Amanda Murphy1, Airton Leonardo de Oliveira Manoel2, R Loch Macdonald3, Andrew Baker4, Ting-Yim Lee5, Tom Marotta6, Walter Montanera6, Richard Aviv7, Aditya Bharatha6. 1. Department of Medical Imaging, University of Toronto, 30 Bond Street, Room 3-077CC, Toronto, ON, M5B 1W8, Canada. amanda.murphy@mail.utoronto.ca. 2. St. Michael's Hospital, Toronto, ON, Canada. 3. Department of Neurosurgery, St. Michael's Hospital, Toronto, ON, Canada. 4. Department of Critical Care, St. Michael's Hospital, Toronto, ON, Canada. 5. Robarts Research Institute, London, ON, Canada. 6. Department of Medical Imaging, St. Michael's Hospital, Toronto, ON, Canada. 7. Department of Medical Imaging, Sunnybrook Health Sciences Centre, Toronto, ON, Canada.
Abstract
BACKGROUND: The effects of induced hypertension (IH) on cerebral perfusion after subarachnoid hemorrhage (SAH) are unclear. The objectives of this investigation are to: (1) determine whether there are differences in cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) measured with computed tomography perfusion (CTP) before and after IH; (2) evaluate differences in the presence of infarction and clinical outcome between patients with and without IH. METHODS: We performed a retrospective cohort analysis of 25 aneurysmal SAH patients. IH was initiated as per the standard institutional protocol when patients showed clinical symptoms of delayed cerebral ischemia (DCI). Differences in CBF, CBV, and MTT between early (<72 h after aneurysm rupture) and late (7-10 days after aneurysm rupture) CTP were quantified in patients with (n = 13) and without IH (n = 12). Outcome measures included cerebral infarction and clinical outcome at 3 months. RESULTS: Early MTT was significantly greater in the IH group compared to the no-IH group. There was no difference in early or late CBV or CBF between the two groups. In patients that received IH, there was a significant decrease in MTT between the early (7.0 ± 1.2 s) and late scans (5.8 ± 1.6 s; p = 0.005). There was no difference in the incidence of infarction (5/13 vs. 2/11) or poor outcome (3/11 vs. 6/13) between the IH and no-IH groups, respectively (p > 0.05). CONCLUSIONS: Elevated MTT is a significant factor for the development of DCI in patients eventually requiring IH therapy and is improved by IH treatment. Therapies to prevent DCI and improve clinical outcome may need to be initiated earlier, when cerebral perfusion abnormalities are first identified.
BACKGROUND: The effects of induced hypertension (IH) on cerebral perfusion after subarachnoid hemorrhage (SAH) are unclear. The objectives of this investigation are to: (1) determine whether there are differences in cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) measured with computed tomography perfusion (CTP) before and after IH; (2) evaluate differences in the presence of infarction and clinical outcome between patients with and without IH. METHODS: We performed a retrospective cohort analysis of 25 aneurysmalSAHpatients. IH was initiated as per the standard institutional protocol when patients showed clinical symptoms of delayed cerebral ischemia (DCI). Differences in CBF, CBV, and MTT between early (<72 h after aneurysm rupture) and late (7-10 days after aneurysm rupture) CTP were quantified in patients with (n = 13) and without IH (n = 12). Outcome measures included cerebral infarction and clinical outcome at 3 months. RESULTS: Early MTT was significantly greater in the IH group compared to the no-IH group. There was no difference in early or late CBV or CBF between the two groups. In patients that received IH, there was a significant decrease in MTT between the early (7.0 ± 1.2 s) and late scans (5.8 ± 1.6 s; p = 0.005). There was no difference in the incidence of infarction (5/13 vs. 2/11) or poor outcome (3/11 vs. 6/13) between the IH and no-IH groups, respectively (p > 0.05). CONCLUSIONS: Elevated MTT is a significant factor for the development of DCI in patients eventually requiring IH therapy and is improved by IH treatment. Therapies to prevent DCI and improve clinical outcome may need to be initiated earlier, when cerebral perfusion abnormalities are first identified.
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