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S Juvela

Publications and source records attributed to S Juvela.

At least 37 records · Page 2Linked to original sources
PubMed1996

Platelets, alcohol consumption, and onset of brain infarction.

OBJECTIVES: Previous investigations have suggested that recurrent rebound thrombocytosis after alcohol misuse may be a factor in the pathogenesis of thromboembolic disease. Alcohol consumption, platelet count, and platelet function were examined among patients of working age with brain infarction. METHODS: Platelet count and risk factors for stroke were studied in 426 stroke patients and 157 control patients in hospital. The measures were platelet count obtained within four days after the stroke onset, in vitro adenosine diphosphate induced platelet aggregation, associated thromboxane B2 formation, and urinary excretion of 11-dehydrothromboxane B2. RESULTS: After adjustment for sex, age, cardiac disease, diabetes, and alcohol intake, hypertension (OR 3.4, 95% confidence interval (95% CI) 2.0-6.0) and current smoking (OR 2.1, 95% CI 1.4-3.3) were associated with an increased risk for brain infarction. Platelet count shortly after the onset of disease was higher in the stroke patients than in the controls (OR 1.05/10(10)/1 platelets; 95% CI 1.02-1.09). The patients with brain infarction who were heavy alcohol drinkers (n = 144) showed both thrombocytosis (OR 2.30, 95% CI 0.82-6.44) and thrombocytopenia (OR 3.20, 95% CI 1.19 to 8.59) more often at the onset of the stroke than the other patients with brain infarction. The thromboxane variables showed inconsistent associations with the onset of stroke. There was no consistent platelet abnormality among alcohol misusers at the onset of ischaemic brain infarction. CONCLUSIONS: Alcohol induced thrombocytopenia and rebound thrombocytosis were both often seen at the onset of brain infarction in patients who were heavy alcohol drinkers. Therefore, other mechanisms which could contribute to the high frequency of recurrences of ischaemic stroke among heavy drinkers should be investigated.

Adenosine Diphosphate↗
PubMed1996

Weekend and holiday increase in the onset of ischemic stroke in young women.

BACKGROUND AND PURPOSE: Chronobiological analyses of stroke onset may throw some light on the mechanisms that trigger stroke. Observations may generate new hypotheses for identifying significant causal relationships. METHODS: In the present study, both the circadian and the weekend and holiday versus workday times of the onset of ischemic cerebral infarction were determined for 723 consecutive subjects, aged 16 to 60 years, who were admitted for hospital treatment in the acute phase without any selection. RESULTS: Among young adults (16 to 40 years) and women, more infarctions occurred during weekends and holidays than were expected. Young women in particular had an increased risk for brain infarction during weekends and holidays (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.26 to 3.63). In a multivariate analysis, age of 16 to 30 years (OR, 3.13; 95% CI, 1.57 to 6.50), female sex (OR 1.71; 95% CI, 1.12 to 2.63), and recent drinking of alcohol (P < .01) were associated with the onset of brain infarction during weekends and holidays, whereas current cigarette smoking was associated with the onset of brain infarction during workdays (P < .001). A morning increase in the onset of brain infarction was observed among middle-aged people during both weekends/holidays and workdays. Among young adults, however, an evening increase was also seen during weekends/holidays and workdays. CONCLUSIONS: We found that young adults and women are frequently stricken by brain infarction during weekends and holidays and that the circadian distribution of the onset of brain infarction among young adults is different from that of middle-aged people. These observations suggest that there may be stroke-triggering activities that are associated with lifestyle.

Adolescent↗
PubMed1995

Risk factors for impaired outcome after spontaneous intracerebral hemorrhage.

