Effects of Induced Hypertension on Cerebral Perfusion in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Background Statins may promote vasodilation following subarachnoid hemorrhage (SAH) and improve the response to blood pressure elevation. We sought to determine whether simvastatin increases cerebral blood flow (CBF) and alters the response to induced hypertension after SAH. Methods Statin-naïve patients admitted <72 hours after WFNS ≥2 aneurysmal SAH were randomly assigned to 80 mg simvastatin/day or placebo for 21 days. Regional cerebral blood flow (CBF) was measured with quantitative 15O PET on SAH day 7–10 before and after raising mean arterial pressure (MAP) 20–25%. Autoregulatory index (AI) was calculated as the ratio of % change in resistance (MAP/CBF) to % change in MAP. Angiography was performed within 24 hours of PET. Results are presented as simvastatin vs. placebo. Results Thirteen patients received simvastatin and 12 placebo. Clinical characteristics were similar. Moderate or severe angiographic vasospasm occurred in 42% vs.45% and delayed cerebral ischemia in 14% vs. 55% (p=0.074). During PET studies MAP (110±10 vs. 111±12), global CBF (41±12 vs. 43±13) and CVR (2.95±1.0 vs. 2.81±1.0) did not differ at baseline. When MAP was raised to 135±7 mm Hg vs. 137±15, global CBF did not change. Global AI did not differ (107±59 % vs 0. 89±52 %, p=0.68). CBF did not change in regions with low baseline flow or in regions supplied by vessels with angiographic vasospasm in either group. Six month modified Rankin Scale scores did not differ. Conclusions Our data indicate that initiation of therapy with high-dose simvastatin does not alter baseline CBF or response to induced hypertension.

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“…They found that raising BP an average of 12 mm Hg did not change global or CBF or CBF asymmetry in the region with the lowest baseline flow. [42]…”

Section: Discussionmentioning

confidence: 99%

Effect of High-Dose Simvastatin on Cerebral Blood Flow and Static Autoregulation in Subarachnoid Hemorrhage

et al. 2015

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“…Hemodynamic interventions are routinely employed for this purpose, including volume expansion, induced hypertension, and augmentation of cardiac output [2–4]. Still, optimal management of DCI remains largely empiric, with no therapeutic strategies being supported by clinical or even convincing physiologic proof-of-efficacy [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

RBC Transfusion Improves Cerebral Oxygen Delivery in Subarachnoid Hemorrhage

Dhar

Zazulia²,

Derdeyn³

et al. 2017

Critical Care Medicine

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Objective Impaired oxygen delivery due to reduced cerebral blood flow (CBF) is the hallmark of delayed cerebral ischemia (DCI) following subarachnoid hemorrhage (SAH). Since anemia reduces arterial oxygen content, it further threatens oxygen delivery increasing the risk of cerebral infarction. Thus, SAH may constitute an important exception to current restrictive transfusion practices, wherein raising hemoglobin could reduce the risk of ischemia in a critically hypoperfused organ. In this physiologic proof-of-principle study we determined whether transfusion could augment cerebral oxygen delivery, particularly in vulnerable brain regions, across a broad range of hemoglobin values. Design Prospective study measuring CBF and oxygen extraction fraction (OEF) using 15O-PET. Vulnerable brain regions were defined as those with baseline oxygen delivery < 4.5 ml/100g/min. Setting PET facility located within the Neurology/Neurosurgery Intensive Care Unit. Patients 52 patients at risk for DCI after aneurysmal SAH with hemoglobin 7–13 g/dl. Interventions Transfusion of one unit of red blood cells (RBCs) over one hour. Measurements and Main Results Baseline hemoglobin was 9.7 g/dl (range 6.9–12.9) and CBF was 43±11 ml/100g/min. After transfusion, hemoglobin rose from 9.6±1.4 to 10.8±1.4 g/dl (12%, p < 0.001) and oxygen delivery from 5.0 (IQR 4.4–6.6) to 5.5 (4.8–7.0) ml/100g/min (10%, p=0.001); the response was comparable across the range of hemoglobin values. In vulnerable brain regions, transfusion resulted in a greater (16%) rise in oxygen delivery associated with reduction in OEF, independent of Hgb level (p=0.002 vs. normal regions). Conclusions This study demonstrates that RBC transfusion improves cerebral oxygen delivery globally and particularly to vulnerable regions in SAH patients at risk for DCI across a wide range of hemoglobin values and suggests that restrictive transfusion practices may not be appropriate in this population. Large prospective trials are necessary to determine if these physiologic benefits translate into clinical improvement and outweigh the risk of transfusion.

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“…It appears that MTT, not CBF, is the key component both to identify those more likely to develop DCI, but also for monitoring the effect of treatment. The authors were able to show a significant change with MTT with one-tenth the patients that have been thought to be needed for a trial of IH if one is looking for changes in CBF [7]. This paper, like others, did not find clinical differences in the DCI versus the non-DCI cohorts.…”

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confidence: 61%

CTP and DCI: We Need Clarification

Mattingly¹

2017

Neurocrit Care

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Effects of Induced Hypertension on Cerebral Perfusion in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Cited by 76 publications

References 5 publications

Effect of High-Dose Simvastatin on Cerebral Blood Flow and Static Autoregulation in Subarachnoid Hemorrhage

Effect of High-Dose Simvastatin on Cerebral Blood Flow and Static Autoregulation in Subarachnoid Hemorrhage

RBC Transfusion Improves Cerebral Oxygen Delivery in Subarachnoid Hemorrhage

CTP and DCI: We Need Clarification

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