Blood coagulation and fibrinolysis in acute ischaemic and haemorrhagic (intracerebral and subarachnoid haemorrhage) stroke: does decreased plasmin inhibitor indicate increased fibrinolysis in subarachnoid haemorrhage compared to other types of stroke?

Antović, Jovan P.; Bakić, Mirjana; Živković, Mladen; Ilić, Ana; Blombäck, M

doi:10.1080/003655102317475452

Cited by 25 publications

(14 citation statements)

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“…Markers of hypercoagulation, (Antovic et al, 2002; Peltonen et al, 1997) and platelet activation (Denton et al, 1971; Ishikawa et al, 2009; Juvela et al, 1991) rapidly increase following aneurysm rupture; values are higher in the CSF and jugular blood compared to systemic levels, suggesting a cerebral origin (Hirashima et al, 1997; Kasuya et al, 1998; Suzuki et al, 1999). In addition, several autopsy studies have detected the presence of small intra-vascular blood clots, termed microclots, and have demonstrated a correlation between microclot density and the location and severity of histological evidence of ischemia (Stein et al, 2006b) or radiographic evidence of infarction (Suzuki et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Microthrombosis after experimental subarachnoid hemorrhage: Time course and effect of red blood cell-bound thrombin-activated pro-urokinase and clazosentan

Pisapia

Kelly

et al. 2012

Experimental Neurology

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Delayed cerebral ischemia (DCI) is a significant cause of morbidity and mortality for patients surviving the rupture of an intracranial aneurysm. Despite an association between vasospasm and DCI, thrombosis and thromboembolism may also contribute to DCI. In this study we investigate the time course of intravascular microclot formation after experimental subarachnoid hemorrhage (SAH) and assess the effects of the following two drugs on microclot burden: mutant thrombin-activated urokinase-type plasminogen activator (scFv/uPA-T), which is bound to red blood cells for use as a thromboprophylactic agent, and clazosentan, an endothelin antagonist. In the first study, adult male C57BL/6 mice were sacrificed at 24 (n=5), 48 (n=6), 72 (n=8), and 96 (n=3) hours after SAH induced by filament perforation of the anterior cerebral artery. Sham animals (n=5) underwent filament insertion without puncture. In the second study, animals received scFv/uPA-T (n=5) 3 hours after hemorrhage, clazosentan (n=5) by bolus and subcutaneous pump after SAH just prior to skin closure, or a combination of scFv/uPA-T and clazosentan (n=4). Control (n=6) and sham (n=5) animals received saline alone. All animals were sacrificed at 48 hours and underwent intra-cardiac perfusion with 4% paraformaldehyde. The brains were then extracted and sliced coronally on a cryostat and processed for immunohistochemistry. An antibody recognizing thrombin–anti-thrombin complexes was used to detect microclots on coronal slices. Microclot burden was calculated for each animal and compared among groups. Following SAH, positive anti-thrombin staining was detected bilaterally in the following brain regions, in order of decreasing frequency: cortex; hippocampus; hypothalamus; basal ganglia. Few microclots were found in the shams. Microclot burden peaked at 48 hours and then decreased gradually. Animals receiving scFv/uPA-T and scFv/uPA-T+clazosentan had a lower microclot burden than controls, whereas animals receiving clazosentan alone had a higher microclot burden (p<0.005). The overall mortality rate in the time course study was 40%; mortality was highest among control animals in the second study. Intravascular microclots form in a delayed fashion after experimental SAH. Microclots may be safely reduced using a novel form of thromboprophylaxis provided by RBC-targeted scFv/uPA-T and represent a potential target for therapeutic intervention in the treatment of DCI.

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Section: Introductionmentioning

confidence: 99%

Microthrombosis after experimental subarachnoid hemorrhage: Time course and effect of red blood cell-bound thrombin-activated pro-urokinase and clazosentan

Pisapia

Kelly

et al. 2012

Experimental Neurology

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“…So blood coagulation profile may become a possible candidate predictor. But the results of blood coagulation profile may be inconsistent in different blood taking time because of their rapid change resulting from consumed clotting factors over time (Antovic et al, 2002). And it was difficult to make uniform in blood taking time in present retrospective study.…”

Section: The Roles Of Laboratorial Candidates In the Prognosis Of Ichmentioning

confidence: 78%

A new prognostic model and score to predict short term outcome after intracerebral hemorrhage