OBJECTIVE: To search out independent prognostic factors, including preictal variables for outcome of spontaneous intracerebral hemorrhage. DESIGN: Prospective follow-up study. PATIENTS: One hundred fifty-six consecutive patients (96 men and 60 women) aged 16 to 60 years admitted as emergencies after bleeding. MAIN OUTCOME MEASURES: Potential risk factors (baseline characteristics, health habits, and clinical variables) for death and impaired outcome were studied prospectively up to 1 year after hemorrhage. RESULTS: One year after hemorrhage, 64 patients (41%) were independent and 34 patients (22%) were dependent in the activities of daily living; 58 patients (37%) had died. Risk of death was predicted, after adjustment for sex, age, hypertension, and body mass index, by clinical condition at admission according to the Glasgow Coma Scale (P < .001) and the occurrence of subcortical hematoma (odds ratio [OR], 0.18; 95% confidence interval [CI], 0.04 to 0.91; P = .04). Risk of poor outcome (dependent state or death) was predicted, after adjustment for sex, hypertension, body mass index, cigarette smoking, presence of intraventricular hemorrhage, and surgery, significantly by the Glasgow Coma Scale (P < .001); presence of subcortical hematoma (OR, 0.04; 95% CI, 0.01 to 0.27; P < .001); volume of hematoma (P = .03); age (P = .004); amount of alcohol consumed within 1 week before hemorrhage (P = .03); and presence of cerebellar hematoma (OR, 0.13; 95% CI, 0.02 to 0.95; P = .04). Significant independent predictors of impaired outcome (assessed with the Glasgow Outcome Scale) were the Glasgow Coma Scale (P < .001); presence of subcortical hematoma (OR, 0.26; 95% CI, 0.10 to 0.67; P = .006); alcohol intake within 1 week (P = .002); and presence of cerebellar (OR, 0.16; 95% CI, 0.04 to 0.60; P = .008), intraventricular (OR, 2.74; 95% CI, 1.19 to 6.28; P = .02), or caudate hemorrhage (OR, 0.13; 95% CI, 0.02 to 0.77; P = .03). The mean erythrocyte corpuscular volume was directly associated with an impaired outcome (P < .05). CONCLUSION: In addition to severity and location of the hemorrhage, the age of the patient and the amount of alcohol consumed within 1 week seem to be independent determinants of outcome after intracerebral hemorrhage.

Adolescent↗
PubMed1995

Recent alcohol consumption, cigarette smoking, and cerebral infarction in young adults.

BACKGROUND AND PURPOSE: The role of recent heavy drinking of alcohol as a risk factor for ischemic brain infarction is unclear. We investigated this problem in young adults, in whom even a thorough workup often fails to reveal any predisposing factor. METHODS: This was a hospital-based case-control study comprising 75 consecutive subjects aged 16 to 40 years with first-ever ischemic brain infarction and 133 control subjects from the same hospital who were group-matched with the case patients for age, sex, day of the onset of symptoms, and acuteness of disease onset. RESULTS: Multiple logistic regression analysis showed that alcohol intake exceeding 40 g of ethanol within the 24 hours preceding disease onset was a significant independent risk factor for brain infarction among both men (odds ratio [OR], 6.0; 95% confidence interval [CI], 1.8 to 20.3) and women (OR, 7.8; 95% CI, 1.0 to 60.8). Cigarette smoking was not found to be an independent risk factor in the model, whereas among men arterial hypertension was (OR, 6.2; 95% CI, 1.5 to 24.7). CONCLUSIONS: We conclude that very recent alcohol drinking, particularly drinking for intoxication, may trigger the onset of brain infarction in young adults and that there might be a variety of mechanisms behind this effect.

Adolescent↗
PubMed1995

Risk factors for spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Spontaneous intracerebral hemorrhage has remained a serious disease despite recent improvements in medical treatment. This study was designed to identify modifiable risk factors for intracerebral hemorrhage. METHODS: Health habits, previous diseases, and medication of 156 consecutive patients with intracerebral hemorrhage aged 16 to 60 years (96 men and 60 women) were compared with those of 332 hospitalized control patients (192 men and 140 women) who did not differ from case subjects in respect to age, day of onset of symptoms, or acuteness of disease onset. RESULTS: After adjustment for sex, age, hypertension, body mass index, smoking status, and alcohol consumption during the last week, patients who had consumed 1 to 40, 41 to 120, or > 120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk (95% confidence interval) of hemorrhage of 0.3 (0.2 to 0.7), 4.6 (2.2 to 9.4), and 11.3 (3.0 to 42.8), respectively, compared with those who had consumed 0 g. In addition, alcohol intake within 1 week before the onset of illness, excluding use within the last 24 hours, increased the risk of hemorrhage; adjusted risks were 2.0 (1.1 to 3.5) for 1 to 150 g, 4.3 (1.6 to 11.7) for 151 to 300 g, and 6.5 (2.4 to 17.7) for > 300 g compared with 0 g. The adjusted risk of hypertension for hemorrhage was 6.6 (3.9 to 11.3). Previous heavy alcohol consumption and current cigarette smoking were not independent risk factors for hemorrhage, but anticoagulant treatment was (P < .01). Erythrocyte mean corpuscular volume and gamma-glutamyl transferase values were also higher in patients with intracerebral hemorrhage than in control subjects. CONCLUSIONS: Recent moderate and heavy alcohol intake as well as hypertension and likely also anticoagulant treatment seem to be independent risk factors for intracerebral hemorrhage.

