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PubMed1999

Factors associated with delayed admission to hospital and in-hospital delays in acute stroke and TIA: a prospective, multicenter study.Seek- Medical-Attention-in-Time Study Group.

BACKGROUND AND PURPOSE: Early admission to hospital followed by correct diagnosis with minimum delay is a prerequisite for successful intervention in acute stroke. This study aimed at clarifying in detail the factors related to these delays. METHODS: This was a prospective, multicenter, consecutive study that explored factors influencing the time from stroke or transient ischemic attack (TIA) onset until patient arrival at the emergency department, stroke unit, and CT laboratory. Within 3 days of hospital admission, the patients and/or their relatives were interviewed by use of a standardized structured protocol, and the patients' neurological deficits were assessed. No information about this study was given to the public or to the staff. RESULTS: Patients (n=329) were studied at 15 Swedish academic or community-based hospitals: 252 subjects with brain infarct, 18 with intracerebral hemorrhage, and 59 with TIA. Among stroke and TIA patients, the median times from onset to hospital admission, stroke unit, and CT scan laboratory were 4.8 and 4.0 hours, 8.8 and 7.5 hours, and 22.0 and 17.5 hours, respectively. From multivariate ANOVA with logarithmically transformed time for increasing delay to hospital admission as the dependent variable, a profile of significant risk factors was obtained. This included patients with a brain infarct, gradual onset, mild neurological symptoms, patients who were alone and did not contact anybody when symptoms occurred, patients who lived in a large catchment area, those who did not use ambulance transportation, and those who visited a primary care site. These factors explained 45.3% of the variance in delayed hospital admission. The median time from arrival at the emergency department to arrival at the stroke unit or CT scan laboratory (whichever occurred first) was 2.6 and 2.7 hours in the stroke and TIA groups, respectively. A large catchment area, moderate to mild neurological deficit, and waiting for the physician at the emergency department were all significantly related to in-hospital delay. CONCLUSIONS: Increased public awareness of the need to seek medical or other attention promptly after stroke onset, to use an ambulance with direct transportation to the acute-care hospital, and to have more effective in-hospital organization will be required for effective acute treatment options to be available to stroke patients.

Acute Disease↗
PubMed1997

Lipoprotein(a) concentration and molecular weight of apolipoprotein(a) in patients with cerebrovascular disease and diabetes mellitus.

Plasma lipoprotein(a) [Lp(a)] concentrations are genetically determined, and hyper-Lp(a)-emia is an independent risk factor for atherosclerosis and thrombosis. To study the implications of Lp(a) in cerebrovascular disease (CVD) and diabetes mellitus (DM), we examined plasma Lp(a) levels and molecular weights of apolipoprotein(a) [apo(a)] in 118 patients with CVD, and 125 cases with DM. Although mean Lp(a) concentrations were higher in those cases with atherothrombotic brain infarction than in those with brain hemorrhage and lacunar infarction, the difference was not statistically significant. Lp(a) levels were significantly higher in the DM cases treated with insulin and in those treated with oral hypoglycemic agents than in those on diet therapy alone, suggesting that insulin and oral agents modulate apo(a) expression. Lp(a) concentrations correlated significantly with the low-molecular-weight isoforms of apo(a) in all CVD and DM groups.

Aged↗
PubMed1998

Apolipoprotein(a) and thrombosis: molecular and genetic bases of hyper-lipoprotein(a)-emia.

The apolipoprotein(a) [APO(a)] gene encodes a protein component of lipoprotein(a) [LP(a)], whose plasma levels vary among individuals. To study the implications of LP(a), we examined plasma LP(a) levels and molecular weights of APO(a) in patients with cerebrovascular disease (CVD) or diabetes mellitus (DM). Mean LP(a) concentrations were higher in the CVD patients with atherothrombotic brain infarction than in those with brain hemorrhage and lacunar infarction. LP(a) levels were lower in the DM cases on diet therapy alone than in those treated with insulin or oral hypoglycemic agents. These results suggest that LP(a) is thrombogenic and atherogenic and that insulin may modulate LP(a) levels. We subclassified the APO(a) gene into four types (A to D) by polymorphisms in the 5'-flanking region. We also measured plasma LP(a) concentrations and examined expression of the gene by an in vitro assay. Homozygotes of type C had higher LP(a) levels than those of type D, and the relative expression of type C was higher than that of type D in vitro. Thus, LP(a) concentrations are genetically determined, and hyper-LP(a)-nemia is related to atherosclerosis and thrombosis.

