[Apoplexy units--European experiments].
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Cerebrovascular Disorders↗
Biomedical subjects
G Boysen
Publications and source records attributed to G Boysen.
Cholesterol and risk of stroke.
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Cerebrovascular Disorders↗
[Thrombolytic therapy in acute cerebral ischemia].
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Acute Disease↗
Influence of systolic and diastolic blood pressure on stroke risk: a prospective observational study.
The purpose of this study was to estimate the influence of systolic (SBP) and diastolic blood pressure (DBP) on stroke risk. The Copenhagen City Heart Study is a prospective survey of 19,698 women and men who were invited to two cardiovascular examinations at 5-year intervals. Blood pressure was measured in participants once at each examination, together with other variables. Initial cases of stroke and transient ischemic attack were recorded from hospital records and death certificates from 1976 through 1988. When entered separately in the Cox regression model, both SBP and DBP had significant effects on stroke risk. In the lower 60% of the blood pressure distribution in the population, the relative risk of stroke was nearly constant, followed by a gradual increase in the upper 40% of blood pressure distribution. However, when SBP and DBP were entered simultaneously in the model, the effect of DBP vanished, while the pattern of the association between SBP and stroke risk remained unchanged. Persons on antihypertensive treatment had higher risk for stroke than non-treated persons with the same blood pressure, relative risk = 1.6 (95% confidence interval (CI) 1.2-2.2). The relative risk for the highest SBP levels, shared by nearly 3% of the population, was 4.0 (95% CI 2.2-7.3). The attributable risk of SBP in the upper 40% of SBP distribution, i.e., above the mean for each age and sex group, was 22%. Our results indicate that: 1) the association between blood pressure and stroke risk was not log-linear, and 2) SBP was a stronger stroke predictor than DBP.
Adult↗
Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study (ECASS)
OBJECTIVE: To evaluate the efficacy and safety of intravenous thrombolysis using recombinant tissue plasminogen activator (rt-PA) in patients with acute ischemic stroke. DESIGN: Randomized, prospective, multicenter, double-blind, placebo-controlled clinical trial. SETTING: A total of 75 hospitals in 14 European countries. PATIENTS: A total of 620 patients with acute ischemic hemispheric stroke and moderate to severe neurologic deficit and without major early infarct signs on initial computed tomography (CT). INTERVENTION: Patients were randomized to treatment with 1.1 mg per kilogram of body weight of rt-PA (alteplase) or placebo within 6 hours from the onset of symptoms. OUTCOME MEASURES: Primary end points included Barthel Index (BI) and modified Rankin Scale (RS) at 90 days. Secondary end points included combined BI and RS, Scandinavian Stroke Scale (SSS) at 90 days, and 30-day mortality. Tertiary end points included early neurologic recovery (SSS) and duration of in-hospital stay. Safety parameters included mortality and incidence of intracranial or extracranial hemorrhage. RESULTS: The distribution of demographic variables was similar among patients in the rt-PA and placebo treatment arms in both the intention-to-treat (ITT) analysis and the explanatory analysis for the target population (TP). A total of 109 patients (17.4%) were included in the trial despite major protocol violations but excluded from the TP. There was no difference in the primary end points in the ITT analysis, while the TP analysis revealed a significant difference in the RS in favor of rt-PA-treated patients (P = .035). Of the secondary end points, the combined BI and RS showed a difference in favor of rt-PA-treated patients in both analyses (P < .001). Neurologic recovery at 90 days was significantly better for rt-PA-treated patients in the TP (P = .03). The speed of neurologic recovery assessed by the SSS was significantly better up to 7 days in the ITT analysis and up to 30 days for the TP in the rt-PA treatment arm. In-hospital stay was significantly shorter in the rt-PA treatment arm in both analyses. There were no statistically significant differences in the mortality rate at 30 days or in the overall incidence of intracerebral hemorrhages among the rt-PA and placebo treatment arms in either analysis. However, the occurrence of large parenchymal hemorrhages was significantly more frequent in the rt-PA-treated patients. CONCLUSIONS: Intravenous thrombolysis in acute ischemic stroke is effective in improving some functional measures and neurologic outcome in a defined subgroup of stroke patients with moderate to severe neurologic deficit and without extended infarct signs on the initial CT scan. However, the identification of this subgroup is difficult and depends on recognition of early major CT signs of early infarction. Therefore, since treating ineligible patients is associated with an unacceptable increase of hemorrhagic complications and death, intravenous thrombolysis cannot currently be recommended for use in an unselected population of acute ischemic stroke patients.