Adolescent↗
PubMed1995

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study was interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

Adult↗
PubMed1993

Cigarette smoking and alcohol consumption as risk factors for aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Aneurysmal subarachnoid hemorrhage is a serious disease despite recent improvements in medical and surgical treatment. Hence, identification of modifiable risk factors for subarachnoid hemorrhage is important. METHODS: We compared the smoking and drinking habits of 278 consecutive patients with aneurysmal subarachnoid hemorrhage, aged 15-60 years (145 men and 133 women) with those of 314 hospitalized control patients (164 men and 150 women) who did not differ in regard to age, day of onset of symptoms, and acuteness of disease onset. RESULTS: Multiple logistic regression analysis showed that recent alcohol intake and smoking, but not hypertension, were significant independent risk factors for hemorrhage. After adjustment for age, hypertension, and smoking status, men who had consumed 1-40, 41-120, or > 120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk of hemorrhage of 0.3 (95% confidence interval [CI], 0.1-0.8), 2.5 (95% CI, 1.1-5.5), and 4.5 (95% CI, 1.5-12.9), respectively, compared with men who had consumed 0 g. Women who had consumed 1-40 or > 40 g of alcohol had a risk of hemorrhage of 0.4 (95% CI, 0.2-0.8) and 6.4 (95% CI, 2.3-17.9), respectively, compared with women without use of alcohol. Heavily smoking (> 20 cigarettes per day) men and currently smoking women had adjusted relative risks of hemorrhage of 7.3 (95% CI, 3.8-14.3) and 2.1 (95% CI, 1.2-3.6), respectively, compared with men who had never smoked and with women who were not current smokers. Higher levels of erythrocyte mean corpuscular volume in patients with subarachnoid hemorrhage than in control subjects supported the notion of different smoking and drinking habits. CONCLUSIONS: Recent heavy alcohol intake and current smoking seem to be independent risk factors for aneurysmal subarachnoid hemorrhage.

Adolescent↗
PubMed1993

Risk factors for cervical atherosclerosis in patients with transient ischemic attack or minor ischemic stroke.

BACKGROUND AND PURPOSE: Our purpose was to study potential determinants of the presence and the severity of cervical atherosclerosis in patients with transient ischemic attack or minor ischemic stroke. METHODS: Two hundred ninety-four patients up to 60 years of age were included in this cross-sectional study. The male to female ratio was 171/123. Atherosclerosis was defined as the presence of any visible atherosclerotic lesion in anteroposterior or left oblique views of cervical arteries in aortic arch angiograms. The severity of atherosclerosis was assessed using three scores, which were computed separately for the total thickness and length of all plaques as well as for the percent stenosis of the vessels. RESULTS: Atherosclerosis was present in 180 patients (61.2%). In a multiple stepwise logistic regression analysis, age, serum triglycerides, smoking history for more than 20 years, arterial hypertension (defined as systolic or diastolic blood pressure values at least 150 or 100 mm Hg, respectively, or the use of antihypertensive medication), regular light alcohol consumption (inversely), and body mass index (marginal inverse association) were independent determinants of the presence of atherosclerosis; the respective odds ratios were 1.1/1 y, 1.8/1 mmol/L, 3.3, 2.4, 0.3, and 0.9/1 kg/m2. In multiple linear regression models, age was associated positively and the ratio of high density lipoprotein to total cholesterol was associated negatively with the severity of atherosclerosis regardless of the scoring method, whereas current smoking and female sex were predictors only of the percent stenosis and the length of the lesions. Arterial hypertension showed a significant association only with the length of the lesions. CONCLUSIONS: Age, cigarette smoking, and arterial hypertension contribute substantially to atherosclerosis in cervical arteries, but this study also confirms the independent associations of lipid or lipoprotein variables with atherosclerotic disease. An independent inverse association of regular light consumption of alcohol with cervical atherosclerosis was also observed.

Adult↗
PubMed1993

Natural history of unruptured intracranial aneurysms: a long-term follow-up study.