Alleles↗
PubMed1998

Multi-modal expression of apolipoprotein (a) gene in vivo.

The apolipoprotein (a) [apo(a)] gene encodes a protein component of lipoprotein (a) [Lp(a)] whose plasma levels vary among individuals. To study the implications of Lp(a), we examined plasma Lp(a) levels and molecular weights of apo(a) in patients with cerebrovascular disease (CVD) or diabetes mellitus (DN). Mean Lp(a) concentrations were higher in the CVD cases with atherothrombotic brain infarction than in those with brain hemorrhage and lacunar infarction. Lp(a) levels were lower in the DM cases on diet therapy alone than in those treated with insulin or oral hypoglycemic agents. These results suggest that Lp(a) is thrombogenic and atherogenic, and that insulin may modulate Lp(a) levels. We subclassified the apo(a) gene into four types (A-D) by polymorphisms in the 5'-flanking region. We also measured plasma Lp(a) concentrations and examined expression of the gene by an in vitro assay. Homozygotes of type C had higher Lp(a) levels than those of type D, and the relative expression of type C was higher than that of type D in vitro. Lp(a) levels, however, varied even within the same 5'-allele having similar apo(a) isoforms. Thus, Lp(a) concentrations are genetically determined and may be modified by some hormones and cytokines. When we examined transcript levels for apo(a) by RT-PCR in various normal tissues, apo(a) was strongly expressed in liver while not in thyroid or leukocytes. Small amounts of apo(a) transcript were observed in all other organs and tissues. Apo(a) in these tissues may also play a role in inframmation, tissue remodeling, cell migration, and other physiological functions.

Apolipoproteins A↗
PubMed1978

[Role of arterio-arterial embolisms in the pathogenesis of cerebral circulatory disorders].

The authors studied 52 patients with brain infarctions and transient disorders of cerebral circulation, which in the opinion of the authors developed as a result of arterio-arterial embolism. Besides, 16 post-mortem cases with arterio-arterial embolism were studied as well. On the basis of clinico-angiographical, clinico-laboratory and clinico-anatomical correlations, the authors come to the conclusion that this mechanism is frequently the main link in the pathogenesis of distrubed cerebral circulation. Embologenic materials in the development of brain infarctions are most often particles of parietal or obturating thrombi in the magistral cerebral vessels. In patients with transient disorders of cerebral circulation most likely embolism of the minor cerebral vessels by thrombocytic aggregates. The authors discuss the functional properties of thrombocytes in the pathogenesis of transient disorders of cerebral circulation and the feasibility of the use of antiaggregates for preventive purposes.

Adult↗
PubMedDate not supplied

Local intraarterial fibrinolysis in the carotid territory.

A series comprising 12 patients who had intraarterial local fibrinolysis in the carotid territory is reported. A classification is proposed that divides the different types of occlusions into three groups on the basis of angiographic location. Group 1 (two cases) comprises occlusion of the extra- and/or intracranial carotid artery with patency of the circle of Willis and the lenticulostriate arteries. In this group, there is no brain infarction, the CT findings are normal, and the clinical signs are mainly hemodynamic and intermittent. Fibrinolysis may be performed late and rather safely and completed by surgery or angioplasty of the neck vessel stenosis responsible for the occlusion. Group 2 (five cases) comprises occlusions of the cortical arteries without involvement of the lenticulostriate arteries. The mechanism of the occlusion can be hemodynamic or embolic. Group 3 (five cases) comprises occlusions of intracerebral arteries involving the lenticulostriate arteries. In groups 2 and 3 with brain infarction, fibrinolysis will only be able to restore viability of the area of cerebral tissue surrounding the infarction (penumbra). The time factor is particularly critical in group 3 because lenticulostriate arteries are terminal vessels whose revascularization may induce hemorrhages with increasing frequency as the occlusion time is prolonged. The time factor is less critical in group 2 because collaterals make the ischemia less severe in the infarcted area and the vital and functional consequences of hemorrhage are not as serious as in group 3 because of the location. In this series, all the symptomatic complications of hemorrhage (two cases) occurred in group 3, in patients treated later than 6 hr after clinical onset. Given the time delay inherent in performing CT and angiography and in making the medical decision, it is considered dangerous to undertake fibrinolytic therapy in group 3, unless it can be started before 4 or 5 hr after clinical onset.

