.07.004Get rights and content

We present the case of a 48 year-old male with a history of cystic fibrosis who presented with massive haemoptysis and was later found to have Takotsubo cardiomyopathy. He subsequently developed a left ventricular (LV) thrombus which was successfully removed via a left apical ventriculotomy. Surgical management of LV thrombus related to Takotsubo cardiomyopathy is warranted in a selected population of patients and a left apical ventriculotomy provides good access with minimal complications in the post operative setting.

Introduction

Here we describe a case of a 48 year-old male presenting with massive haemoptysis on a background of cystic fibrosis who was later found to have Takotsubo cardiomyopathy with an associated left ventricular thrombus. The thrombus was successfully removed by an apical left ventriculotomy and the patient subsequently made a full recovery. To our knowledge, this is the first case described in the literature where a ventricular thrombus secondary to Takotsubo cardiomyopathy has been successfully treated surgically.

Section snippets

Case

A 48 year-old male non-smoker with a history of cystic fibrosis was brought to a suburban hospital by ambulance with massive haemoptysis, dyspnoea, and respiratory arrest at home.

On arrival to the suburban hospital he was hypotensive, hypoxic and had a decreased level of consciousness – he required intubation and a noradrenaline infusion. He was transferred to a tertiary hospital for further management. A presumptive diagnosis of bronchial arterio-alvelolar fistula was made due to CF-related

Discussion

Thrombus formation in the LV is common following acute myocardial infarction and other events, such as cardiomyopathy or heart failure [1], [2]. Takotsubo cardiomyopathy or stress induced cardiomyopathy is a rare condition in which the apical segments of the LV are depressed, which results in compensatory hyperkinesis of the basal segments and ballooning of the apex during systole. The exact mechanism is still unknown; however, most authors suggest a catecholamine-mediated mechanism via cardiac

Acknowledgements

There were no grants or financial support received by the authors in preparing this paper.

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