Role of platelet function in symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Ohkuma, Hiroki; Suzuki, Shigeharu; Kimura, Masaomi; Sobata, E

doi:10.1161/01.str.22.7.854

Cited by 79 publications

(42 citation statements)

References 32 publications

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“…Increased platelet aggregability might play a role in the pathogenesis of DCI. [22][23][24] An observational study has shown that patients who had taken Kaplan-Meier curve for the composite outcome event of death or DCI, according to the duration of unconsciousness. The height under the curves refers to the proportion of patients who are still alive and did not develop DCI.…”

Section: Discussionmentioning

confidence: 99%

Initial Loss of Consciousness and Risk of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Hop¹,

Rinkel²,

Algra³

et al. 1999

Stroke

131

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Background and Purpose-Delayed cerebral ischemia (DCI) is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. We studied the prognostic value for DCI of 2 factors: the duration of unconsciousness after the hemorrhage and the presence of risk factors for atherosclerosis. Methods-In 125 consecutive patients admitted within 4 days after hemorrhage, we assessed the presence and duration of unconsciousness after the hemorrhage, the neurological condition on admission, the amount of subarachnoid blood, the size of the ventricles, and a history of smoking, hypertension, stroke, or myocardial infarction. The relationship between these variables and the development of DCI was analyzed by means of the Cox proportional hazards model. Results-The univariate hazard ratio (HR) for the development of DCI in patients who had lost consciousness for Ͼ1 hour was 6.0 (95% CI 3.0 to 12.0) compared with patients who had no loss or a Ͻ1-hour loss of consciousness. The presence of any risk factor for atherosclerosis yielded an HR of 1.4 (95% CI 0.6 to 3.5). The HR for unconsciousness remained essentially the same after adjustment for other risk factors for DCI. The HR for a poor World Federation of Neurological Surgeons score (grade IV or V) on admission was 2.9 (95% CI 1.5 to 5.5); that for a large amount of subarachnoid blood on CT was 3.4 (95% CI 1.6 to 7.3). Conclusions-The duration of unconsciousness after subarachnoid hemorrhage is a strong predictor for the occurrence of DCI. This observation may contribute to a better understanding of the pathogenesis of DCI and increased attention for patients at risk. (Stroke. 1999;30:2268-2271.)

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Section: Discussionmentioning

confidence: 99%

Initial Loss of Consciousness and Risk of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Hop¹,

Rinkel²,

Algra³

et al. 1999

Stroke

131

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“…Increased platelet activation and aggregation are suggested by increased levels of b-thromboglobulin, thromboxane B2, soluble platelet selectin (sP-selectin), and platelet-activating factor (Ohkuma et al, 1991;Hirashima et al, 1997a;Frijns et al, 2006 b;Nissen et al, 2001). Interestingly, increased procoagulant activity is already present within a few days after SAH, that is, in a time period before vasospasm develops.…”

Section: Activation Of the Coagulation Cascadementioning

confidence: 99%

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

Vergouwen

Vermeulen

Coert

et al. 2008

J Cereb Blood Flow Metab

289

195

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Patients with aneurysmal subarachnoid hemorrhage (SAH) who experience delayed cerebral ischemia (DCI) have an increased risk of poor outcome. Delayed cerebral ischemia is considered to be caused by vasospasm. However, not all patients with DCI have vasospasm. Inversely, not all patients with vasospasm develop clinical symptoms and signs of DCI. In the past, treatments aiming at vasospasm were not successful in preventing ischemia. The purpose of this review is to give an overview of clinical data showing that DCI cannot always be attributed to vasospasm, and to present an in-depth analysis of clinical and autopsy studies on the role of microthrombosis in the pathogenesis of DCI. Clinical studies show that DCI is associated with an activation of the coagulation cascade within a few days after SAH, preceding the time window during which vasospasm occurs. Furthermore, impaired fibrinolytic activity, and inflammatory and endotheliumrelated processes, lead to the formation of microthrombi, which ultimately result in DCI. The presence of microthrombi is confirmed by autopsy studies. Insight in the pathophysiology of DCI is crucial for the development of effective therapies against this complication. Because multiple pathways are involved, future research should focus on drugs with pleiotropic effects.

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“…Then serotonin and thromboxane released from platelets enhance vasoconstriction and produce microemboli that accelerate brain ischemia, leading to symptomatic vasospasm. 26 …”

Section: Hypothesismentioning

confidence: 99%

The role of superoxide anions in the pathogenesis of cerebral vasospasm.

Shishido

Suzuki

Liang

et al. 1994

Stroke

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To determine the role of superoxide anions in the pathogenesis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage, we studied the preventive effect of human recombinant copper-zinc superoxide dismutase (h-r SOD) in a rabbit subarachnoid hemorrhage (SAH) model. Forty-five rabbits receiving intracisternal injection of 3 mL autologous nonheparinized blood or 3 mL saline were divided into four groups as follows: (1) saline injected and no treatment (control group, n = 6); (2) blood injected and no treatment (SAH group, n = 20); (3) blood injected and treated by multiple intracisternal injections of 30,000 U of h-r SOD in 0.5 mL saline (SOD group, n = 9); and (4) blood injected and treated by multiple intracisternal injections of 0.5 mL saline (saline group, n = 10). Serial angiograms were performed after the blood injection, and the diameter of the basilar artery was measured. Three animals from the control group and five animals from the SAH and SOD groups each were killed 2 days after SAH, and their basilar arteries were processed for transmission electron microscopic observations. In the SAH and saline groups, the diameter of the basilar arteries was significantly reduced (28 +/- 14% and 27 +/- 9%, respectively) at 2 days after the blood injection, then recovered to pre-SAH levels until 11 days. In the SOD group, the diameter of the basilar artery was only minimally changed during the follow-up period. Transmission electron microscopy revealed endothelial injury in all basilar arteries in the SAH group, whereas endothelial injury was minimal in the SOD group. We determined that h-r SOD prevents the occurrence of vasospasm, possibly as a result of preventing endothelial injury initiated by superoxide anions.

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Role of platelet function in symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Cited by 79 publications

References 32 publications

Initial Loss of Consciousness and Risk of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Initial Loss of Consciousness and Risk of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

The role of superoxide anions in the pathogenesis of cerebral vasospasm.

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