Adult↗
PubMed1996

The effect of oral antiplatelet agents on tissue plasminogen activator-mediated thrombolysis in a rabbit model of thromboembolic stroke.

OBJECTIVE: The success of thrombolytic therapy in acute stroke relies on timely reperfusion. The current study examines the efficacy of antiplatelet agents as adjuvants for thrombolytic therapy. METHODS: Using an established rabbit model of clot embolization and a randomized blinded design, rabbits (n = 8 in each group) were orally pretreated daily for 5 days with adjuvant aspirin (1 mg/kg of body weight or 20 mg/kg), ticlopidine (100 mg/kg), or vehicle (sodium carbonate). On the 6th day, tissue plasminogen activator (6.3 mg/kg administered intravenously over 2 h), was initiated 1 hour after embolization. RESULTS: In all groups, cerebral blood flow (CBF) was reduced to < 10 ml/100 g/min immediately after clot embolization. After the initiation of tissue plasminogen activator (t-PA), there was significant restoration of CBF in the control (t-PA only) and ticlopidine groups (P < 0.05) only. Restoration of CBF generally correlated with brain infarct size (percent hemisphere, mean +/- standard error of the mean), which was 18.0 +/- 7.0 in the t-PA only group versus 11.0 +/- 3.3, 26.5 +/- 5.8, and 21.5 +/- 3.4 in the ticlopidine, low-dose aspirin, and high-dose aspirin groups, respectively (ticlopidine versus aspirin, P < 0.05). Clot lysis was identical in the control and ticlopidine groups, with 6 of 8 animals demonstrating complete clot lysis. Aspirin antagonized clot lysis in a dose-related manner, with low-and high-dose aspirin groups noting clot lysis in four of eight and two of eight animals, respectively. CONCLUSIONS: Pretreatment with ticlopidine significantly reduced brain infarct size when compared with aspirin treatment (P < 0.05). Moreover, whereas ticlopidine treatment did not affect clot lysis or CBF relative to t-PA alone, aspirin therapy resulted in antagonism of clot lysis and was associated with a more modest restoration of blood flow. This study provides a background for a more comprehensive understanding of the balance of thrombogenicity and thrombolysis and may assist in the development of novel therapies to expedite cerebrovascular patency and reduce ischemic and reperfusion-mediated neuronal injury.

Animals↗
PubMed2004

Delayed neurological deficits detected by an ischemic pattern in the extracellular cerebral metabolites in patients with aneurysmal subarachnoid hemorrhage.

OBJECT: In the treatment of patients with aneurysmal subarachnoid hemorrhage (SAH), early occlusion of the aneurysm is necessary as well as monitoring and treatment of complications following the primary bleeding episode. Monitoring with microdialysis has been studied for its ability to indicate and predict the occurrence of delayed ischemic neurological deficits (DINDs) in patients with SAH. METHODS: In 42 patients with aneurysmal SAH microdialysis monitoring of metabolites was performed using a 0.3-microl/minute perfusion flow over several days, and the results were correlated to clinical events and to brain infarction observed on computerized tomography scans. The microdialysis probe was inserted into the territory of the parent artery of the aneurysm. The authors defined an ischemic pattern as increases in the lactate/glucose (L/G) and lactate/pyruvate (L/P) ratios that were greater than 20% followed by a 20% increase in glycerol concentration. This ischemic pattern was found in 17 of 18 patients who experienced a DIND and in three of 24 patients who did not experience a delayed clinical deterioration. The ischemic pattern preceded the occurrence of a DIND by a mean interval of 11 hours. Maximum L/G and L/P ratios did not correlate with the presence of DIND or outcome, and there was no association between the glycerol level and subsequent brain infarction. CONCLUSIONS: Microdialysis monitoring of the cerebral metabolism in patients with SAH may predict with high sensitivity and specificity the occurrence of a DIND. Whether an earlier diagnosis results in better treatment of DINDs and, therefore, in overall better outcomes remains to be proven, as it is linked to an efficacious treatment of cerebral vasospasm.

