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PubMed2005

Functional recovery after embolic stroke in rodents by activated protein C.

A serine protease activated protein C has been shown to be a powerful neuroprotectant in stressed neurons and in hypoxic brain endothelium. In a clinically relevant model of embolic stroke in rodents, we now show that administration of activated protein C alone or in combination with tissue plasminogen activator, or both, 4 hours after embolic stroke improves the functional outcome and reduces brain infarction within 7 days of stroke. In contrast, tissue plasminogen activator alone was not protective. Thus, activated protein C may be useful as a new stand-alone therapy for clinical stroke and to extend the time window of thrombolytic therapy.

Animals↗
PubMed1990

[Clinical results of open heart surgery within 2 weeks after cardiogenic embolic stroke].

Fourteen patients, 5 with infective valvular disease (IVD), 7 with non-infective valvular disease (NVD) and 3 with LA myxoma, underwent open heart surgery within 2 weeks after cardiogenic embolic stroke because of uncontrolled heart failure or recurrent embolism. Fifty percent of patients experienced a second embolism within 2 weeks of the initial stroke. Preoperative brain CT revealed no hemorrhagic infarction in all patients. However, in 3 of 5 patients with IVD, who had large brain infarction, one patient died from massive brain edema and two patients from severe brain hemorrhage. The other 2 patients with IVD, who had small infarction, and the remaining 7 patients with NVD and LA myxoma, even having large or small infarction, recovered without any complications. From these results, we concluded that 1) Open heart surgery within 2 weeks after initial stroke was safe in patients with no brain infarction and small non-hemorrhagic infarction, 2) Patients with IVD should be treated surgically before embolic stroke, because mortality rate was so high even in patients with non-hemorrhagic infarction.

Adult↗
PubMed2003

Recovery of apparent diffusion coefficient after embolic stroke does not signify complete salvage of post-ischemic neuronal tissue.

BACKGROUND AND PURPOSE: It has been shown in previous studies that recovery of apparent diffusion coefficient (ADC) of water is not necessarily associated with a reversal of tissue damage. We examined the relationships between temporal ADC change and histological outcome after embolic stroke in rat using an experimental MRI scanner. SUBJECTS AND METHODS: Male Wistar rats underwent embolization of the right middle cerebral artery with autologous clot. ADC and relative cerebral blood flow (rCBF) were measured consecutively for 3 hours after embolization. The brains were prepared for histological examination. RESULTS: Transient decline of ADC was observed during the initial 2 hours after embolization. In these areas, serial rCBF measurement revealed incomplete recovery. In some other areas, ADC decrease without rCBF recovery was observed during 3 hours postischemia. Histological examination revealed infarction in areas with persistent ADC decrease. Scattered neuronal death was noticeable in areas with a transient--in some areas less than 0.5 hour--ADC decrease. CONCLUSION: Consecutive MRI analysis demonstrated postischemic transient ADC decrease in an embolic stroke model of rat. The normalization of ADC does not signify normalization of postischemic tissue, since the areas often evolve postischemic neuronal death at a later time.

Animals↗
PubMed1995

Fibrinolytic therapy for acute embolic stroke: intravenous, intracarotid, and intra-arterial local approaches.

To clarify the efficacy and limitations of the intra-arterial local infusion of a high-dose fibrinolytic agent for acute embolic stroke, we analyzed the results of 44 patients and compared them with those of 51 patients treated with intracarotid (18 patients) or intravenous (33 patients) infusion therapy. Ten megaunits of recombinant tissue plasminogen activator or 24 x 10(4) IU of urokinase were administered through a microcatheter placed into or proximal to an embolus for 20 minutes. When arterial recanalization was not achieved, a second or third infusion was performed. The rates of complete and partial recanalization just after the local infusion were 52 and 32%, respectively. They were high in middle cerebral and basilar artery occlusion and low in internal carotid artery occlusion (69, 78, and 20%, respectively). In our use, there was no difference between tissue plasminogen activator and urokinase in restoring blood flow. The mean time interval from onset to recanalization in patients with middle cerebral artery occlusion showing marked improvement was 4.8 hours, and it was 5.8 hours with basilar artery occlusion. The size of infarction was reduced, and the outcome was good in patients with complete recanalization achieved. The incidence of hemorrhagic infarction within 24 hours was 22%, and only one patient clinically deteriorated. In the intracarotid infusion group (20 x 10(4) IU of urokinase for 30 min), only two patients showed partial recanalization without clinical improvement. The incidence of hemorrhagic infarction was 28%. The outcome in this group and the intravenous infusion group (18 x 10(4) IU of urokinase a day for 1 wk) was poor compared with that in the local infusion group showing complete recanalization. This preliminary study appears to suggest that intra-arterial local fibrinolytic therapy could be a new strategy for acute embolic stroke.