Acute Disease↗
[An insufficient report on neurosurgical research].
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Denmark↗
[Plasma total cholesterol, high density lipoprotein-cholesterol and triglycerides as risk factors for cerebrovascular diseases. A 12-year follow-up by the Osterbro survey].
The aim of this study was to estimate the effect of plasma total cholesterol, HDL-cholesterol and triglycerides on risk of cerebrovascular disease. The Copenhagen City Heart Study is a prospective population study with 14.223 and 12.411 participants in first (1976-78) and second (1981-83) examination, respectively, where plasma lipids were measured along with other variables. Acute cerebrovascular cases were recorded during 12-year follow-up and the associations between lipid levels and risk of cerebrovascular disease were estimated using the Cox regression model. Significantly increased risk of ischaemic cerebrovascular disease was associated with: total cholesterol levels > 8 mmol/l, decreasing HDL-cholesterol, and increasing triglyceride levels. The association with HDL-cholesterol and triglycerides was log-linear and relative risks (95% confidence intervals) corresponding to increase by 1 mmol/l were: 0.53 (0.34-0.83) and 1.12 (1.07-1.16), respectively. The relative risk for total cholesterol < or = 8 mmol/l was constant (non log-linear association). These associations did not vary significantly between women and men.
Cerebrovascular Disorders↗
Thrombolysis in ischaemic stroke--how far from a clinical breakthrough?
Thromboembolic occlusions of the cerebral arteries often recanalize spontaneously, and patients with early recanalization have a better outcome than patients who do not recanalize. Clinical as well as experimental data support the concept of a time window within which brain tissue will profit from restoration of blood flow. In occlusion of middle cerebral artery, internal carotid artery, as well as vertebrobasilar arteries, open studies of intra-arterial administration of thrombolytic agents have demonstrated recanalization within hours in 40-100% of patients in small series. In intravenous drug administration, recanalization rate was obtained in 34-59% of patients. Favourable outcome was associated with recanalization. Intracerebral bleeding complications with clinical deterioration occurred in about 10% of patients. Three randomized controlled trials comprising 156 patients with acute ischaemic stroke have reported favourable outcome in treated patients, with no difference of intracerebral haemorrhagic complications between treated and controls. Results of ongoing randomized placebo controlled trials are expected in 1995 to disclose whether a clinical breakthrough is achieved or whether haemorrhagic complications will outweigh a beneficial effect of thrombolytic therapy in acute cerebral ischaemia.
Animals↗
Influence of total cholesterol, high density lipoprotein cholesterol, and triglycerides on risk of cerebrovascular disease: the Copenhagen City Heart Study.
OBJECTIVE: To estimate the influence of plasma total cholesterol, high density lipoprotein cholesterol, and triglycerides on risk of cerebrovascular disease. DESIGN: The Copenhagen City Heart Study is a prospective observational survey with two cardiovascular examinations at five year intervals. Non-fasting plasma lipids were measured in participants once at each examination, along with other variables. The Cox regression model was used to establish the effect of the factors recorded on cerebrovascular events of mostly, but not exclusively, ischaemic origin. SUBJECTS: 19,698 women and men at least 20 years old, randomly selected after age stratification from an area of central Copenhagen. MAIN OUTCOME MEASURES: Initial cases of stroke and transient ischaemic attack recorded from hospital records and death certificates from 1976 through 1988. RESULTS: 660 non-haemorrhagic and 33 haemorrhagic events were recorded. Total cholesterol was positively associated with risk of non-haemorrhagic events, but only for levels > 8 mmol/l, corresponding to the upper 5% of the distribution in the study population. For lower plasma cholesterol values the relative risk remained nearly constant. Plasma triglyceride concentration was significantly, positively associated with risk of non-haemorrhagic events. The relative risk corresponding to an increase of 1 mmol/l was 1.12 (95% confidence interval 1.07 to 1.16). There was a negative, log linear association between high density lipoprotein cholesterol and risk of non-haemorrhagic events (0.53 (0.34 to 0.83)). There was no indication that the effects of plasma lipids were different in women and men. CONCLUSIONS: The pattern of the association between plasma cholesterol and risk of ischaemic cerebrovascular disease was not log linear, and the increased risk was confined to the upper 5% of the cholesterol distribution. Further studies should concentrate on the association between plasma cholesterol and verified haemorrhagic stroke.
