Elsevier

World Neurosurgery

Volume 124, April 2019, Pages 157-160
World Neurosurgery

Case Report
Takotsubo Cardiomyopathy and Neurogenic Pulmonary Edema After Carotid Endarterectomy

https://doi.org/10.1016/j.wneu.2018.12.206Get rights and content

Background

Takotsubo cardiomyopathy (TCM) and neurogenic pulmonary edema (NPE) are rare complications of an acute ischemic stroke. In particular, TCM and NPE following carotid endarterectomy (CEA) are extremely rare. In general, TCM- and NPE-associated ischemic strokes are caused by excess catecholamine release after sympathetic nervous stimulation following stroke onset, but the mechanism triggering this stimulation is still unknown.

Case Description

An 88-year-old man underwent left CEA for symptomatic carotid artery stenosis (North American Symptomatic Carotid Endarterectomy Trial, 65%). After the surgery, his respiratory condition rapidly worsened, and chest radiography revealed an infiltrative shadow on both lung fields. Transthoracic echocardiography revealed left ventricular dysfunction, suggesting TCM. Postoperative magnetic resonance imaging revealed a small infarction in the left anterior insular cortex. Eventually, his respiratory and cardiac functions gradually improved. He was finally discharged on his own from the hospital on postoperative day 9.

Conclusions

We described a very rare case of TCM and NPE following CEA. The mechanisms of TCM and NPE involve excess catecholamine release after sympathetic nervous stimulation. Our findings suggest that surgery-associated transient ischemia and reperfusion injury to the left insular cortex stimulate sympathetic nerves.

Introduction

Takotsubo cardiomyopathy (TCM) is characterized by a transient left ventricular apical ballooning that resembles a Japanese octopus catcher pot (takotsubo) with a short narrow neck and round bottom.1 Neurogenic pulmonary edema (NPE) is the condition of noncardiac abnormal accumulation of extravascular liquid in the lungs because of acute central nervous system injury.2 Recently, it is reported that patients with acute-stage ischemic stroke rarely present with complications such as TCM and NPE. Here, we describe a case of TCM and NPE following carotid endarterectomy (CEA). Furthermore, we discuss the mechanism of TCM and NPE following CEA.

Section snippets

Case Presentation

An 88-year-old man presented with gait disturbance. His medical history included angina, arteriosclerosis obliterans, hypertension, and hyperlipidemia. He had previously been treated with medication for hypertension and hyperlipidemia. On admission, his neurologic examination revealed no symptoms, and the National Institute Health Stroke Scale score was 0. Magnetic resonance (MR) imaging of the brain on admission revealed multiple infarctions in the right hemisphere (Figure 1A–B). MR

Discussion

Initially, patients with acute-stage ischemic stroke rarely present with complications such as TCM and NPE. In general, TCM- and NPE-associated ischemic strokes are caused by excess catecholamine release after sympathetic nervous stimulation following stroke onset, but the mechanism triggering this stimulation is still unknown.3 The mechanisms of TCM and NPE involve excess catecholamine release after sympathetic nervous stimulation.4, 5, 6, 7 The central autonomic network, a recently defined

Conclusions

TCM and NPE following CEA are extremely rare. In general, TCM- and NPE-associated ischemic strokes are caused by excess catecholamine release after sympathetic nervous stimulation following stroke onset, but the mechanism triggering this stimulation is unknown. In this report, we concluded that the mechanisms of TCM and NPE due to CEA involved the following: 1) a small infarction occurred in the left insular cortex, which indicated ischemia of the left insula cortex due to clamp during the

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Cited by (11)

  • Neurogenic pulmonary edema following acute stroke: The progress and perspective

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    Citation Excerpt :

    The theory of lateralization, that the right Ic mainly controls the sympathetic nervous system while the left Ic mainly controls the parasympathetic nervous system, supports the perspective that sympathetic activation and the onset of NPE are closely related to a right insular infarction [13]. However, the case report about NPE in left insular infarction patients suggests that the left Ic can also affect sympathetic nerves through some unknown mechanism [14]. In fact, it is indeed complex that how the Ic damage change automatic nervous function, because different noxious stimulus applies different impacts to automatic nervous system.

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Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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