Reduced Platelet Activity Is Associated With Early Clot Growth and Worse 3-Month Outcome After Intracerebral Hemorrhage

Naidech, Andrew M.; Jovanovic, Borko; Liebling, Storm; Garg, Rajeev; Bassin, Sarice L.; Bendok, Bernard R.; Bernstein, Richard A.; Alberts, Mark J.; Batjer, H. Hunt

doi:10.1161/strokeaha.109.550939

Cited by 189 publications

(125 citation statements)

References 26 publications

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“…With regard to antiplatelet pretreatment, clinical studies revealed much more controversial results (Wijman, 2009). Some authors reported a significant influence of antiplatelet pretreatment on hematoma growth and outcome (Naidech et al, 2009;Roquer et al, 2005;Saloheimo et al, 2006;Toyoda et al, 2005), whereas others did not (Foerch et al, 2006;Moussouttas et al, 2010;Sansing et al, 2009). Interestingly, adjusting for baseline factors such as premorbid disability and concomitant diseases seems to be a crucial factor (Foerch et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Our study is the first to provide experimental evidence that ASA and clopidogrel pretreatment does not increase hematoma volume and does not worsen functional outcome in this scenario. It has been suggested that reduced platelet activity in acute ICH (e.g., resulting from antiplatelet pretreatment) may be increased rapidly by platelet transfusion (Naidech et al, 2009)). This topic is currently investigated in the PATCH (Platelet Transfusion in Cerebral Hemorrhage) study (de Gans et al, 2010) However, our results imply that potential hemostatic approaches to prevent hematoma expansion should rather concentrate on the coagulation side of hemostasis (Mayer et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Accordingly, observational studies have indicated that previous use of platelet inhibitors in ICH is associated with higher mortality rates (Roquer et al, 2005;Saloheimo et al, 2006). Furthermore, reduced platelet activity may also be related to an increased early hematoma growth and a worse functional outcome at 3 months (Naidech et al, 2009;Toyoda et al, 2005). In contrast, several investigations have failed to identify the previous usage of antiplatelet agents as an independent risk factor of hematoma expansion and functional outcome in patients with ICH (Foerch et al, 2006;Moussouttas et al, 2010;Sansing et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Antiplatelet Pretreatment does not Increase Hematoma Volume in Experimental Intracerebral Hemorrhage

Lauer

Schlunk

Cott

et al. 2011

J Cereb Blood Flow Metab

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While oral anticoagulants are associated with greater hematoma expansion and higher mortality rates in patients with intracerebral hemorrhage (ICH), there is ongoing discussion whether pretreatment with antiplatelet drugs also worsens prognosis. Using an experimental model of ICH, we investigated the effects of antiplatelet pretreatment on hematoma volume and functional outcome. CD-1 mice were treated with acetyl-salicylic acid (ASA, 60 mg/kg per 24 hours), clopidogrel (22.5 mg/kg per 24 hours), or both (ASA + clopidogrel) through drinking water for 3 days (n = 20 per group). Thereafter, platelet aggregation was found to be significantly reduced. Untreated mice and mice pretreated with warfarin served as controls. A stereotactic injection of collagenase into the right striatum was used to induce ICH. Twenty-four hours after ICH induction, hematoma volume was measured to be 15.0±4.4 lL in controls, 14.1±5.3 lL in ASA mice, 16.8±5.1 lL in clopidogrel mice, and 16.4 ± 5.1 lL in ASA + clopidogrel animals. These differences were not statistically significant. However, mice pretreated with warfarin revealed largely increased hematoma volumes (25.0 ± 7.4 lL versus controls, P = 0.001). Neurologic outcome was not different between antiplateletpretreated animals and untreated controls. Our results suggest that plasmatic coagulation rather than platelet function is the most critical element for preventing hematoma expansion in acute ICH. Future therapeutic strategies may take these findings into account.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antiplatelet Pretreatment does not Increase Hematoma Volume in Experimental Intracerebral Hemorrhage

Lauer

Schlunk

Cott

et al. 2011

J Cereb Blood Flow Metab

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“…All patients were prospectively diagnosed by a boardcertified neurologist using computed tomography. We measured change in hematoma volume as previously described (16). Patients were excluded if their ICH was attributable to trauma, hemorrhagic conversion of ischemic stroke, or structural lesions (aneurysm, tumor, arteriovenous malformation, vessel dissection, and so forth).…”