Adult↗
The influence of body temperature on infarct volume and thrombolytic therapy in a rat embolic stroke model.
The effect of body temperature on cerebral infarcts and thrombolytic therapy was investigated in 91 rats embolized in the right carotid territory. Hypothermia of 32 degrees C for 2 h with preembolic onset (n = 15) or hyperthermia of 39 degrees C for 2 h with postembolic onset (n = 22) was compared to normothermic controls (n = 17). After 48 h of survival, neuropathological evaluation with measurement of infarct volume was performed. Median infarct volume in percent of affected hemisphere volume was 11% (9-21, quartiles) in rats treated with hypothermia alone, compared to 46% (14-59, quartiles) in normothermic controls (P = 0.04). Hyperthermia for 2 h increased median infarct volume to 65% (37-75, quartiles). There was a positive and significant correlation between infarct volume and body temperature (R = 0.53, P = 0.0002, n = 54). Mortality rate was significantly higher among rats treated with hyperthermia compared to normothermic controls (P = 0.005). A subset of 37 rats exposed to the same temperature regimen were treated with tissue plasminogen activator (20 mg/kg i.v. during 45 min) 2 h after embolization. Judged by posttreatment carotid angiography, hyperthermic rats (n = 11) had the best degree of recanalization (P = 0.03) compared to controls (n = 17), but median infarct volume in this group was (58% (27-67, quartiles)) significantly larger (P < 0.02) than normothermic (21% (15-39, quartiles), n = 14) and hypothermic (13% (7-31, quartiles), n = 12) rats treated with thrombolytic therapy. Thrombolytic therapy following 2 h of hypothermia, could not improve the effect of hypothermia alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of delayed thrombolysis with rt-PA in a rat embolic stroke model.
The effect of delayed thrombolysis with recombinant tissue plasminogen activator was tested in an embolic stroke model. The carotid territory was embolized in 103 rats with fibrin-rich clots formed and washed in polyethylene tubes. Hemispheric cerebral blood flow before and after embolization was measured by the intra arterial 133Xe injection method. At five delay times, 15-240 min after embolization, 69 animals were treated with tissue plasminogen activator, 20 mg/kg, and 34 animals with saline. Carotid angiography displayed the grade of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed after 2 days, evaluated neuropathologically, and infarct volume measured. Cerebral blood flow was reduced by 56-71% after embolization. Reperfusion induced by thrombolytic therapy was demonstrated by comparing the posttreatment angiography of the pooled five treatment groups to control animals. Thrombolytic therapy significantly reduced the infarct volume and improved the prekill clinical score by up to 2 h of treatment delay, and treatment might have been beneficial even after 4 h delay. Prolonging the delay of treatment increased the infarct volume (p < 0.001, Jonck-heere-Terpstra test). Only a few hemorrhagic complications were observed. Thus, thrombolytic therapy in embolic stroke induced recanalization. The effect on clinical outcome and infarct volume was dependent on delay time.
Animals↗
Effect of hypothermia and delayed thrombolysis in a rat embolic stroke model.
