• Takehiro Kitagawa, Hisashi Ishikawa, Junkoh Yamamoto, and Shinzo Ota.
• Department of Neurosurgery, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, Japan. Electronic address: tkitagawa0626@gmail.com.
• World Neurosurg. 2019 Apr 1; 124: 157160157-160.

BackgroundTakotsubo 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 DescriptionAn 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.ConclusionsWe 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.Copyright © 2019 Elsevier Inc. All rights reserved.

5 keywords...

hide…