To investigate the natural history of unruptured aneurysms and predictive risk factors determining subsequent rupture, the authors followed 142 patients with 181 unruptured aneurysms until death or subarachnoid hemorrhage intervened, or for at least 10 years after the unruptured aneurysm was diagnosed. Six patients had a symptomatic aneurysm, five had an incidentally discovered aneurysm, and 131 had multiple aneurysms, of which the ruptured lesion was clipped at the beginning of the follow-up study. The median follow-up time was 13.9 years (range 0.8 to 30.0 years). During 1944 patient-years of follow-up study there were 27 first episodes of hemorrhage from a previously unruptured aneurysm, giving an average annual rupture incidence of 1.4%. Fourteen of these bleeding episodes were fatal. The cumulative rate of bleeding was 10% at 10 years, 26% at 20 years, and 32% at 30 years after the diagnosis. The only predictor for the rupture was the size of the aneurysm (p = 0.036). However, in patients with multiple aneurysms (the main subgroup) the only variable that tended to predict rupture was the age of the patient: risk of rupture was inversely associated with age (p = 0.080). The median diameter of the aneurysms was 4 mm at the beginning of the follow-up period, both in those with and those without a later hemorrhage. During the angiographic monitoring period, a ruptured aneurysm significantly (p < 0.001) increased in size in 17 patients with hemorrhage but aneurysms did not increase significantly in 14 patients without hemorrhage. In addition, a new aneurysm was found in six of 31 patients. The authors conclude that an unruptured aneurysm should be operated on, irrespective of its size, if it is technically possible and the patient's age and concurrent diseases are not contraindications to surgery.

Adolescent↗
PubMed1992

Alcohol consumption as a risk factor for poor outcome after aneurysmal subarachnoid haemorrhage.

OBJECTIVE: To evaluate the effect of factors existing before aneurysmal subarachnoid haemorrhage on outcome of haemorrhage. DESIGN: Prospective follow up study. SETTING: Helsinki University Hospital. PATIENTS: 291 consecutive patients (149 men) aged 15 to 65 years admitted within 96 hours after the bleeding. MAIN OUTCOME MEASURES: Potential risk factors (baseline characteristics, health habits, and clinical variables) for poor outcome after haemorrhage (dependent state in the activities of daily living, or death) were studied using multiple logistic regression. RESULTS: One year after haemorrhage, 179 (62%) patients were independent in the activities of daily living and 28 (10%) dependent; 84 (29%) had died. Risk of poor outcome was predicted, after adjustment for sex and age, by clinical condition at admission according to the Glasgow coma scale (p less than 0.0001); occurrence of rebleeding (relative risk 7.1, 95% confidence interval 2.8 to 18.0, p less than 0.0001) or delayed cerebral ischaemia (10.3, 4.2 to 25.4, p less than 0.0001); surgery on an aneurysm (0.13, 0.05 to 0.35, p less than 0.0001); and heavy consumption of alcohol (4.5, 1.8 to 11.0, p = 0.0014). Heavy drinking remained a significant risk factor after additional adjustment for hypertension, body mass index, and presence of intracerebral haematoma. Heavy drinkers had a more unfavourable outcome after rebleeding and delayed ischaemia than did others with rebleeding or ischaemia. Those who had salicylates in urine on admission had delayed ischaemia with fixed neurological deficits less commonly than others. CONCLUSIONS: Heavy drinking impairs outcome mainly through severe rebleeding and delayed ischaemia and to a lesser extent through a poor initial condition and presence of intracerebral haematoma.

Adolescent↗
PubMed1992

Minor leak before rupture of an intracranial aneurysm and subarachnoid hemorrhage of unknown etiology.

Of 312 consecutive patients who were admitted to an emergency hospital because of subarachnoid hemorrhage (SAH), data on premonitory minor leaks were available on 303. Patients with an aneurysmal SAH had significantly (P less than 0.05) more frequently (100 of 273, or 37%) a history of symptoms consistent with a previous minor leak than those with a hemorrhage of unknown etiology (4 of 30, or 13%). Aneurysmal SAH was associated with a poorer prognosis, more frequent occurrence of repeated bleeding and cerebral ischemia compared with SAH of unknown etiology, even in the good grade patients. The possible occurrence of a minor leak in poor grade patients may be even more frequent because the history obtained from family members was quite often uncertain. The outcome did not differ according to the evidence of previous minor leaks, but those who were admitted before a major rupture had a good outcome. The median time between a minor leak and major rupture was 14 days (range, 1 day to 4 mo). The correct diagnosis of a minor leak is important because early diagnosis and management can improve the overall outcome of this disastrous disease.

Adolescent↗
PubMed1991

Angiographic vasospasm and release of platelet thromboxane after subarachnoid hemorrhage.