Effect of hypothermia on cerebral infarcts was studied in rats embolized in the right carotid territory. Thirty-four served as normothermic controls receiving saline infusion only. In 16 rats hypothermia of 32 degrees C was induced by cooling with a fan, followed by embolization. The rats were kept hypothermic for the following 3 h before body temperature was raised to 37 degrees C. In 26 rats, treatment with human recombinant tissue plasminogen activator (20 mg/kg i.v. during 45 min), started 2 h after embolization. Finally, 14 rats were treated similarly with hypothermia for 3 h followed by additional rt-PA treatment starting after 2 h. Thrombolytic therapy reduced median infarct volume from 19.5% of affected hemisphere among controls to 4.6% (p = 0.006) in the treated group. Three hours of hypothermia reduced infarct volume to 1.6% (p = 0.0007). Additional rt-PA could not demonstrate further improvement in this experimental setting.
Animals↗
Comparison of probability of stroke between the Copenhagen City Heart Study and the Framingham Study.
BACKGROUND AND PURPOSE: We wished to test the validity of a stroke probability point system from the Framingham Study for a sample of the population of Copenhagen, Denmark. In the Framingham cohort, the regression model of Cox established the effect on stroke of the following factors: age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease, atrial fibrillation, and left ventricular hypertrophy. Derived from this model, stroke probabilities were computed for each sex based on a point system. The authors claimed that a physician can use this system for individual stroke prediction. METHODS: The Copenhagen City Heart Study is a prospective survey of 19,698 women and men aged 20 years or older invited to two cardiovascular examinations at 5-year intervals. The baseline examination included 3015 men and 3501 women aged 55 to 84 years; 474 stroke events occurred during 10 years of follow-up. In both cohorts initial cases of stroke and transient ischemic attack recorded during 10 years of follow-up were used. We used the statistical model from the Framingham Study to establish a corresponding stroke probability point system using data from the Copenhagen City Heart Study population. We then compared the effects of the relevant risk factors, their combinations, and the corresponding stroke probabilities. We also assessed stroke events during 10 years of follow-up in several subgroups of the Copenhagen population with different combinations of risk factors. RESULTS: For the Copenhagen City Heart Study population some of the risk factors (diabetes mellitus, cigarette smoking, atrial fibrillation, and left ventricular hypertrophy) had regression coefficients different from those of the Framingham Study population. Consequently, the probability of stroke for persons presenting these risk factors and their combinations varied between the two studies. For some other risk factors (age, blood pressure, and cardiovascular disease), no major differences were found. The recorded frequency of stroke events in subgroups of the Copenhagen population was compatible with the estimated probability intervals of stroke from the Copenhagen City Heart Study and with those from the Framingham Study, but these intervals were very large. CONCLUSIONS: The majority of risk factors for stroke identified by the Framingham Study also had a significant effect in the Copenhagen City Heart Study population. The differences found could be due partly to different definitions of these factors used by the two studies. Although estimated stroke probabilities based on point systems from the Copenhagen City Heart Study and the Framingham Study were similar, the points scored in the two systems did not always correspond to the same combination of risk factors. Such systems can be used for estimating stroke probability in a given population, provided that the statistical confidence limits are known and the definitions of risk factors are compatible. However, because of the large statistical uncertainty, a prognostic index should not be applied for individual prediction unless it is used as an indicator of high relative risk associated with the simultaneous presence of several risk factors.
Adult↗
Stroke scale comparisons.
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Cerebrovascular Disorders↗
[Apoplexy--the acute phase].
This review concerns the acute phase of stroke. It describes incidence, prevalence, etiology, diagnosis and treatment together with the possibilities for prevention. The incidence of stroke in the Danish population is about 2/1000 person years and has been largely unchanged during the last 20 years. About 85% of strokes are caused by cerebral infarcts, ten percent by intracerebral haemorrhages and about five percent by subarachnoid bleeding. The incidence increases with age. Up till age 65 years the ratio between men and women is two to one, while the ratio in the oldest age group approaches one to one. The most important risk factors for stroke are smoking, arterial hypertension, previous cerebrovascular disease, heart disease and diabetes mellitus. Till now, no treatment has been documented as effective in reducing the cerebral damage caused by acute stroke. Ongoing controlled clinical trials in the acute state of ischaemic stroke are testing the effect of thrombolytic therapy, treatment with calciumantagonists, aspirin and heparin. The general medical treatment including nursing and physiotherapy in the acute phase is described. Within recent years benefit of various strategies of stroke prevention has been documented.
