Angiography‐Negative Subarachnoid Hemorrhage Detected After Emergent Percutaneous Coronary Intervention for Non‐ ST ‐Segment Elevation Myocardial Infarction: A Case Report

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  FIGURE 1. Prehospital rhythm strip documenting ventricular fibrillation as the initial cardiac arrest rhythm. All patient‐identifying information, including calendar date, clock‐time identifiers, patient name, registration number, and emergency medical service identifiers, was removed or masked.

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  FIGURE 2. Coronary angiography showing critical thrombotic stenosis of the mid‐left anterior descending artery (A, arrow). Balloon dilatation and stent deployment during percutaneous coronary intervention are shown (B); the red arrowheads indicate the deployed coronary stent. Final angiography demonstrates restoration of coronary blood flow with no residual significant stenosis and Thrombolysis in Myocardial Infarction grade 3 flow (C).

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  FIGURE 3. Axial brain computed tomography images obtained after neurological deterioration, with subarachnoid hemorrhage detected after percutaneous coronary intervention, showing diffuse thick subarachnoid hemorrhage centered in the basal cisterns, bilateral Sylvian cisterns, and anterior brainstem cisterns, with intraventricular extension and acute hydrocephalus, consistent with modified Fisher grade 4 subarachnoid hemorrhage (A–D).

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  FIGURE 4. Neurovascular imaging findings after subarachnoid hemorrhage detection. (A) Computed tomography angiography did not identify a definite ruptured aneurysm or other causative vascular lesion. (B) Initial digital subtraction angiography showed no definite aneurysm, dissection, arteriovenous shunt, or other causative vascular abnormality. (C) A small vascular pouch measuring approximately 3 × 3 mm was noted at the right posterior communicating artery origin. The right posterior communicating artery arose from the apex of the pouch, and the lesion had an infundibular configuration without a discrete aneurysmal neck. The magnified inset in the upper right corner highlights the vascular pouch more clearly, supporting the multidisciplinary interpretation of junctional or infundibular dilatation rather than a definite ruptured aneurysm. (D) Right vertebral artery anteroposterior digital subtraction angiography without manual neck compression showed opacification of the contralateral left posterior inferior cerebellar artery. (E) Lateral view of right vertebral artery digital subtraction angiography. (F) Rotational three‐dimensional vertebral artery angiography showed no definite aneurysm,…

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  FIGURE 5. Follow‐up magnetic resonance angiography. Magnetic resonance angiography obtained on hospital day 6 (A) and hospital day 13 (B) showed no definite aneurysm, dissection, or other causative vascular abnormality. Multifocal arterial narrowing compatible with secondary vasospasm was noted on early follow‐up studies. Repeat magnetic resonance angiography obtained more than 5 years after the initial presentation (C) again showed no identifiable causative vascular lesion. These findings support the absence of an identified vascular cause on serial imaging but do not definitively exclude an initially occult ruptured lesion.