Search PubMed⌕ Search

Biomedical subjects

Gudrun Boysen

Publications and source records attributed to Gudrun Boysen.

At least 19 recordsLinked to original sources
PubMed2006

Relationship between outcome and baseline blood pressure and other haemodynamic measures in acute ischaemic stroke: data from the TAIST trial.

BACKGROUND: A poor outcome after stroke is associated independently with high blood pressure during the acute phase; however, relationships with other haemodynamic measures [heart rate (HR), pulse pressure (PP), rate-pressure product (RPP)] remain less clear. METHODS: The Tinzaparin in Acute Ischaemic Stroke Trial is a randomised, controlled trial assessing the safety and efficacy of tinzaparin versus aspirin in 1484 patients with acute ischaemic stroke. Systolic blood pressure (SBP), diastolic blood pressure (DBP) and HR measurements taken immediately prior to randomization were averaged, and the mid-blood pressure (MBP), PP, mean arterial pressure (MAP), pulse pressure index, and RPP were calculated. The relationship between these haemodynamic measures and functional outcome (death or dependency, modified Rankin Scale > 2) and early recurrent stroke, were studied with adjustment for baseline prognostic factors and treatment group. Odds ratios (OR) and 95% confidence intervals (CI) refer to a change in haemodynamic measure by 10 points. RESULTS: A poor functional outcome was associated with SBP (adjusted OR; 1.11; 95% CI, 1.03-1.21), HR (adjusted OR; 1.15; 95% CI, 1.00-1.31), MBP (adjusted OR; 1.15, 95% CI, 1.03-1.29), PP (adjusted OR; 1.14; 95% CI, 1.02-1.26), MAP (adjusted OR; 1.15; 95% CI, 1.02-1.31) and RPP (adjusted OR; 1.01; 95% CI, 1.00-1.02). Early recurrent stroke was associated with SBP, DBP, MBP and MAP. CONCLUSIONS: A poor outcome is independently associated with elevations in blood pressure, HR and their derived haemodynamic variables, including PP and the RPP. Agents that modify these measures may improve functional outcome after stroke.

Aged↗
PubMed2005

Abnormalities on ECG and telemetry predict stroke outcome at 3 months.

BACKGROUND: ECG is a useful tool in monitoring vital functions in patients with acute stroke; however, fairly little evidence is available concerning the prevalence and the prognostic impact of ECG findings in patients with acute cerebral infarction and acute intracerebral haemorrhage (ICH). METHODS: This analysis was based on data from 692 patients with acute cerebral infarction, 155 patients with intracerebral haemorrhage (ICH), and 223 patients with transient ischaemic attack (TIA), who were admitted to hospital within 6 h of symptom onset. A 12 lead ECG was obtained on admission, and the patient was on telemetry for the first 12-24 h of hospitalisation. RESULTS: ECG abnormalities were observed in 60% of patients with cerebral infarction, 50% of patients with ICH, and 44% of patients with TIA. In multivariate analyses 3-month mortality in patients with ischaemic stroke was predicted by atrial fibrillation OR 2.0 (95% CI 1.3-3.1), atrio-ventricular block OR 1.9 (95% CI 1.2-3.9), ST-elevation OR (2.8, 95% CI 1.3-6.3), ST-depression OR 2.5 (95% CI 1.5-4.3), and inverted T-waves OR 2.7 (95% CI 1.6-4.6). This was independent of stroke severity, pre-stroke disability and age. In patients with ICH, sinus tachycardia OR 4.8 (95% CI 1.7-14.0), ST-depression OR 5.2 (95% CI 1.1-24.9), and inverted T-wave 5.2 (95% CI 1.2-22.5) predicted poor outcome. None of the changes reached significance in patients with TIA. In patients with severe cerebral infarction or ICH, heart rate did not decrease within the first 12 h after admission, which was the case in patients with mild to moderate stroke. Rapid heart rate predicted 3-month mortality in multivariate testing OR 1.7 (95% CI 1.02-2.7). CONCLUSIONS: ECG abnormalities are frequent in acute stroke and may predict 3-month mortality.

Aged↗
PubMed2005

The Scandinavian stroke scale predicts outcome in patients with mild ischemic stroke.

