Relative brain density is superior to absolute density in predicting hemorrhagic transformation of brain infarction post thrombectomy.

Purpose Hyper-attenuating lesions, or contrast staining, on a non-contrast brain computed tomography (NCCT) scan have been investigated as a predictor for hemorrhagic transformation after endovascular treatment of acute ischemic stroke (AIS). However, the association of hyper-attenuating lesions and final ischemic areas are poorly investigated in this setting. The aim of the present study was to assess correlations between hyper-attenuating lesions and final brain infarcted areas after thrombectomy for AIS. Methods Data from patients with AIS of the anterior circulation who underwent endovascular treatment were retrospectively assessed. Images of the brain NCCT scans were analyzed in the first hours and late after treatment. The hyper-attenuating areas were compared to the final ischemic areas using the Alberta Stroke Program Early CT Score (ASPECTS). Results Seventy-one of the 123 patients (65.13%) treated were included. The association between the hyper-attenuating region in the post-thrombectomy CT scan and final brain ischemic area were sensitivity (58.3% to 96.9%), specificity (42.9% to 95.6%), positive predictive values (71.4% to 97.7%), negative predictive values (53.8% to 79.5%), and accuracy values (68% to 91%). The highest sensitivity values were found for the lentiform (96.9%) and caudate nuclei (80.4%) and for the internal capsule (87.5%), and the lowest values were found for the M1 (58.3%) and M6 (66.7%) cortices. Conclusions Hyper-attenuating lesions on head NCCT scans performed after endovascular treatment of AIS may predict final brain infarcted areas. The prediction appears to be higher in the deep brain regions compared with the cortical regions.

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Hemorrhagic transformation in ischemic stroke and its treatment during thrombolysis

Reviews in Health Care ◽

10.7175/rhc.v2i1s.39 ◽

2011 ◽

Vol 2 (1S) ◽

pp. 99-107

Author(s):

Maurizio Paciaroni ◽

Luca Masotti ◽

Valeria Caso

Keyword(s):

Ischemic Stroke ◽

Brain Infarction ◽

Hemorrhagic Transformation ◽

Stroke Patients ◽

Adequate Treatment ◽

Haemorrhagic Transformation ◽

Hemorrhagic Infarction ◽

Brain Infarcts ◽

Secondary Bleeding ◽

Key Points

Haemorrhagic transformation (HT) of brain infarction or hemorrhagic infarction is a complication of acute ischemic stroke, especially in cardioembolic stroke, and represents the most feared complication of thrombolysis. HT is a multifocal secondary bleeding into brain infarcts with innumerable foci of capillary and venular extravasation either remaining as discrete petechiae or emerging to form confluent purpura. HT is evidenced as a parenchymal area of increased density within an area of low attenuation in a typical vascular distribution on non-contrasted CT scans and is subdivided into two major categories on the basis of standardised definition: haemorrhagic infarct (HI) and parenchymal haematoma (PH). PH has been associated to poor outcome in ischemic stroke patients. Thus, its prevention, early detection and adequate treatment represent key points in the management of acute stroke.

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Abstract WMP84: Effects of a New Thrombolytic Compound DC007d in Acute Brain Tissue Damage After Focal Embolic Stroke in Rats

Stroke ◽

10.1161/str.51.suppl_1.wmp84 ◽

2020 ◽

Vol 51 (Suppl_1) ◽

Author(s):

Yinghua Jiang ◽

Ning Liu ◽

Xiao-ying Wang ◽

Iris Yuwen Zhou ◽

Chienhsi Chen ◽

...