Acute Disease↗
Enhancing the efficacy of thrombolysis by AMPA receptor blockade with NBQX in a rat embolic stroke model.
Efficacy and safety of combined alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor blockade and thrombolytic therapy with human recombinant tissue plasminogen activator (TPA) was tested in a rat embolic stroke model. Sixty-three rats were embolized in the right internal carotid territory with a 200 microliters suspension of microclots formed by alternate moving of 150 microliters whole blood and 50 microliters of thrombin between two interconnected syringes for 4 min. Sixteen embolized rats served as controls, and 16 rats were treated with NBQX immediately after embolization. Thirty-one rats were treated with TPA 2 h following embolization, and in 16 of these rats additional NBQX treatments were initiated 90 min following embolization. Hemispheric cerebral blood flow (CBF) was measured by an intraarterial 133Xenon injection method before and after embolization. Carotid angiography displayed the rate of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed after 2 days, evaluated neuropathologically, and infarct volumes were measured. Median CBF was reduced by 70-77% in the affected hemispheres following embolization. Significant recanalization occurred in all groups except those treated with NBQX. TPA-treated rats had significantly better reperfusion compared to controls judged by angiography 3 h following embolization (P = 0.04). NBQX alone and TPA alone caused insignificant reduction in infarct volume but, when combined, total infarct volume was reduced by 77% compared to controls (P = 0.02). Separate measurement of cortical infarct revealed significantly smaller infarcts (P = 0.05) in the combined treatment group compared to the TPA treatment group.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Neuroprotection with NBQX and thrombolysis with rt-PA in rat embolic stroke.
The efficacy of delayed thrombolysis with recombinant tissue plasminogen activator was tested in combination with the ischaemic protecting drug NBQX in an embolic stroke model. In 113 rats the carotid territory was embolized with a fibrin-rich clot formed in polyethylene tube. Hemispheric cerebral blood flow (CBF) was measured by intra-arterial 133Xenon injection method before and after embolization. Two hours after embolization 67 animals were treated with tissue plasminogen activator 20 mg kg-1, 46 control animals with saline. NBQX was given to 53 animals, of which 41 animals also received thrombolytic therapy and 12 were saline controls. Carotid angiography displayed the rate of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed after two days, evaluated neuropathologically, and infarct volume was measured. Embolization caused a 60-78% reduction of median CBF. The comparison of post-treatment angiography of thrombolytic treated animals to controls showed significant (p < 0.01) reperfusion in thrombolytic treated animals, while NBQX alone did not enhance reperfusion. Thrombolytic therapy significantly reduced the total infarct volume from 19.5% to 4.5% of embolized hemisphere volume (p = 0.006). NBQX alone reduced total infarct volume from 19.5% to 6.5% and cortical infarct volume from 7.9% to 0.3% (p = 0.03). In thrombolytic treated animals NBQX reduced total infarct volume from 4.5% to 2.1%. The more than 50% reduction of total infarction volume caused by NBQX was not statistically significant due to the variation of infarct size in this model. Small haemorrhagic lesions in infarcts were observed in thrombolytic treated animals. The clinical outcome correlated well with infarct volume.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Risk factors for stroke in Copenhagen, Denmark. I. Basic demographic and social factors.
The Copenhagen City Heart Study is a prospective study based on a randomly selected sample of an urban population of, initially, 19,698 participants followed since 1976. Risk factor analysis was based on the initial examination of 13,000 persons > or = 35 years old without previous stroke who responded to the first invitation. In the period 1976-1988, 696 initial cases were identified: 584 strokes, 106 transient ischemic attacks and 6 retinal-artery occlusions. We used the regression model of Cox based on a hierarchic system of risk factors that indicated the way they influence each other. This method distinguishes independent risk factors and estimates their causal influences on the risk of stroke. Among the basic variables analyzed in this paper, significant effects were found for age, sex, length of school education and income. There was a tendency for living alone to be a risk factor as opposed to living with someone, while no influence could be demonstrated for family history of stroke.
Adult↗