Section: Methods Standard Protocol Approvals Registrations and Patimentioning

confidence: 99%

Intracerebral Hemorrhage and Delirium Symptoms. Length of Stay, Function, and Quality of Life in a 114-Patient Cohort

Naidech

Beaumont²,

Rosenberg³

et al. 2013

Am J Respir Crit Care Med

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105

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Rationale: The prognostic significance of delirium symptoms in intensive care unit (ICU) patients with focal neurologic injury is unclear. Objectives: To determine the relationship between delirium symptoms and subsequent functional outcomes and quality of life (QOL) after intracerebral hemorrhage. Methods: We prospectively enrolled 114 patients. Delirium symptoms were routinely assessed twice daily using the Confusion Assessment Method for the ICU by trained nurses. Functional outcomes were recorded with modified Rankin Scale (scored from 0 [no symptoms] to 6 [dead]), and QOL outcomes with Neuro-QOL at 28 days, 3 months, and 12 months. Measurements and Main Results: Thirty-one (27%) patients had delirium symptoms ("ever delirious"), 67 (59%) were never delirious, and the remainder (14%) had persistent coma. Delirium symptoms were nearly always hypoactive, were detected mean 6 days after intracerebral hemorrhage presentation, and were associated with longer ICU length of stay (mean 3.5 d longer in ever vs. never delirious patients; 95% confidence interval, 1.5-8.3; P ¼ 0.004) after correction for age, admit National Institutes of Health (NIH) Stroke Scale, and any benzodiazepine exposure. Delirium symptoms were associated with increased odds of poor outcome at 28 days (odds ratio, 8.7; 95% confidence interval, 1.4-52.5; P ¼ 0.018) after correction for admission NIH Stroke Scale and age, and with worse QOL in the domains of applied cognition-executive function and fatigue after correcting for the NIH Stroke Scale, age, benzodiazepine exposure, and time of follow-up. Conclusions: After focal neurologic injury, delirium symptoms were common despite low rates of infection and sedation exposure, and were predictive of subsequent worse functional outcomes and lower QOL. Keywords: delirium; outcomes; quality of lifeThe symptoms of delirium, a potential consequence of multiple clinical disease states and physiologic aberrations, include a shift in baseline mental status, inattention, and disorganized thinking or altered level of consciousness. Although nonspecific, this syndrome is an independent predictor of higher mortality (1), longer length of stay (LOS), higher cost of care, and worse long-term cognitive outcomes in medical, surgical, burn, and trauma intensive care unit (ICU) patients (2). There are few such data, however, in ICU patients with focal neurologic injury without systemic illness.Risk factors for delirium symptoms are typically global (infection [3] and intravenous sedation, particularly benzodiazepines [BZDs]) (4, 5) as opposed to focal lesions (e.g., hematoma). Most mechanically ventilated patients are delirious during hospitalization (1), potentially because of the sedation regimen (e.g., BZD infusion), but sedation is typically minimized in neurologically injured patients to permit repeated neurologic assessment that may lead to an acute intervention (6).Screening tests for delirium have been recently validated in neurologically ill patients (7-9), including ischemic stroke (7, 10) and intracerebra...

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“…The outcomes in individuals on antiplatelet therapy with an ICH are variable according to the available literature [135][136][137][138][139]. The best evidence includes a post-hoc analysis of the placebo arm of the CHANT study, which included 70 patients who were on antiplatelet therapy at onset of their ICH.…”

Section: Management Of Ich In Patients On Concurrent Antithrombotic Tmentioning

confidence: 99%

Treatment Targets in Intracerebral Hemorrhage

Sangha

Gonzales

2011

Neurotherapeutics

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Intracerebral hemorrhage (ICH) imparts a higher mortality and morbidity than ischemic stroke. The therapeutic interventions that are currently available focus mainly on supportive care and secondary prevention. There is a paucity of evidence to support any one acute intervention that improves functional outcome. This chapter highlights current treatment targets for ICH based on the pathophysiology of the disease.

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Reduced Platelet Activity Is Associated With Early Clot Growth and Worse 3-Month Outcome After Intracerebral Hemorrhage

Cited by 189 publications

References 26 publications

Antiplatelet Pretreatment does not Increase Hematoma Volume in Experimental Intracerebral Hemorrhage

Antiplatelet Pretreatment does not Increase Hematoma Volume in Experimental Intracerebral Hemorrhage

Intracerebral Hemorrhage and Delirium Symptoms. Length of Stay, Function, and Quality of Life in a 114-Patient Cohort

Treatment Targets in Intracerebral Hemorrhage

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