Keyword(s):

Rat Model ◽

Brain Infarction ◽

Serum Levels ◽

Hemorrhagic Transformation ◽

Brain Swelling ◽

Infarction Size ◽

Swelling Rate ◽

Pai 1

Background and Purpose: DC007D is a novel small molecule designed to have thrombolytic and free radical scavenging activities. In this study, we aimed to test the potential neuroprotective effects of DC007D in embolic clot model of focal ischemic stroke in rats. Methods: All animals received intravenous infusion of either saline, 10 mg/kg DC007D or 10 mg/kg tPA at each experimental time point (1.5, 3 and 4.5 hrs after stroke, respectively). In first set of experiments, animals were treated at 1.5-hr after stroke. We performed a time course of multi-parametric MRI analysis including perfusion, diffusion and T2 relaxation. Brain infarction size and swelling rate were measured by TTC staining at 24 hrs after stroke. Next, in 3- and 4.5-hrs treatment experiments, we examined acute brain infarct volume, brain swelling rate, hemorrhagic transformation, neurological deficits. Additionally, we also tested potentially direct neuroprotection effects of DC007D in a mechanical filament pMCAO rat model. Lastly, the effect of DC007D in tPA activity in vitro, INR, and serum levels of tPA and PAI-1 activities in vivo at 24 hrs after stroke were assessed and compared. Results: Both tPA and DC007D treated at 1.5 hrs after stroke reduced hypoperfused area, diffusion, T2 lesion size and TTC-stained infarction. When treated at 3 hrs after stroke, DC007D had significantly better therapeutic effects in reducing brain infarction size, swelling rate and hemorrhagic transformation compared to conventional tPA treatment group. When treated at 4.5 hrs after stroke, both tPA and DC007D had no effects in brain infarction. However, tPA, but not DC007D, significantly increased brain swelling and intracerebral hemorrhagic transformation compared to saline controls. Our experimental results also showed that DC007D failed to have direct neuroprotection in the mechanical pMCAO rat model. Lastly, DC007D did not interfere tPA activity in vitro, and also did not significantly alter INR, serum levels of tPA and PAI-1 activities post stroke in vivo. Conclusions: DC007D is neuroprotective to embolic focal stroke of rats, likely via tPA/PAI-1 activity independent thrombolytic mechanism. It might be developed as a new and novel thrombolytics or adjunct for tPA thrombolytic reperfusion therapy.

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Abstract W P374: Coated-Platelet Levels Correlate With HAS-BLED Scores in Stroke Patients With Atrial Fibrillation

Stroke ◽

10.1161/str.45.suppl_1.wp374 ◽

2014 ◽

Vol 45 (suppl_1) ◽

Author(s):

Calin Prodan ◽

Andrea Vincent ◽

Angelia Kirkpatrick ◽

George Dale

Keyword(s):

Atrial Fibrillation ◽

Ischemic Stroke ◽

Intracerebral Hemorrhage ◽

Brain Infarction ◽

Pearson Correlation ◽

Preventive Treatment ◽

Bleeding Risk ◽

Hemorrhagic Transformation ◽

Stroke Patients ◽

Increased Risk

Background: Coated-platelets are a subset of procoagulant platelets observed upon dual agonist stimulation with collagen and thrombin. Coated-platelet levels are increased in non-lacunar ischemic stroke compared to controls; however, patients with early hemorrhagic transformation have lower coated-platelet levels than those without. In contrast to brain infarction, coated-platelet levels are decreased in intracerebral hemorrhage and inversely correlated with the size of the bleed. Because anticoagulation is a key preventive treatment in cardioembolic stroke, we investigated the existence of a relationship between coated-platelets and bleeding risk in stroke patients with atrial fibrillation. Methods: Coated-platelet levels, reported as percent of platelets converted to coated-platelets, were determined in 45 consecutive patients with acute stroke and atrial fibrillation. Exclusion criteria consisted of dementia, stroke due to other causes than atrial fibrillation, > 96 hours between onset of symptoms and coated-platelet assay, current anticoagulation, prior thrombolytics or abnormal PT/PTT/INR. Bleeding risk was determined for each patient using the HAS-BLED score. The correlation between individual coated-platelet levels and HAS-BLED scores was determined using the Pearson correlation coefficient. Results: Coated-platelet levels for the 45 patients were 41.0 ± 13.9% (mean ± SD, range 13.2 to 69.7%), consistent with previous data in patients with non-lacunar ischemic stroke. Mean HAS-BLED score was 3.2 ± 1.6, with a range between 1 and 7. A highly significant inverse linear correlation between coated-platelet levels and HAS-BLED scores was observed (p < 0.001, r = -0.67). Conclusions: Lower coated-platelet levels correlate with higher HAS-BLED scores in patients with stroke due to atrial fibrillation, suggesting that decreased coated-platelet synthesis is present in patients with an increased risk for bleeding. Our results are consistent with previously published research showing lower coated-platelet levels in intracerebral hemorrhage and early hemorrhagic transformation of ischemic stroke, and support a role played by this subset of activated platelets in the balance between thrombosis and hemorrhage.

