Case ReportTakotsubo Cardiomyopathy and Neurogenic Pulmonary Edema After Carotid Endarterectomy
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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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.