Adult↗
PubMed2007

Effects of edaravone on singlet oxygen released from activated human neutrophils.

The effects of edaravone, a curative agent for acute brain infarction, on singlet oxygen ((1)O2) released from activated human neutrophils were examined, and the effects were compared to those of histidine, a (1)O2 singlet oxygen scavenger. The neutrophils, stimulated with opsonized zymosan, released (1)O2 that was detected by chemiluminescence using a (1)O2 specific probe, trans-1-(2'-methoxyvinyl)pyrene. Edaravone dose-dependently suppressed the (1)O2 release with an IC(50) of approximately 0.3 microM, while the IC(50) of histidine was approximately 1 mM. This (1)O2 scavenging activity of edaravone might be involved in its curative effects on acute brain infarction.

Adult↗
PubMed1980

Outcome of stroke in the Espoo--Kauniainen area, Finland.

A prospective study of all stroke cases in the Espoo--Kauniainen area (population 113 000) in South-Finland was carried out during 1972 and 1973 by the WHO stroke register method. 286 stroke patients were registered; 61% of them had a brain infarction, 16% an intracerebral haemorrhage and 15% a subarachnoid haemorrhage. The total incidence was 200/100 000/year after age adjustment of the results to the population of Finland. The incidence of subarachnoid haemorrhage, 23.9/100 000/year was especially high. The mortality within three months was 40%, and that after median follow-up periods of four and six years was 62% and 67% respectively. In the intracerebral haemorrhage group the 3-month mortality was very high (72%), but it did not change during the follow-up period. In the subarachnoid haemorrhage group the 3-month mortality was 43%, which increased slightly, but in the brain infarction group the 3-month mortality of 30% increased steadily up to 66% during the follow-up period. The causes of death after the acute stage were cardiovascular as often as cerebrovascular. After four and six years, 71% of the survivors were fully independent in activities of daily living. After four years 21% had even returned to work. 16% of the survivors were still working after six years.

Activities of Daily Living↗
PubMed1989

[Infection and tissue ischemia: what role does the rheologic behavior of blood cells play?].

It is not clear how acute infection is associated with a subsequent ischaemic brain infarction. Infection may, in fact, cause changes in blood fluidity. Abnormalities in blood flow, particularly in white blood cell rheology, are known to be precipitating factors for ischaemic events. Therefore the rheological behaviour of the erythrocytes and the leukocytes were studied 30 days after the onset of acute bacterial infections in 30 patients and in a group of 50 controls (matched for sex, body mass index and cardiovascular risk factors). Our results show a significant impairment in the flow properties of the leukocytes in the patients compared to the controls, and indicate disturbances in leukocyte rheology might be considered an additional risk factor for ischaemic brain infarction when it occurs shortly after febrile infection.

Aged↗
PubMedDate not supplied

Outcome of surgical treatment of 110 patients with transient ischemic attack.

Between 1980 and 1982, 227 consecutive patients with transient ischemic attack (TIA) or ischemic brain infarction (IBI) were evaluated as possible candidates for carotid surgery in the Department of Neurology, University of Helsinki. One hundred and ten patients (mean age 58, range 41-72 years) were selected for surgery; 82 of them had had TIA and 28 IBI as the presenting symptom. After a total of 128 operations (84 unilateral and 18 bilateral endarterectomies, and 8 arterial reconstructions), 16 patients (14.5%) developed neurological deficits. In 7 patients (6.4%), the deficit was severe and 4 of them (3.6%) died within the first four days after surgery. Ten patients had occlusion of the contralateral internal carotid artery and/or severe hypertension. Five of them suffered ischemic brain infarction after the operation and two died. Operation on an occluded internal carotid artery in 7 patients was complicated by hemiparesis in two patients, one of whom died. Patients with surgical complications more often had severe hypertension (p less than .001), total occlusion of the contralateral internal carotid artery, (n.s.) and severe angiographic changes (n.s.) compared with patients without complications. During the follow-up the annual rate for IBI was 3.3% and for acute myocardial infarction (AMI) 4.4%. Vascular death occurred with a frequency of 1.7% per year. The results emphasize that patients with TIA or IBI should be carefully evaluated before recommending surgical treatment for prevention of threatened stroke. Patients with severe risk factors may fare better on medical treatment than with surgical intervention.