Acute Disease↗
PubMed1987

Prophylactic anticoagulants in managing embolic stroke.

The primary risk of anticoagulant therapy in cardiac embolic stroke is hemorrhage--particularly cerebral hemorrhage in the elderly. Improving the benefit/risk ratio for indicated anticoagulation involves consideration of the following: hemostatic competence, blood pressure, drug interactions, falls, interval surgery, diet, aspirin and last but not least, the intensity of anticoagulant prophylaxis. For the present it would be prudent to limit heparin administration to a low-dose regimen not exceeding 20,000 units/24 hours and warfarin maintenance to a low-dose prothrombin time ratio of 1.5.

Accidental Falls↗
PubMed2006

Characterization of cerebral tissue by MRI map ISODATA in embolic stroke in rat.

ISODATA using MRI parameter-weighted images has been previously employed to characterize ischemic cell damage after stroke in rats. In an effort to increase the objectivity and to further automate the ISODATA, MRI parameter maps were now employed. Male Wistar rats were subjected to embolic stroke and received treatment via a femoral vein at 4 h post-stroke. The control rats received saline and were sacrificed at 6, 24 and 48 h after stroke, respectively. Treated rats received rtPA alone or were treated with a combination of rtPA and an antibody, 7E3 F(ab')2, against the glycoprotein receptor that binds the platelet to fibrin. These rats were sacrificed at 24, or 48, h post-stroke. T1, T2 and diffusion maps were employed for map ISODATA analysis. H&E histological analysis of coronal sections of tissue was performed and compared with map ISODATA from the corresponding sections. ISODATA signatures were highly correlated (R approximately 0.80, P < 0.0001) with the ischemic cell damage analyzed at 6, 24 and 48 h post-stroke. At 24 and 48 h after stroke, ISODATA lesion sizes were highly correlated (R > 0.97, P < 0.001) with lesion sizes measured histologically. The combination treatment of rtPA and 7E3 F(ab')2 reduced both infarction size (P < 0.002) and average signature (P < 0.03) at 48 h after stroke, compared to saline-treated animals. No significant difference was found between saline and rtPA-alone-treated rats. The map ISODATA successfully provides objective and automated quantitation of the ischemic damage in both size and severity in an embolic stroke model of rat with and without a therapeutic intervention.

Animals↗
PubMed2006

Single-vessel versus multivessel territory acute ischemic stroke: value of transesophageal echocardiography in the differentiation of embolic stroke.

OBJECTIVES: We sought to assess the presence of potential aortic or cardiac sources of embolism in patients presenting with acute ischemic stroke in one or more vascular territories. BACKGROUND: In patients with acute ischemic stroke, involvement of multiple vascular territories has been used to implicate a cardiac or aortic source of embolus. It remains unclear whether patients with multivessel stroke have a higher frequency of cardiac or aortic embolic sources on transesophageal echocardiography (TEE) compared with patients with single-territory stroke. METHODS: We identified 210 patients with acute ischemic stroke documented by neuroimaging undergoing TEE for identification of a potential embolic source. Patients were divided into 3 groups (lacunar stroke, nonlacunar stroke/single-vessel involvement, nonlacunar stroke/multivessel involvement) and the frequency of potential embolic sources on TEE was compared. RESULTS: Of the 210 patients, 121 (58%) were male and the mean age was 61 years. In all, 139 patients (66%) were classified as having single-vessel stroke, 47 (22%) as having multivessel stroke, and 24 (11%) as having lacunar stroke. On TEE, 87 patients (41%) had at least one potential source of embolism. Patients with multivessel strokes had fewer potential embolic sources on TEE than patients with single-vessel or lacunar strokes (26% vs 46% and 46%, respectively; P = .043). CONCLUSIONS: In patients with acute ischemic stroke, the incidence of a potential cardiac or aortic source of embolism is high, regardless of the vascular distribution of the stroke. TEE may be a useful tool to assess the source of stroke in single-vessel, multivessel, and lacunar territory stroke distribution. We aimed to assess the presence of potential aortic or cardiac sources of embolism in patients presenting with acute ischemic stroke in one or more vascular territories. A total of 210 patients with acute ischemic stroke were divided into 3 groups (lacunar stroke, nonlacunar stroke/single-vessel involvement, nonlacunar stroke/multivessel involvement) and the frequency of potential embolic sources on transesophageal echocardiography was compared. Patients with multivessel strokes had fewer potential embolic sources on transesophageal echocardiography than patients with single-vessel or lacunar strokes, but the frequency of a potential cardiac or aortic source of embolism was high, regardless of the vascular distribution of stroke.

