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M Kaste

Publications and source records attributed to M Kaste.

197 records · Page 11Linked to original sources

Effects of ethanol on platelet function.

To obtain evidence for an ethanol mediated disruption of hemostasis we compared the effects of acute and chronic ethanol ingestion on platelet reactivity. Since ADP may be important for hemostasis in vivo it was used to induce platelet aggregation in platelet-rich plasma. Thromboxane B2 (TXB2) formed during the aggregation was measured by radioimmunoassay. Ethanol (1.5 g/kg) given to 8 healthy non-alcoholic male volunteers increased platelet reactivity to ADP and the associated TXB2 formation rose from 289 +/- 60 (mean +/- SE) to 984 +/- 263 fmol/10(7) platelets (p less than 0.025). The effects lasted for as long as ethanol was present in blood. In 13 non-cirrhotic male alcoholics the withdrawal of ethanol caused a 4-fold increase in TXB2 formation within one week but the basal levels before ethanol withdrawal were the same as in controls. These findings are discussed in relation to the higher risk of brain infarction seen in alcoholics and even associated with binge drinking. Further studies are needed to establish the effects of ethanol on prostacyclin formation.

Adenosine Diphosphate↗

Prevention of alcohol withdrawal seizures with carbamazepine and valproic acid.

To evaluate the value of the nonsedative anticonvulsants carbamazepine and valproic acid a controlled study including drug monitoring was carried out. Intoxicated alcoholics (n = 138) were admitted for inpatient detoxication and randomly assigned to either carbamazepine (n = 43), sodium valproate (n = 46) or placebo (n = 49) in a double-blind fashion. Drug treatment lasted for four days and the daily doses of both drugs amounted to 1200 mg in the beginning of the study. Sodium valproate induced gastric distress, nausea and vomiting more frequently than placebo. About half of the subjects had to stop carbamazepine because of intolerable side-effects including vertigo, nausea, vomiting, diplopia and rash. Serum carbamazepine levels (18-89 mumol/l) were found to be high (greater than 40 mumol/l) in many but not all of these subjects. Seizures occurred in 3 subjects on placebo, 2 on carbamazepine and 1 on sodium valproate. Delirium tremens developed in 2 on sodium valproate and 1 on placebo. The study demonstrates that drug side-effects may seriously hamper the utility of carbamazepine and sodium valproate as routine treatment for the prevention of alcohol withdrawal symptoms.

Adult↗

Evaluation of various methods of assessing symptoms of cognitive impairment and dementia.

BACKGROUND AND PURPOSE: The effect of different diagnostic criteria for detecting dementia in both epidemiological and stroke cohort studies has been shown, but comparison between different assessment methods has only seldom been done. We compared both assessment methods and diagnostic criteria for dementia in a large well-defined stroke cohort. SUBJECT AND METHODS: A group of 227 of 486 patients aged 55 to 85 years who 3 months after ischemic stroke completed a comprehensive neuropsychological test battery, structured clinical mental status examination of defined cognitive domains with expanded Mini-Mental State Examination. The criteria for dementia were those of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III, DSM-III-R) and the National Institute of Neurological Disorders and Stroke-Associated Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN). RESULTS: The main differences between clinical and neuropsychological examinations were seen in memory functions: clinically 24.7% and neuropsychologically 54.2% had impairment in short-term memory and 10.4% versus 5.3% in long-term memory. Accordingly, the prevalence of dementia varied greatly: It was clinically 14.1% by DSM-III, 9.7% by DSM-III-R and 8.4% by NINDS-AIREN criteria. The corresponding frequencies based on neuropsychological evaluation were 27.3%, 4.0% and 25.6%. Between these 3 diagnostic criteria the concordance varied in clinical testing between 59.4%-68.8% (kappa 0.72-0.79) and in neuropsychological testing between 14.5%-81.1% (kappa 0.20-0.86). The concordance between clinical and neuropsychological testing was 56.8% (kappa 0.42) by DSM-III, 31.6% (kappa 0.35) by DSM-III-R and 25.5% (kappa 0.24) by NINDS-AIREN. CONCLUSIONS: The frequency of poststroke dementia and cognitive decline varied sharply when different systems of diagnostic classification and methods were used. This may have serious influences on investigation and treatment of patients. We underline the importance of further debate and studies to refine the categories of cognitive impairment used in the setting of CVD.