Adult↗
PubMed2002

Resection of thymic carcinoma in a patient with thoracic aortic aneurysm.

A 72-year-old man with a history of brain infarction presented with left sided anterior chest pain secondary to a thymic carcinoma. He received induction radiotherapy, 45 Gy. Preoperative computed tomography showed the tumor was adherent to a thoracic aortic aneurysm (TAA) which had extensive mural thrombus and calcification. To obtain adequate exposure without exerting tension on the fragile aneurysmal wall, ribs were resected to allow us to separate the tumor from the TAA, after which median sternotomy was performed uneventfully, creating generous exposure. The tumor had invaded the sternum, ribs, innominate vein, phrenic and recurrent laryngeal nerves, and lung. The tumor was removed en bloc, and the chest wall was reconstructed. Intra- and post-operative brain infarction and rupture of the TAA were avoided. The patient is alive and well without recurrence 10 months after surgery.

Aged↗
PubMedDate not supplied

[Clinico-roentgenologic evaluation of the efficacy of extra-intracranial microvascular anastomoses in patients with stenoses in the internal carotid artery system].

The authors analyse the results of clinical and X-ray examination of 20 patients with stenosing lesions in the system of the internal carotid artery after operations for establishing extra-intracranial microvascular anastomoses (EICMA). Marked stable neurological symptomatology was encountered before the operation in arterial stenosis of a high degree (more than 50%) and the presence of brain infarctions. In functioning EICMA, evolution of stenoses in the system of the internal carotid arteries was found, which was characterized both by their increase (even to the development of thrombosis) and by their involution. Evolution of the stenoses did not occur if the EICMA failed to function. The operation leads to a less marked character of the neurological symptoms or has no particular effect on their dynamics. Changed amplitude and volume of active movements, muscular tone and strength, as well as of speech function, were found to be the most sensitive indicators of the operation efficacy. Regression of the neurologic symptoms after the operation was observed even in extensive brain infarctions and long standing of the disease.

Adolescent↗
PubMed2004

Defense mechanism to oxidative DNA damage in glial cells.

Astrocytosis is a sequential morphological change of astrocytic reaction to tissue damage, and is associated with regulation of antioxidant defense mechanisms to reduce oxidative damage. The repair enzymes to oxidative DNA damage, oxidized purine-nucleoside triphosphatase (hMTH1) and a mitochondrial type of 8-oxoguanine DNA glycosylase (hOGG1-2a) in brain tumors and neurons of Alzheimer's disease, were previously reported. In the present study, glial expression of these repair enzymes under such pathological conditions as cerebrovascular diseases and metastatic brain tumors, were investigated. Furthermore, an in-vitro experiment using a glioma cell-line under oxidative stress was performed to verify the immunohistochemical results of post-mortem materials. As a result, hOGG1-2a immunoreactivities in reactive astrocytes were more intense than those to hMTH1. Oligodendrocytes of acute or subacute stage of brain infarction were strongly immunoreactive to both repair enzymes. In-vitro study revealed that, hOGG1-2a is constitutively expressed in both untreated glioma cells and the glioma cells under oxidative stress. However, although no immunoreactivity to hMTH1 was found in the control cells, accumulation of hMTH1 was rapidly induced by oxidative stress. These results indicate that the two repair enzymes to oxidative DNA damage are differentially regulated in glial cells, and that there is a difference in the expression of the repair enzymes between reactive astrocytes and oligodendrocytes.

Adult↗
PubMedDate not supplied

Characterization of CNS lesions by using high-resolution 1H MR spectroscopy of CSF: preliminary results.