Brain Ischemia↗
PubMed2003

Ebselen, a seleno-organic antioxidant, is neuroprotective after embolic strokes in rabbits: synergism with low-dose tissue plasminogen activator.

BACKGROUND AND PURPOSE: It has been proposed that antioxidants and spin-trap agents may be neuroprotective after acute ischemia stroke. Although the antioxidant ebselen is currently in clinical trials, little is known about the effectiveness of ebselen, which has glutathione peroxidase-like and anti-inflammatory properties in embolic stroke models. Therefore, we determined the effects of ebselen when administered alone or with the thrombolytic tissue plasminogen activator (tPA), the only Food and Drug Administration-approved pharmacological agent for the treatment of stroke. METHODS: Male New Zealand White rabbits were embolized by injection of a suspension of small blood clots into the middle cerebral artery via a catheter. Five minutes after embolization, ebselen (10 to 50 mg/kg) was infused intravenously. Control rabbits received infusions of the vehicle required to solubilize ebselen. In additional rabbits, ebselen (20 mg/kg) was administered 60 minutes after embolization, either alone or in combination with tPA (0.9 or 3.3 mg/kg tPA). Behavioral analysis was conducted 24 hours after embolization, allowing determination of the effective stroke dose (P50) or clot amount (mg) that produces neurological deficits in 50% of the rabbits. RESULTS: A drug is considered neuroprotective if it significantly increases the P50 compared with the vehicle-treated control group. The P50 of controls 24 hours after embolization was 1.35+/-0.30 mg. Rabbits treated 5 minutes after embolization with 10, 20, or 50 mg/kg ebselen had P50 values of 2.12+/-0.56, 2.82+/-0.75 (P<0.05), and 0.49+/-0.54 mg, respectively. A significant neuroprotective effect was observed with the 20-mg/kg dose, but not if there was a 60-minute delay before administration (P50=1.69+/-0.32 mg). When tPA (3.3 mg/kg) was infused 60 minutes after embolization and ebselen (20 mg/kg) was injected at either 5 (P50=2.98+/-0.18 mg) or 60 (P50=3.60+/-0.79 mg) minutes, there was no additional neuroprotective effect compared with tPA alone (P50=3.38+/-0.55 mg). However, if ebselen (20 mg/kg) was administered concomitantly with low-dose tPA (0.9 mg/kg) 60 minutes after embolization, the P50 was 3.52+/-0.73 mg (P<0.05), indicating a synergistic effect of the drug combination because neither alone was effective (P50=1.69+/-0.32 and 1.54+/-0.36 mg, respectively). CONCLUSIONS: This study indicates that ebselen may be neuroprotective when administered shortly after an embolic stroke, but the time- and dose-response analyses suggest that it has a narrow therapeutic window. Nevertheless, ebselen may be beneficial if administered concomitantly with a thrombolytic because it significantly enhanced the neuroprotective activity of low-dose tPA.

Animals↗
PubMed2002

Rotational vertebral artery occlusion from occipital bone anomaly: a rare cause of embolic stroke. Case report.