Aged↗

The ECASS 3-hour cohort. Secondary analysis of ECASS data by time stratification. ECASS Study Group. European Cooperative Acute Stroke Study.

OBJECTIVES: (1) To determine whether and how outcome measurements in the ECASS trial are influenced by a shorter time window (0-3 vs. 3-6 h) between onset of symptoms and start of thrombolytic therapy using recombinant tissue plasminogen activator (rt-PA) in acute ischemic stroke. (2) To discuss the results of the ECASS 0- to 3-hour cohort with the results of the National Institute of Neurological Disorders and Stroke Study (NINDSS). DESIGN AND ANALYSIS: Analysis of the 0- to 3-hour and the 3- to 6-hour cohort in accordance with the ECASS protocol. Comparative analysis of the ECASS and NINDSS results following the NINDSS protocol using dichotomized endpoints. MAIN OUTCOME MEASURES: Primary endpoints: modified Rankin Scale, Barthel Index; secondary endpoints: combined Barthel/Rankin, long-term Scandinavian Stroke Scale, National Institutes of Health Stroke Scale, mortality at 30 and 90 days, occurrence of intracranial hemorrhage. NINDS trial endpoint: favorable outcome as defined in the NINDS trial. RESULTS: In ECASS, 87 patients were randomized within 3 h of stroke onset. Differences in favor of rt-PA treatment can be found for all primary and secondary outcome measures in the ECASS 0- to 3-hour cohort, except for mortality at day 30, which is somewhat higher in the rt-pA-treated group. However, due to the small sample size, the differences do not reach statistical significance. Early infarct signs (as defined by the ECASS protocol) are found as early as 2 h after stroke onset. Parenchymal hemorrhages are found significantly more often among rt-PA-treated patients. The results in the ECASS 0- to 3-hour cohort fit well with the results in NINDSS. CONCLUSION: Data from the 3-hour ECASS cohort support the efficacy of early thrombolytic therapy in acute hemispheric stroke patients. Comparing bleeding complications between the ECASS and NINDSS is difficult because of differences in the definition and occurrence of hemorrhagic events.

Aged↗

Correlates of dependent living 3 months after ischemic stroke.

To examine the correlates of dependent living after ischemic stroke, a consecutive cohort of 486 patients aged 55-85 years was examined 3 months after the index stroke. Detailed medical, neurological and radiological stroke evaluation, structured measures of cognition, emotion and behavior, activities of daily living (ADL), physical disability, and assessment of dependent living were performed. Independent correlates of dependent living 3 months after stroke were the presence of the major hemispheral stroke syndrome (odds ratio, OR, 11.8, 95% confidence interval, CI, 7.2-19.9), and a combination of handicap (Rankin Scale, OR 3.9, 95% CI 2.6-6.1), cognition (DSM-III-R dementia, OR 3.9, CI 1.5-10.7, any cognitive decline, OR 4.5, CI 2.0-11.2), and ADL [Functional Activities Questionnaire (FAQ), OR 1.2, 95% CI 1.1-1.2]. The Rankin Scale explained 51.5%, FAQ 5.9% and presence of DSM-III-R dementia or any cognitive decline 3.4% of the total variance between dependent and independent patients after stroke. Independent of the effects of physical disability, presence of cognitive impairment has important functional consequences on stroke patients. Our findings emphasize the importance of the evaluation of cognitive functions in both observational and interventional clinical trials, as well as in treatment planning, rehabilitation and guidance of patients with ischemic stroke.

Activities of Daily Living↗

Effect of nimodipine on final infarct volume after acute ischemic stroke.

