Takotsubo Cardiomyopathy and Neurogenic Pulmonary Edema After Carotid Endarterectomy

被引:10
作者
Kitagawa, Takehiro [1 ]
Ishikawa, Hisashi [2 ]
Yamamoto, Junkoh [1 ]
Ota, Shinzo [2 ]
机构
[1] Univ Occupat & Environm Hlth, Dept Neurosurg, Kitakyushu, Fukuoka, Japan
[2] Ota Mem Hosp, Brain Attack Ctr, Dept Neurosurg, Fukuyama, Hiroshima, Japan
关键词
Carotid endarterectomy; Insular cortex; Neurogenic pulmonary edema; Postoperative complication; Takotsubo cardiomyopathy; INSULAR CORTEX; BRAIN; PATHOGENESIS; STRESS;
D O I
10.1016/j.wneu.2018.12.206
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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.
引用
收藏
页码:157 / 160
页数:4
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