Abstract FR402: Bilateral Vertebral Artery Stenosis and Severe Aortic Valve Stenosis Trigger Functional Hypotension With Neurologic Collapse and Syncope

Case Presentation: 62-year-old woman with hypertension on lisinopril and uncontrolled type 2 DM (HbA1c 12.6) presented with left eyelid ptosis, diplopia, new-onset left lower extremity weakness, and 5 episodes of syncope. She had multiple prior ED visits for syncope with normal-to-high blood pressure. Code stroke was activated due to focal neurologic findings. CT angiography revealed severe bilateral vertebral artery stenosis, raising concern for posterior circulation insufficiency. Brain MRI showed no infarct and preserved perfusion. Cerebral angiography confirmed high-grade vertebral stenosis with robust collateral flow. Echocardiography revealed severe aortic valve stenosis (valve area 0.72 cm2 , mean gradient 55 mmHg). Differential Diagnosis: Included diabetic cranial neuropathy, posterior circulation ischemia, structural compression, and stroke. Diabetic ischemia could explain the cranial nerve palsy but not the leg weakness or syncope, which suggested vertebrobasilar hypoperfusion. Despite normotension, the patient was functionally hypotensive due to impaired cerebrovascular reserve, producing a dynamic low-flow state that mimicked stroke. Treatment and Management: Lisinopril was discontinued. A permissive hypertension protocol targeted systolic blood pressures ≥130 mmHg. Midodrine was administered for dips, and gentle intravenous hydration supported preload. After adequate collateral perfusion was confirmed by cerebral angiography, the patient underwent combined AVR and CABG. She remained neurologically stable postoperatively. Discussion: This case illustrates the challenge of diagnosing and managing patients with both AVS and bilateral VAS. The patient’s focal neurologic deficits and syncope were suggestive of stroke, but imaging revealed no infarction. The underlying pathology was functional cerebral hypoperfusion, from a posterior circulation that failed to maintain adequate flow despite normal systemic pressures. The case demonstrates that standard vital signs do not ensure brain perfusion when vascular reserve is compromised. Stroke diagnosis in such cases requires a flow-based assessment of structurally fragile cerebrovascular systems, rather than a simple distinction between infarction and no infarction. Ultimately, this case emphasizes that “normal” is not always safe. It highlights the importance of dynamic diagnostics and interdisciplinary collaboration in managing patients with overlapping cardiovascular and cerebrovascular compromise