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Christoph J. Griessenauer, R. Shane Tubbs, Paul M. Foreman, Michelle H. Chua, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Ramaswamy Iyer, Rishikesh Haridas, Beverly C. Walters, Salman Chaudry, Aisana Malieva, Samantha Wilkins, Mark R. Harrigan, Winfield S. Fisher III, and Mohammadali M. Shoja

. Exclusion criteria were age under 19 years and any associated genetic predisposition known to contribute to cerebral aneurysm formation (polycystic kidney disease, Turner syndrome, Noonan syndrome, Ehlers-Danlos syndrome Type 4, Marfan syndrome, or neurofibromatosis Type 1), as well as systemic diseases (congestive heart failure or cirrhosis) that could interfere with RAS activity. 14 The control group comprised trauma patients, 19 years of age and older, with unremarkable findings on CTA of the head and neck (no cerebral aneurysm or other vascular malformation) and

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Christoph J. Griessenauer, R. Shane Tubbs, Paul M. Foreman, Michelle H. Chua, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Ramaswamy Iyer, Rishikesh Haridas, Beverly C. Walters, Salman Chaudry, Aisana Malieva, Samantha Wilkins, Mark R. Harrigan, Winfield S. Fisher III, and Mohammadali M. Shoja

ruptured cerebral aneurysm was confirmed by CT angiography (CTA) or digital subtraction angiography (DSA). Exclusion criteria were age younger than 19 years and any associated genetic syndrome that could explain the presence of a cerebral aneurysm (such as polycystic kidney disease, Ehler-Danlos syndrome Type 4, and Marfan syndrome) or systemic diseases (e.g., congestive heart failure and cirrhosis) that could interfere with RAS activity. All patients were enrolled within 72 hours of admission. General Management Patients presenting with aSAH were treated in accordance