Vertebral artery (VA) occlusion by rotation of the head is uncommon, but can result from mechanical compression of the artery, trauma, or atlantoaxial instability. Occipital bone anomalies rarely cause rotational VA occlusion, and patients with nontraumatic intermittent occlusion of the VA usually present with compromised vertebrobasilar flow. A 34-year-old man suffered three embolic strokes in the vertebrobasilar system within 2 months. Magnetic resonance imaging demonstrated multiple infarcts in the vertebrobasilar territory. Angiography performed immediately after the third attack displayed an embolus in the right posterior cerebral artery. Radiographic and three-dimensional computerized tomography bone images exhibited an anomalous osseous process of the occipital bone projecting to the posterior arch of the atlas. Dynamic angiography indicated complete occlusion of the left VA between the osseous process and the posterior arch while the patient's head was turned to the right. Surgical decompression of the VA resulted in complete resolution of rotational occlusion of the artery. An occipital bone anomaly can cause rotational VA occlusion at the craniovertebral junction in patients who present with repeated embolic strokes resulting from injury to the arterial wall.

Adult↗
PubMed2004

Transcranial infrared laser therapy improves clinical rating scores after embolic strokes in rabbits.

BACKGROUND AND PURPOSE: Because photon energy delivered using a low-energy infrared laser may be useful to treat stroke, we determined whether transcranial laser therapy would improve behavioral deficits in a rabbit small clot embolic stroke model (RSCEM). METHODS: In this study, the behavioral and physiological effects of laser treatment were measured. The RSCEM was used to assess whether low-energy laser treatment (7.5 or 25 mW/cm2) altered clinical rating scores (behavior) when given to rabbits beginning 1 to 24 hours postembolization. Behavioral analysis was conducted from 24 hours to 21 days after embolization, allowing for the determination of the effective stroke dose (P50) or clot amount (mg) that produces neurological deficits in 50% of the rabbits. Using the RSCEM, a treatment is considered beneficial if it significantly increases the P50 compared with the control group. RESULTS: In the present study, the P50 value for controls were 0.97+/-0.19 mg to 1.10+/-0.17 mg; this was increased by 100% to 195% (P50=2.02+/-0.46 to 2.98+/-0.65 mg) if laser treatment was initiated up to 6 hours, but not 24 hours, postembolization (P50=1.23+/-0.15 mg). Laser treatment also produced a durable effect that was measurable 21 days after embolization. Laser treatment (25 mW/cm2) did not affect the physiological variables that were measured. CONCLUSIONS: This study shows that laser treatment improved behavioral performance if initiated within 6 hours of an embolic stroke and the effect of laser treatment is durable. Therefore, transcranial laser treatment may be useful to treat human stroke patients and should be further developed.

Animals↗
PubMed1997

Intravenous thrombolysis with recombinant staphylokinase versus tissue-type plasminogen activator in a rabbit embolic stroke model.

BACKGROUND AND PURPOSE: Timely intravenous administration of recombinant tissue-type plasminogen activator (alteplase, rTPA) to patients with evolving ischemic stroke improves neurological outcome. The present study was designed to compare the effects of rTPA and recombinant staphylokinase (Sak), a highly fibrin-specific thrombolytic agent, in an experimental model of rabbit embolic stroke. METHODS: Groups of 5 to 12 rabbits were given intravenous saline or heparin and aspirin with, in addition, either Sak (1 or 2 mg/kg infused over 30 minutes or 2 mg/kg injected over 1 minute) or rTPA (3 or 6 mg/kg infused over 30 minutes or 6 mg/kg injected over 1 minute). Infusions were started 15 minutes after selective injection of standardized 125I-fibrin labeled rabbit plasma clots into the internal carotid artery. RESULTS: Mean clot lysis over 60 minutes increased from 3.8% after saline to between 27% and 44% after Sak regimens (P = .0001 versus control) and to between 15% and 34% after rTPA regimens (P = .0001). Median volume of the ischemic lesion at 5 hours decreased from 190 mm3 after saline to between 11 and 17 mm3 after Sak (P = .02) and to between 0.5 to 54 mm3 after rTPA (P = .04). Mean neurological impairment at 5 hours (on a scale of 0 to 3) decreased from 2.3 after saline to between 1.3 to 1.6 after Sak (P = .003) and to between 1.1 to 1.9 after rTPA (P = .02). At the highest doses used, fibrinogen depletion was marginal with Sak but total with rTPA. Marked prolongation of car puncture and cuticle bleeding times was only observed after bolus administration of rTPA. CONCLUSIONS: In the present rabbit model of embolic stroke, Sak was significantly more fibrin-specific than rTPA and at least as effective in lysing arterial emboli and limiting ischemia and neurological impairment.