Sixty-six samples of CSF from 66 patients with a variety of diseases, including tumors, arteriovenous malformations, aneurysms, brain infarctions, and lumbar back pain, were studied with 1H MR spectroscopy at 360 MHz. 1H MR spectroscopy offers a simple means to obtain fast information about different metabolites simultaneously. As compared with the control group, which consisted of 19 CSF samples from the same group of 66 patients, but from individuals who had no abnormal findings on neurologic examination, common clinicochemical tests, or neuroradiologic studies, our preliminary results suggest that tumors and hemorrhages may be differentiated by 1H MR spectroscopy. MR peak intensities relative to lactate peak intensity were used as variables in a statistical analysis to determine the significance of individual resonance intensities in predicting CNS abnormalities. The most important factors for diagnosis were analyzed by means of a multivariate general linear hypothesis and a principal component method. The most important factors for predicting CNS abnormalities in the studied diseases were creatinine, glucose, creatine, citrate, protein content, glutamine, amount of cells, and valine. By using this model for discriminant analysis, we could predict hemorrhages correctly in 88% of cases and tumors in 75% of cases. All samples of controls were determined correctly. In cases of brain infarctions, different signals were observed, which may lead to further characterization of such lesions. 1H MR spectroscopy may offer a simple means for further characterizing CNS lesions. However, this needs confirmation by a prospective study, which would include a larger patient population with different diseases.

Central Nervous System Diseases↗
PubMedDate not supplied

Echo-lucency of computerized ultrasound images of carotid atherosclerotic plaques are associated with increased levels of triglyceride-rich lipoproteins as well as increased plaque lipid content.

BACKGROUND: Echo-lucency of carotid atherosclerotic plaques on computerized ultrasound B-mode images has been associated with a high incidence of brain infarcts as evaluated on CT scans. We tested the hypotheses that triglyceride-rich lipoproteins in the fasting and postprandial state predict carotid plaque echo-lucency and that echo-lucency predicts a high plaque lipid content. METHODS AND RESULTS: The study included 137 patients with neurological symptoms and > or = 50% stenosis of the relevant carotid artery. High-resolution B-mode ultrasound images of carotid plaques were computer processed to yield a measure of echogenicity (gray-scale level). Lipoproteins were measured before and hourly for 4 hours after a standardized fatty meal. A subgroup of 58 patients underwent endarterectomy. On linear regression analysis, echo-lucency (low gray-scale level) was associated with elevated levels of fasting and postprandial plasma triglycerides (P=.0002 and P=.002), IDL cholesterol (P=.0009 and P=.006), and VLDL/chylomicron remnant cholesterol (P=.0003 and P=.0004) and triglycerides (P=.0003 and P=.003), the area under the plasma triglyceride curve 0 to 4 hours after a fatty meal (P=.001), and body mass index (P=.0001). On ANCOVA, body mass index, fasting IDL cholesterol, and fasting plasma triglycerides were independent predictors of echo-lucency. Echo-lucency was associated with increased relative plaque lipid content (P=.02). CONCLUSIONS: Increased plasma levels of triglyceride-rich lipoproteins predict echo-lucency of carotid plaques, which is associated with increased plaque lipid content. Because echo-lucency has been associated with a high incidence of brain infarcts on CT scans, triglyceride-rich lipoproteins may predict a plaque type particularly vulnerable to rupture.

Arteriosclerosis↗
PubMed2006

Blood pressure changes during the initial week after different subtypes of ischemic stroke.

BACKGROUND AND PURPOSE: The purpose of this study was to clarify the differences in the acute blood pressure course among different ischemic stroke subtypes. METHODS: We divided 588 consecutive patients with acute brain infarction into four clinical subgroups to study the blood pressure levels during the initial 6 hospital days. RESULTS: During the 6 days, systolic blood pressure of lacunar and atherothrombotic patients was higher (P=0.0001) and diastolic blood pressure of lacunar patients was higher (P=0.0371) than of patients with the other subtypes. Preexisting hypertension was associated with elevated acute systolic blood pressure in all patients and in each subtype and with elevated acute diastolic blood pressure in all patients, cardioembolic patients, and patients with stroke of other etiology. After adjustment by preexisting hypertension, diabetes mellitus with a hemoglobin A1c >7.0% was associated with elevated systolic blood pressure in all, lacunar, and cardioembolic patients and with diastolic blood pressure in all patients. CONCLUSIONS: Blood pressure course of patients sustaining acute stroke varied widely according to stroke subtypes. Poorly controlled diabetes mellitus, as well as preexisting hypertension, appeared to influence blood pressure during the initial week of stroke.

Acute Disease↗