Placebo-controlled clinical trials with nimodipine in acute ischemic stroke have not fulfilled the early optimistic expectations. Nimodipine has in some experimental studies, when administered either before or up to 90 min after induction of cerebral ischemia, resulted in a reduction of infarct size. No studies on the effects of nimodipine on infarct size in man have been published. We measured the infarct volumes in the admission and control CT examinations 3 weeks to 3 months later in 153 patients who had participated in a multicenter, randomized and placebo-controlled study. No statistically significant differences overall were found within or between the treatment groups. Subgroup analyses revealed in the placebo, but not in the nimodipine arm, an increase in the median infarct volumes if the treatment was started within 24 h of onset, and if the volume in the admission CT was less than median. A beneficial effect of nimodipine in prevention of infarct size increase in these circumstances cannot be excluded.

Adolescent↗

Tranexamic acid in subarachnoid hemorrhage. A double-blind study.

The effects of intravenous tranexamic acid were compared with placebo in 64 patients with subarachnoid hemorrhage. A double-blind procedure was used. One gram of tranexamic acid was given intravenously every 4 hours up to the time of operation on an intracranial arterial aneurysm or for up to 21 days after the first bleeding if operative treatment was not feasible. There were no differences in re-bleeds, morbidity or mortality between the tranexamic and placebo-treated groups. No thromboembolic complications were noted in either group. Our results do not support the use of tranexamic acid in subarachnoid hemorrhage in daily doses of 6 g.

Adolescent↗

Ethanol intoxication: a risk factor for ischemic brain infarction in adolescents and young adults.

Between January 1978 and December 1979 23 consecutive patients aged under 40 years with acute ischemic brain infarction were admitted to the department of neurology, Meilahti University Hospital in Helsinki. In 10 patients (43%) the onset of symptoms was preceded within 24 hours by ethanol intoxication, and all but one symptom occurred at weekends when most liquor is consumed in Finland. Ethanol intoxication preceding the stroke was 4 times as common in female and 5 times as common in male patients as ethanol intoxication in the general Finnish population of the same age and sex. The present results support those of our previous study and suggest that occasional ethanol intoxication increases the risk of ischemic brain infarction both in adolescents and young adults.

Adolescent↗

Outcome of 314 patients with transient ischemic attacks.

Between 1967 and 1976, 314 patients with transient ischemic attack (TIA) were evaluated and treated. Follow-up has been from 2.8 to 13.2 years (mean 7.8). As of 1979, 55 of the patients had succumbed to cardiovascular disease (28), cerebrovascular disease (9), malignancy (10), and other causes (8). During the follow-up period, 15 patients suffered brain infarction (4.8% under the risk) while 40 had myocardial infarction (12.7%) under the risk). Brain infarction occurred as often in patients with carotid TIA as in those with vertebral-basilar TIA, and was more common in patients under anticoagulation therapy than in those without it (p less than 0.05). Arterial hypertension, heart disease, peripheral arterial disease and diabetes did not increase the risk of brain infarction, but all (except diabetes) increased the risk of myocardial infarction. Combination of TIA with arterial hypertension, heat disease, or peripheral arterial disease increased the mortality (p less than 0.001). A life table analysis of surviving 1, 5, and 10 years gave probabilities of 99 and 100%, 89 and 91%, and 60 and 75% for males and females respectively. In the case of normotensive and hypertensive patients, a life table analysis of chances of surviving 1, 5, and 10 years gave probabilities of 100 and 95%. 94 and 80%, and 76 and 49% in both groups respectively. The result clearly emphasize treating of arterial hypertension, and demonstrate that TIA is not only a warning sign of impending stroke but also that of myocardial infarction.

Adolescent↗

Increase of low serum concentrations of high-density lipoprotein (HDL) cholesterol in TIA-patients treated with phenytoin.

