Kitagawa Takehiro, Ishikawa Hisashi, Yamamoto Junkoh, Ota Shinzo
Department of Neurosurgery, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, Japan.
Department of Neurosurgery, Brain Attack Center, Ota Memorial Hospital, Fukuyama, Hiroshima, Japan.
World Neurosurg. 2019 Apr;124:157-160. doi: 10.1016/j.wneu.2018.12.206. Epub 2019 Jan 17.
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.
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.
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.
应激性心肌病(TCM)和神经源性肺水肿(NPE)是急性缺血性卒中的罕见并发症。特别是,颈动脉内膜切除术(CEA)后发生的TCM和NPE极为罕见。一般来说,与TCM和NPE相关的缺血性卒中是由卒中发作后交感神经刺激导致儿茶酚胺释放过多引起的,但触发这种刺激的机制仍不清楚。
一名88岁男性因有症状的颈动脉狭窄接受了左颈动脉内膜切除术(北美症状性颈动脉内膜切除术试验,65%)。术后,他的呼吸状况迅速恶化,胸部X线检查显示双肺野有浸润性阴影。经胸超声心动图显示左心室功能障碍,提示应激性心肌病。术后磁共振成像显示左侧前岛叶皮质有小梗死灶。最终,他的呼吸和心脏功能逐渐改善。术后第9天,他最终自行出院。
我们描述了一例CEA术后非常罕见的应激性心肌病和神经源性肺水肿病例。应激性心肌病和神经源性肺水肿的机制涉及交感神经刺激后儿茶酚胺释放过多。我们的研究结果表明,手术相关的左侧岛叶皮质短暂缺血和再灌注损伤刺激了交感神经。