BACKGROUND: The prognostic value of the Scandinavian Stroke Scale (SSS) in patients with mild ischemic stroke has not previously been examined. We investigated if differences in SSS score predicted risk of death or dependency within 12 months after stroke onset. PATIENTS AND METHODS: The analysis included 353 patients with acute cerebral infarction and SSS of at least 40 points on admission, 157 of whom with SSS of at least 50 points. Patients with 40-49 points on the SSS were compared with patients with 50-58 points; and patients with SSS 50-53 were compared to patients with 54-58 points on the SSS. Death or dependency was defined as 3-6 points on the modified Rankin scale (MRS), 3 and 12 months after stroke onset. The frequencies of death or dependency were compared between groups by chi2; the risk of death or dependency 1 year after stroke was calculated by multiple logistic regression analysis, adjusting for age, gender, prestroke MRS, arterial hypertension and tobacco smoking. RESULTS: The risk of death or dependency 1 year after stroke onset was higher in patients with SSS 40-49 than with SSS 50-58, OR 2.0 (CI 95% 1.2-3.5). Three months after stroke, 46.5% of patients with SSS 40-49 were dead or dependent in comparison with 23.9% of patients with SSS > 49, p < 0.001. One year after stroke, 53.6% of patients with SSS 40-49 were dead or dependent in comparison with 30.1% of patients with SSS > 49, p <0.001. A significant 15% difference in living in own home was observed 1 year after stroke onset between patients with SSS 40-49 and SSS > 49. In very mild stroke, 32.7% of patients with SSS 50-53 were dead or dependent 3 months after stroke in comparison with 18.1% of patients with SSS 54-58 on admission, p = 0.048. CONCLUSIONS: The SSS predicts death and dependence in patients with mild ischemic stroke.

Brain Ischemia↗
PubMed2004

C-reactive protein and white blood cell count increases in the first 24 hours after acute stroke.

UNLABELLED: Levels of C-reactive protein (CRP) and white blood cell count (WBC) in acute stroke may reflect the stroke lesion itself or pre-existing factors such as infections, smoking or atherosclerosis. The aim of this study was to investigate the relation between CRP and WBC levels and time from onset of stroke, stroke severity and outcome. PATIENTS AND METHODS: The analyses were based on 719 patients in whom WBC test material was obtained within 9 h of stroke onset and CRP test material within 24 h of stroke onset. Stroke severity was assessed by the Scandinavian Stroke Scale Score on admission and outcome by death 7 days, 3 months and 1 year after symptom onset as well as modified Rankin Scale 3 months after stroke onset. RESULTS: CRP and WBC levels correlated significantly with time from symptom onset as well as with stroke severity and outcome. Levels of CRP and WBC were higher in later determinations in severe stroke. In multivariate logistic regression analysis, CRP(+10 mg/l) was independently related to 1-year mortality (OR 1.1, 95% CI 1.02-1.2). CONCLUSION: Levels of WBC and CRP increase within the first 24 h in patients with severe stroke. CRP but not WBC is related to long-term mortality possibly by reflecting the vascular risk profile.

Aged↗
PubMed2004

Serum cardiac troponin I in acute stroke is related to serum cortisol and TNF-alpha.

BACKGROUND: Serum cardiac troponin I (cTnI) is a specific marker of myocardial injury related to in-patient fatality and cardiac injury in acute stroke. We investigated whether cTnI in acute stroke is related to serum cortisol, acute inflammatory response, and insular damage. We also investigated whether cTnI predicted outcome at 3 months. PATIENTS AND METHODS: The study was based on 155 patients with CT-confirmed acute cerebral infarction and study inclusion within 24 h (50% within 12 h) of stroke onset. Blood samples were obtained on inclusion. Stroke severity was assessed by the Scandinavian Stroke Scale (SSS) and outcome was assessed by the modified Rankin Scale (mRS), death or dependency was defined as mRS > or =3 three months after stroke. RESULTS: 35% of all patients and 63% of patients who died within 3 months were troponin positive. Tumor necrosis factor-alpha (TNF-alpha) and cortisol were independently related to detection of cTnI: TNF-alpha(+100 pg/ml) OR 1.5 (CI 95% 1.1-2.2), cortisol(+100 nmol/l) OR 1.1 (CI 95% 1.01-1.2). SSS and age were also included in this model and did not reach significance. cTnI positivity was, together with age, stroke severity and prestroke mRS, but not s-cortisol, an independent explanatory variable of outcome at 3 months (death or dependency) with OR 4.1 (CI 95% 1.1-14.5). cTnI did not relate to insular involvement. CONCLUSION: In this study, cortisol and TNF-alpha were independently related to cTnI, which was predictive of 3-month prognosis.

Aged↗
PubMed2004

Serum-cortisol reflects severity and mortality in acute stroke.

BACKGROUND: The adrenal glucocorticoid stress response in humans causes catabolism, increasing blood glucose and heart rate, and possibly potentiates ischaemic damage to neurons. These effects could induce secondary brain damage in acute stroke. MATERIALS AND METHODS: This prospective study was based on a single determination of s-cortisol in 172 patients included within 24 h of stroke onset, 50% within 12 h of stroke onset. All patients were admitted to hospital within 6 h of stroke onset. We investigated the relations of s-cortisol to neurological deficit measured by Scandinavian Stroke Scale (SSS), lesion volume on CT-scan, blood glucose on admission, pulse rate, blood pressure, body temperature, deteriorating stroke, cytokines and cytokine receptors, and outcome. RESULTS: In a multivariate logistic regression analysis, s-cortisol was independently related to death within 7 days of stroke onset, odds ratio (OR) Cortisol(+100 nmol/l) 1.9 (95% CI 1.01-3.8); serum-cortisol was, however, not a predictor of death or dependency within 3 months. S-cortisol correlated to SSS (rho=-0.45, p<0.001), body temperature (rho=0.27, p<0.001), pulse rate (rho=0.26, p<0.001), and lesion volume (rho=0.33, p<0.001). S-cortisol was related to the presence of insular damage. CONCLUSION: Acute stroke mortality related to increasing serum-cortisol levels. S-cortisol was associated with stroke severity and markers reflecting stroke severity.