Animals↗
PubMed1990

Incidence of cerebral hemorrhage after treatment with tissue plasminogen activator or streptokinase following embolic stroke in rabbits [corrected].

We studied thrombolysis in an animal model of embolic stroke to determine the safety of tissue plasminogen activator and streptokinase. We occluded the middle cerebral arteries of 137 rabbits with radiolabeled blood clots and administered tissue plasminogen activator (n = 49), streptokinase (n = 40), or saline (n = 48) at various times after embolization. We assessed the rate of thrombolysis and cerebral hemorrhage 24 hours later. Both drugs were very effective in producing thrombolysis. Compared with saline, streptokinase caused a significant increase in the rate of cerebral hemorrhage (p less than 0.05), but tissue plasminogen activator did not. We conclude that thrombolytic therapy for acute stroke should be safer with tissue plasminogen activator than with streptokinase.

Animals↗
PubMed1998

Diffusion-, T2-, and perfusion-weighted nuclear magnetic resonance imaging of middle cerebral artery embolic stroke and recombinant tissue plasminogen activator intervention in the rat.

Thrombolysis of embolic stroke in the rat was measured using diffusion (DWI)-, T2 (T2WI)-, and perfusion (PWI)-weighted magnetic resonance imaging (MRI). An embolus was placed at the origin of the middle cerebral artery (MCA) by injection of an autologous single blood clot via an intraluminal catheter placed in the intracranial segment of internal carotid artery. Rats were treated with a recombinant tissue plasminogen activator (rt-PA) 1 hour after embolization (n = 9) or were not treated (n = 15). Diffusion-weighted imaging, T2WI, and PWI were performed before, during, and after embolization from 1 hour to 7 days. After embolization in both rt-PA-treated and control animals, the apparent diffusion coefficient of water (ADCw) and cerebral blood flow (CBF) in the ischemic region significantly declined from the preischemic control values (P < 0.001). However, mean CBF and ADCw in the rt-PA-treated group was elevated early after administration of rt-PA compared with the untreated control group, and significant differences between the two groups were detected in CBF (24 hours after embolization, P < 0.05) and ADCw (3, 4, and 24 hours after embolization, P < 0.05). T2 values maximized at 24 (control group, P < 0.001) or 48 hours (treated group, P < 0.01) after embolization. The increase in T2 in the control group was significantly higher at 24 hours and 168 hours than in the rt-PA-treated group (P < 0.05). Significant correlations (r > or = 0.80, P < 0.05) were found between lesion volume measured 1 week after embolization and CBF and ADCw obtained 1 hour after injection of rt-PA. Within a coronal section of brain, MRI cluster analysis, which combines ADCw and T2 data maps, indicated a significant reduction (P < 0.05) in the lesion 24 hours after thrombolysis compared with nontreated animals. These data demonstrate that the values for CBF and ADCw obtained 1 hour after injection of rt-PA correlate with histologic outcome in the tissue, and that the beneficial effect of thrombolysis of an intracranial embolus by means of rt-PA is reflected in an increase of CBF and ADCw, a reduction in the increase of T2, and a reduction of the ischemic lesion size measured using MRI cluster analysis.

Animals↗
PubMed1987

Can embolic stroke be diagnosed on the basis of neurologic clinical criteria?

Diagnosis of embolic stroke is based on identification of a source of embolus (SOE) and on neurologic symptoms acknowledged as "clinical criteria." To test the validity of these criteria, we analyzed the symptoms at onset in 193 patients hospitalized after acute cerebral infarction. Patients were grouped according to identification of a cardiac SOE (106 patients), an arterial SOE (38 patients), or no SOE (49 patients). Cross-tabulations demonstrated that only rapidity and loss of consciousness at onset were associated with the presence of a cardiac SOE to a significant degree. Although these symptoms were highly specific for cardiac SOE, they were not sensitive. A distinct clinical neurologic profile from the symptoms and mode of onset was not identified.