Serum high density lipoprotein (HDL) cholesterol and other lipoproteins were measured in 27 TIA-patients with a mean age of 49 +/- 10 years before and during phenytoin therapy. The pretreatment concentrations of HDL-cholesterol (mmol/l, mean +/- SD) were lower (p less than 0.001) in male (1.03 +/- 0.25) and in female patients (1.15 +/- 0.44) than in healthy male (1.28 +/- 0.34) and female controls (1.52 +/- 0.31) respectively. After one month's phenytoin therapy HDL cholesterol concentrations reached normal levels (men 1.33 +/- 0.38, women 1.61 +/- 0.27) and after 9 months of therapy even surpassed them (men 1.47 +/- 0.27, p less than 0.05; women 1.91 +/- 0.33, p less than 0.01). Percent increase of HDL cholesterol after 9 months of therapy was 42 +/- 25 in men and 68 +/- 46 in women. There was a positive correlation (r = 0.43, p less than 0.05) between serum phenytoin level and increase of HDL cholesterol. HDL/LDL cholesterol ratio increased (p less than 0.01) also during 9 months of therapy (men from 0.26 +/- 0.05 to 0.36 +/- 0.10, women from 0.26 +/- 0.07 to 0.43 +/- 0.13) and showed a positive correlation (r = 0.91, p less than 0.001) with increase of serum HDL cholesterol. The HDL cholesterol levels achieved have been maintained with a mean serum phenytoin level of 5.6 +/- 3.6 mg/l. Phenytoin induced increase in serum HDL levels should not yet be equated with protection against atherosclerosis.

Cholesterol↗

Ethanol intoxication: a risk factor for ischemic brain infarction.

One hundred consecutive patients (67 men, 33 women) aged from 15-55 with acute ischemic brain infarction verified by computed tomography and/or angiography and/or brain scanning were studied. In 40 cases the onset of symptoms was preceded within 24 hours by ethanol intoxication. Ethanol intoxication preceding brain infarction was 4-7 times as common in men and 6-15 times as common in women as ethanol intoxication in the general Finnish population of the same age and sex. Nineteen of the patients were heavy drinkers. Heavy drinking was twice as common in men and 5 times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of ischemic brain infarction. The ethanol-induced risk was highest in middle-aged women and young men.

Adolescent↗

Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke?

The effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B2 rose from 303 +/- 56 to 950 +/- 212 fmol per 10(7) platelets (p less than 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.

Adenosine Diphosphate↗

Prognosis of patients with unilateral extracranial occlusion of the internal carotid artery.

One hundred fifty-five patients (121 men and 34 women) had an angiographically verified unilateral internal carotid artery (ICA) occlusion immediately after carotid bifurcation. The median follow-up period was 53 months. Forty-five percent of the patients were fully independent in the activities of daily living (ADL), 22% required assistance in ADL, 11% were disabled, and 22% died within the follow-up period. The mortality rate was exceptionally low compared with previous series. A life-table analysis of the material gave a 94% probability of surviving the first year, 84% the third year, and 78% the fifth year. Young age was favorable in regard to functional recovery, but it had no influence on mortality. The condition at the acute stage was the most important clinical sign in predicting the prognosis. The prognosis of mortality and functional recovery was poorer for smokers than for nonsmokers, and hypertension had no effect on prognosis. Cerebrovascular disease and coronary heart disease were found to be the cause of death with equal frequency in this study.

Activities of Daily Living↗

Prognosis of patients with middle cerebral artery occlusion.

The long-term prognosis of 78 stroke patients with occlusion of the middle cerebral artery (MCA) or its branches is described. The mean age of the patients was 44 years. The mortality rate in the acute phase was 5%. The acute and total mortality rates of men were higher than those of women (p less than 0.05). Life-table analysis gave 94% probability for one year's survival, 84% for three years' survival, and 78% for five years' survival. Subsequent strokes were twice as common as cardiovascular events as the cause of death. Seventy-two percent of the survivors became fully independent in activities of daily living (ADL) , 27% required assistance, 1% was totally disabled, and 43% returned to work. Left-sided occlusion was overrepresented in those who died (p less than 0.00(1) and those who returned to work (p less than 0.05), and right-sided occlusion was overrepresented in those who required assistance in ADL (p less than 0.05).

Activities of Daily Living↗