Aged↗
PubMed2003

Homocysteine and risk of recurrent stroke.

BACKGROUND AND PURPOSE: The goals of this work were to investigate whether elevated total homocysteine (tHcy) measured within 24 hours of acute stroke was an independent risk factor for recurrent stroke and to compare levels of tHcy in groups of patients with diagnoses of ischemic and hemorrhagic cerebrovascular events. METHODS: We performed a longitudinal study of 1039 stroke patients (mean age, 75 years). Fasting tHcy was measured the morning after primary admission. Patients were followed up for 15 months. RESULTS: Serum homocysteine was significantly higher in the 105 patients who experienced a recurrent stroke during the follow-up period than in patients without recurrence. The geometric mean+/-SD was 13.4+/-10.7 versus 11.8+/-7.1 micromol/L (P=0.008), and the mean difference was 1.2 micromol/L [95% confidence interval (CI), 1.05 to 2.3]. In a multiple logistic regression model, tHcy was an independent explanatory variable of recurrent stroke within 15 months (odds ratio, 1.3; 95% CI, 1.1 to 1.5) for each increase in tHcy of 10 micromol/L. At the index event, serum homocysteine was significantly higher in 909 patients with ischemic cerebrovascular events than in 130 patients with intracerebral hemorrhage (geometric mean, 12.1+/-7.3 versus 10.4+/-5.2 micromol/L; P<0.001). CONCLUSIONS: The data in this study indicate that elevated tHcy is an independent risk factor for recurrent stroke.

Aged↗
PubMed2003

Self-reported stress and risk of stroke: the Copenhagen City Heart Study.

BACKGROUND AND PURPOSE: Lay people often mention stress as one of the most important risk factors for stroke. Stress might trigger a cerebrovascular event directly or could be associated with higher levels of blood pressure or an unfavorable lifestyle. To examine these possibilities, we analyzed the association between self-reported stress frequency and intensity and risk of stroke. METHODS: Data from the second examination, 1981 to 1983, of participants in the Copenhagen City Heart Study were analyzed with Cox regression after a mean of 13 years of follow-up. A total of 5604 men and 6970 women were included, and 929 first-ever strokes occurred, of which 207 (22%) were fatal within 28 days after onset of symptoms. The stress frequency categories were never/hardly ever, monthly, weekly, or daily. The stress intensity categories were never/hardly ever, light, moderate, or high. RESULTS: Subjects with high stress intensity had almost a doubled risk of fatal stroke compared with subjects who were not stressed (relative risk [RR], 1.89; 95% CI, 1.11 to 3.21). Weekly stress was associated with an RR of 1.49 (95% CI, 1.00 to 2.23). There was no significant effect of stress in analyses of nonfatal strokes. Subjects who reported to be stressed often were more likely to have an adverse risk factor profile. CONCLUSIONS: Self-reported high stress intensity and weekly stress were associated with a higher risk of fatal stroke compared with no stress. However, there were no significant trends, and the present data do not provide strong evidence that self-reported stress is an independent risk factor for stroke.

Adult↗
PubMed2002

Deteriorating ischaemic stroke. cytokines, soluble cytokine receptors, ferritin, systemic blood pressure, body temperature, blood glucose, diabetes, stroke severity, and CT infarction-volume as predictors of deteriorating ischaemic stroke.

BACKGROUND AND PURPOSE: Although the causes of neurological deterioration in acute cerebral infarction have not yet been identified, many variables have been associated with deterioration. The aim of this study was to investigate deteriorating ischaemic stroke. METHODS: Deterioration was defined as a decrease in Scandinavian Stroke Scale (SSS) of at least 2 points occurring within 72 h of stroke onset and lasting at least 6 h. The earlier found associations between neurological deterioration and systemic blood pressure, blood glucose, body temperature, stroke severity, and diabetes were investigated in a population of 896 consecutive patients with acute cerebral infarction. In a substudy of 162 of these patients, we evaluated the relations of neurological deterioration to s-ferritin, p-tumor necrosis factor-alpha, p-interleukin-1beta, p-interleukin-1 receptor antagonist, p-interleukin-6, p-interleukin-10, and p-soluble tumor necrosis factor receptors 1 and 2. RESULTS: Patients with neurological deterioration had more severe strokes than nondeteriorating patients: median SSS on admission 31 versus 40, p<0.001, Mann-Whitney. We could not confirm previous reports of an association of deteriorating stroke with blood pressure, blood glucose, body temperature, diabetes, s-ferritin or cytokines. CONCLUSIONS: Severe stroke was a predictor of neurological deterioration. This study did not confirm other reported predictors of deterioration.

Blood Glucose↗