PMC6911677_01
Twelve-lead electrocardiography on admission showed atrial fibrillation with a heart rate of 78 beats/min and ST elevation at II, III, and aVF and ST depression at V2-V6.
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Twelve-lead electrocardiography showed atrial fibrillation with a heart rate of 78 beats/min and ST elevation at II, III, and aVF and ST depression at V2- V6 [Figure 1].
The head computed tomography (CT) image showed no intracranial hemorrhages (a), but the hyper-dense arterial sign was observed at the basilar artery (b, arrowhead), which suggested the basilar artery occlusion. The contrast-enhanced chest CT did not indicate aortic dissection nor cardiac tamponade (c). The coronary angiography revealed distal occlusion in the posterior descending branch of the right coronary artery (d, arrow). Mild stenotic lesions suggestive of atherosclerotic pathology were observed in some parts (e and f). The diffusion-weighted image showed hyper-intense lesions in the region of the posterior inferior cerebellar artery (g and h). Magnetic resonance angiography did not reveal the flow of the basilar artery, and severe stenotic lesions of the major arteries were scarcely observed (i).
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The head computed tomography (CT) image showed no intracranial hemorrhages [Figure 2a], but the hyperdense arterial sign was observed at the basilar artery [Figure 2b], which suggested the basilar artery occlusion. The contrast-enhanced chest CT did not indicate aortic dissection nor cardiac tamponade [Figure 2c]. We immediately performed coronary angiography for salvage of the myocardial ischemic area, and it revealed distal occlusion in the posterior descending branch of the right coronary artery [Figure 2d]. Mild stenotic lesions suggestive of atherosclerotic pathology were observed in some parts [Figure 2e and f]. Magnetic resonance imaging was subsequently performed, and the diffusion-weighted image showed hyperintense lesions in the region of the posterior inferior cerebellar artery [Figure 2g and h]. Magnetic resonance angiography did not reveal the flow of the basilar artery, and severe stenotic lesions of the major arteries were scarcely observed [Figure 2i].
After 38 h from the onset, his consciousness level was depressed as Japan coma scale I-3. The head computed tomography (CT) 38 h after the onset showed hydrocephalus (a) due to cerebellar edema and hemorrhagic infarction of the ischemic cerebellum, which compressed the aqueduct (b). The head CT after cerebral ventricular drainage showed improvement in hydrocephalus (c). The chest CT showed cardiac tamponade (d). Emergency pericardiotomy was immediately performed to allow the fluid to drain. A left mural and atrial appendage thrombi were observed. There were no apparent bleeding sources, aortic dissections, nor myocardial ruptures intraoperatively (e).
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The head CT showed hydrocephalus [Figure 3a] due to cerebellar edema and hemorrhagic infarction of the ischemic cerebellum, which compressed the aqueduct [Figure 3b]. After stabilizing circulatory dynamics with adrenaline and noradrenaline, the head CT showed improvement in hydrocephalus [Figure 3c]. The chest CT showed cardiac tamponade [Figure 3d], considered as the cause of shock. Emergency pericardiotomy was immediately performed to allow the pericardial fluid to drain [Figure 3e].