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in 49 patients with subarachnoid hemorrhage in relation to angiographic vasospasm. Postoperative cerebral angiography was performed less than or equal to 3 (median 1) days after surgery for an aneurysm 5-14 days after subarachnoid hemorrhage. Correspondingly, one sample from each patient was taken within 24 hours either before or after angiography. The occurrence of severe as well as diffuse, moderate, or severe angiographic vasospasm was associated with the presence of delayed cerebral ischemia (p less than 0.05). Patients with diffuse angiographic vasospasm had significantly higher (p less than 0.05) values for thromboxane B2 release than the others, even after adjustment by the clinical grades on admission and before surgery, the timing of surgery, the time from subarachnoid hemorrhage to angiography and blood sampling, and nimodipine therapy. Severe and diffuse angiographic vasospasm were also associated with poor outcome at 1 year (p less than 0.05). Our results suggest that augmented release of platelet thromboxane may be involved in the pathogenesis of vasospasm in large cerebral arteries.

Adenosine Diphosphate↗
PubMed1991

Reduced platelet aggregability and thromboxane release after rebleeding in patients with subarachnoid hemorrhage.

Serial blood samples were obtained from 80 patients with subarachnoid hemorrhage (SAH) to study adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release. The goal of the investigation was to detect whether reduced platelet function is involved in rebleeds. Seventeen patients (21%) suffered a rebleed, six of those experiencing their first rebleed within 24 hours after SAH. Therefore, most platelet function studies were performed after rebleeds. Thromboxane release was lower in patients with rebleeds than in the others, both before and after rebleeding, although statistical significance was reached only in samples collected after rebleeds. Patients rebleeding within 24 hours after SAH had lower platelet aggregability (p = 0.037) than patients without a rebleed in the samples taken within 3 days after SAH. The results suggest that reduced platelet aggregability and thromboxane release are involved in rebleeds following primary SAH.

Adenosine Diphosphate↗
PubMed1991

Platelet thromboxane release and delayed cerebral ischemia in patients with subarachnoid hemorrhage.

Adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release were studied in 52 patients with subarachnoid hemorrhage (SAH) in order to detect a possible association between altered platelet function and development of cerebral ischemic complications after SAH. Compared to the values on admission, the patients showed significantly increased platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001) 1 to 2 weeks after SAH. The highest values of thromboxane release were seen in patients who deteriorated due to delayed cerebral ischemia with a permanent neurological deficit. Thromboxane release was significantly higher (p less than 0.05) before the onset of severe delayed ischemia in six patients with preoperative ischemia compared to the patients without delayed ischemia. In five others, both ischemic deterioration and elevated thromboxane release occurred after operation. These patients had preoperative values similar to the values in those without ischemic symptoms. The observations suggest that increased platelet aggregability and thromboxane release are associated with delayed cerebral ischemia both before and after surgery.

Adult↗
PubMed1990

Cerebral infarction and release of platelet thromboxane after subarachnoid hemorrhage.

Platelet aggregation induced by adenosine diphosphate and the release of thromboxane B2 were studied in 68 patients with subarachnoid hemorrhage during the second week after the hemorrhage, when delayed ischemic deterioration most often occurs. Follow-up computed tomographic scans were performed later than 1 month after subarachnoid hemorrhage to reveal permanent hypodense areas consistent with cerebral infarction. Occurrence of hypodense lesions on the follow-up computed tomographic scan was significantly associated with the presence of delayed ischemic deterioration (DID) (P less than 0.01). Patients with subcortical or cortical cerebral infarctions due to DID released more platelet thromboxane B2 than those with no evidence of a hypodense lesion on the computed tomographic scan (P less than 0.05). Hypodense areas caused by an intracerebral hematoma or small, deep-seated infarcts due to DID were not associated with significantly elevated release of thromboxane B2, but the lacunar type infarcts were associated with increased aggregation of platelets. The results suggest that augmented platelet function may be involved in the pathogenesis of cerebral infarction due to DID.

Adult↗
PubMed1990

Platelet thromboxane release after subarachnoid hemorrhage and surgery.

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in platelet-rich plasma from 88 patients with subarachnoid hemorrhage and 26 healthy controls. During the first 3 days after subarachnoid hemorrhage, the patients showed significantly decreased (p less than 0.05) platelet aggregability and thromboxane release relative to the controls, but these effects disappeared in a few days. Platelet count increased for 3 weeks after subarachnoid hemorrhage. Surgery in 67 patients was followed by significant increases in platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001). Greatest thromboxane release was found in the eight patients showing delayed (postoperative) ischemic deterioration with a permanent neurologic deficit. Although platelet hyperaggregability and increased thromboxane release were particularly prominent in these eight patients, the role of these hematologic parameters in the pathogenesis of delayed ischemic deterioration remains unclear.

Adult↗