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Updated: Apr 19, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Hypotension-driven continuous watershed cerebral infarction secondary to critical coronary artery disease: A case
Huizhen Lu1, Dejun Wu2, Xiaoqiang Mao2
1Department of Neurology, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital, Quzhou, China.
Rationale:
Refractory hypotension may aggravate cerebral hypoperfusion in acute ischemic stroke, but occult coronary artery disease is often overlooked.
Patient Concerns:
A 67-year-old man presented with sudden right-sided weakness. Within 24 hours, he developed persistent hypotension (approximately 90-100/50-60 mm Hg) and neurological worsening.
Diagnoses:
Brain magnetic resonance imaging revealed an acute left frontoparietal watershed infarction. Despite fluid resuscitation and vasopressors, hemodynamic instability persisted. Hypovolemia, endocrine disorders, and cervico-cephalic stenosis were excluded. Although cardiac biomarkers and ejection fraction were normal, electrocardiography showed inferior Q waves. Coronary angiography confirmed critical left anterior descending (LAD) artery stenosis with distal occlusion.
Interventions:
Fluid resuscitation and vasopressor support failed to stabilize blood pressure. Balloon angioplasty was performed for the left anterior descending artery lesion.
Outcomes:
After intervention, blood pressure normalized without vasopressors, and neurological function improved.
Lessons:
In acute ischemic stroke patients with unexplained refractory hypotension and watershed infarction, occult coronary ischemia should be considered even when troponin is normal. Early coronary evaluation and timely revascularization may improve cerebral perfusion and outcomes.
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