Li¹,

Chen²,

Wang³

et al. 2011

Sci. Res. Essays

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Spontaneous intracerebral hemorrhage (ICH) accounts for the highest mortality of all strokes. An early and reliable prognostic indication in ICH patients is potentially useful for initiating individual treatment and for informing patients and families. The published predictive models are largely based on neurological features; however, a part of them need to be judged with the subjective viewpoint of physician. Recently, we reviewed the data of 716 patients of ICH within 30 days. By univariate analysis and receiver operating characteristic (ROC) curves, four independent predictors for death outcome were identified from 11 laboratorial items and patient's basic information, such as blood glucose (Glu), white blood cell count (WBC), lactate dehydrogenase (LDH) and age. With the AUC of 0.769, the prognostic model was developed by logistic regression. When the threshold of prediction index was set to 0.106, the sensitivity (88.9%) and specificity (55.6%) for death outcome were obtained by ROC curves. Furthermore, a simple predictive score was developed, whose AUC was 0.745. On a range from 0 -4, the score of ≥3 could predict death outcome with good sensitivity (71.4%) and specificity (72.3%). The objective regression model and score had perfect discriminatory power for the prognosis of ICH within 30 days without the subjective judgment of physicians. It should be easily used by both neurological specialists and community doctors.

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“…However in group II, as in group III (with no deaths), the concentration of fibrinogen was increased and maintained in the following days. An increased concentration of fibrinogen in the acute phase of stroke is usually interpreted as an acute-phase response [1,19].…”

Section: Discussionmentioning

confidence: 99%

“…These studies recommend the determination of fibrinogen, PT, APTT, D-dimers, AT and PLT [5,19,21,26].…”

Section: Discussionmentioning

confidence: 99%

The character of haemostatic disorders and level of protein S-100 in acute ischaemic stroke can affect survival in the first week of follow-up

Jastrzębska

Chełstowski²,

Siennicka³

et al. 2011

Blood Coagulation & Fibrinolysis

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Disorders of haemostasis which result in ischaemic stroke usually appear as thromboembolism in peripheral veins and the pulmonary circulation, and to a lesser extent as coagulopathy. The S-100 protein, a marker of stroke, correlates positively with the neurological deficit National Institutes of Health Stroke Scale (NIHSS). We adopted the hypothesis that early death of patients with acute ischaemic stroke can be explained by changes in blood coagulation and fibrinolysis. The study included 84 patients hospitalized with acute ischaemic stroke. Three groups were created: I (death between 1 and 2 days), II (death between 5 and 7 days) and III (with no deaths in hospital). We measured levels of fibrinogen, antithrombin, D-dimers, plasmin-antiplasmin complexes, plasminogen and clotting times (prothrombin time and activated partial thromboplastin time), platelet number, euglobulin clot lysis time (ECLTindex) and S-100 protein, C-reactive protein and white blood cells (WBCs). Group I had lower concentrations of fibrinogen compared to groups II (3.13 vs. 4.18, P<0.01) and III (3.13 vs. 3.77, P<0.02) and higher levels of D-dimers (3643 vs. 2278, P<0.05), higher concentrations of plasmin-antiplasmin complexes (1410 vs. 882, P=0.03) and a lower ECLTindex (152 vs. 219, P<0.02) when compared with group III. Group I also had higher concentrations of protein S-100 (2.09 vs. 0.61, P<0.001), higher NIHSS (18.0 vs. 13.2, P=0.073) and number of WBC (14.1 vs. 11.1, P<0.02) than in group III. The observed abnormalities in haemostasis, either found systemically or locally as cerebral microvascular thrombosis, may be factors potentially associated with death of patients with the shortest survival time.

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Blood coagulation and fibrinolysis in acute ischaemic and haemorrhagic (intracerebral and subarachnoid haemorrhage) stroke: does decreased plasmin inhibitor indicate increased fibrinolysis in subarachnoid haemorrhage compared to other types of stroke?

Cited by 25 publications

References 1 publication

Microthrombosis after experimental subarachnoid hemorrhage: Time course and effect of red blood cell-bound thrombin-activated pro-urokinase and clazosentan

Microthrombosis after experimental subarachnoid hemorrhage: Time course and effect of red blood cell-bound thrombin-activated pro-urokinase and clazosentan

A new prognostic model and score to predict short term outcome after intracerebral hemorrhage

The character of haemostatic disorders and level of protein S-100 in acute ischaemic stroke can affect survival in the first week of follow-up

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