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Annexin A2 Combined with Low-Dose tPA Improves Thrombolytic Therapy in a Rat Model of Focal Embolic Stroke

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2009.279 ◽

2010 ◽

Vol 30 (6) ◽

pp. 1137-1146 ◽

Cited By ~ 53

Author(s):

Haihao Zhu ◽

Xiang Fan ◽

Zhanyang Yu ◽

Jianxiang Liu ◽

Yoshihiro Murata ◽

...

Keyword(s):

Low Dose ◽

Time Window ◽

Thrombus Formation ◽

Brain Infarction ◽

Hemorrhagic Transformation ◽

Annexin A2 ◽

Embolic Stroke ◽

Model Combination

Recent studies showed that soluble annexin A2 dramatically increases tissue plasminogen activator (tPA)-mediated plasmin generation in vitro, and reduces thrombus formation in vivo. Here, we hypothesize that combining annexin A2 with tPA can significantly enhance thrombolysis efficacy, so that lower doses of tPA can be applied in ischemic stroke to avoid neurotoxic and hemorrhagic complications. In vitro activity assays confirmed tPA-specific amplification of plasmin generation by recombinant annexin A2. In a rat focal embolic stroke model, combination therapy with tPA and recombinant annexin A2 protein at 2 h post-ischemia decreased the effective dose required for tPA by four-fold and reduced brain infarction. Combining annexin A2 with tPA also lengthened the time window for thrombolysis. Compared with tPA (10 mg/kg) alone, the combination of annexin A2 (5 mg/kg) plus low-dose tPA (2.5 mg/kg) significantly enhanced fibrinolysis, attenuated mortality, brain infarction, and hemorrhagic transformation, even when administered at 4 h post-ischemia. Combination with recombinant annexin A2, the effective thrombolytic dose of tPA can be decreased. As a result, brain hemorrhage and infarction are reduced, and the time window for stroke reperfusion prolonged. Our present findings provide a promising new approach for enhancing tPA-based thrombolytic stroke therapy.

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Hemorrhagic transformation in ischemic stroke and its treatment during thrombolysis

Reviews in Health Care ◽

10.7175/rhc.3921s99-107 ◽

2011 ◽

Vol 2 (1S) ◽

pp. 99

Author(s):

Maurizio Paciaroni ◽

Luca Masotti ◽

Valeria Caso

Keyword(s):

Ischemic Stroke ◽

Brain Infarction ◽

Hemorrhagic Transformation ◽

Stroke Patients ◽

Adequate Treatment ◽

Haemorrhagic Transformation ◽

Hemorrhagic Infarction ◽

Brain Infarcts ◽

Secondary Bleeding ◽

Key Points

Haemorrhagic transformation (HT) of brain infarction or hemorrhagic infarction is a complication of acute ischemic stroke, especially in cardioembolic stroke, and represents the most feared complication of thrombolysis. HT is a multifocal secondary bleeding into brain infarcts with innumerable foci of capillary and venular extravasation either remaining as discrete petechiae or emerging to form confluent purpura. HT is evidenced as a parenchymal area of increased density within an area of low attenuation in a typical vascular distribution on non-contrasted CT scans and is subdivided into two major categories on the basis of standardised definition: haemorrhagic infarct (HI) and parenchymal haematoma (PH). PH has been associated to poor outcome in ischemic stroke patients. Thus, its prevention, early detection and adequate treatment represent key points in the management of acute stroke.

Download Full-text