Adult↗
PubMed2006

MRI of combination treatment of embolic stroke in rat with rtPA and atorvastatin.

To test the hypothesis that combination treatment of embolic stroke with rtPA and statins improves the efficacy of thrombolytic therapy in rats. Rats subjected to embolic MCA occlusion (MCAo) were randomized into control (n = 10) and treatment (n = 9) groups. Four hours after MCAo, a combination of rtPA and atorvastatin (treatment) or saline (control) was administered. MRI measurements were performed on all animals at 2 h, 24 h and 48 h after MCAo. The patency of cerebral microvessels was examined using fluorescent microscopy. MRI images showed complete blockage of the right MCA and a reduction of CBF in the territory supplied by the MCA 2 h after MCAo for all animals. By 48 h after stroke, MRI showed that the decreased lesion size, elevated CBF and increased incidence of recanalization were found in treated rats compared with the control rats. The combination treatment significantly increased microvascular patency (16.3 +/- 5.5% vs. 12.4 +/- 3.5%, of field-of-view) and reduced the infarct volume (23.1 +/- 9.6% vs. 38.8 +/- 13.3%, of hemisphere). These data demonstrate that the co-administration of rtPA and atorvastatin 4 h after ischemia is efficacious and is reflected by the MRI indices of recanalization of the MCA, reduction of secondary microvascular perfusion deficits and reduction of the ischemic lesion.

Animals↗
PubMed2003

A unique atrial primary cardiac lymphoma mimicking myxoma presenting with embolic stroke: a case report.

An immunocompetent 29-year-old male presented with an embolic stroke from an unusual primary cardiac lymphoma. The cardiac lesion consisted of a polypoid, left atrial, mural fibrin thrombus with anaplastic tumor cells lining the surface of the clot. Histologic, immunophenotypic, and molecular characterizations were consistent with a diagnosis of CD30+ large B-cell lymphoma with anaplastic cytology. While tumor emboli from invasive primary cardiac lymphomas have been reported, this noninvasive fibrin thrombus-associated lymphoma appears to be unique and previously unreported.

Adult↗
PubMed1988

Benign disappearance of ventricular thrombus after embolic stroke. A case report.

The source for a patient's middle cerebral artery territory embolic stroke was found by echocardiography to be a left ventricular cardiac thrombus. The apical mass was large, pedunculated, and moved with systole into the ventricular cavity. The absence of ventricular dyskinesia was thought to favor a tumor, and surgery was considered before repeat echocardiography showed disappearance of the mass, making thrombus the likely diagnosis. No further embolic events occurred during or since the disappearance of the thrombus while on anticoagulation therapy. Serial echocardiography for change in or disappearance of a ventricular mass may be critical in distinguishing thrombus from tumor.

Aged↗
PubMed2005

A model of mini-embolic stroke offers measurements of the neurovascular unit response in the living mouse.

BACKGROUND AND PURPOSE: To measure cerebral vascular and neuronal responses after stroke in the living mouse, we generated a mouse model of embolic stroke localized to the parietal cortex. METHODS: Male C57/6J or male transgenic mice (2 to 3 months old) expressing yellow fluorescent protein (YFP) were used in the present study. A single fibrin-rich clot (8 mm in length) was injected into a branch of the right middle cerebral artery (MCA). MRI measurements were performed to measure ischemic lesion. Using confocal and 2-photon microscopy, changes in the embolus, dendrites, and dendritic spines were measured in the living mouse. RESULTS: Eight of 11 mice (73%) had the embolus localized to a branch of the right MCA in the parietal cortex. Expansion of the embolus within the artery was observed 24 hours after stroke. The presence of ischemic lesion in the parietal cortex was verified by MRI measurements, and histopathological analysis revealed that these mice (n=8) had a cortical infarct volume of 4.9+/-3.6% of the contralateral hemisphere. In the living mouse, substantial loss of YFP-labeled axonal and dendritic structures as well as the formation of abnormal dendritic bulbs were detected in the ischemic boundary regions 24 hours after stroke compared with that 1 hour after stroke. CONCLUSIONS: This model offers a novel approach to study the neurovascular unit in cerebral cortex after stroke in the living mouse.

Animals↗