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S Juvela

Publications and source records attributed to S Juvela.

At least 19 recordsLinked to original sources
PubMed2002

Natural history of unruptured intracranial aneurysms: risks for aneurysm formation, growth, and rupture.

Several studies concerning risk factors for SAH and for subsequent rupture of an unruptured aneurysm have been published, but not risk factor studies for formation and growth rate of aneurysms. Because less than half of all aneurysms ever rupture, it is essential to know risk factors separately both for aneurysm formation and for its growth. Before 1979, unruptured aneurysms were not operated on in Helsinki. Recently, the results of risk factors for rupture of unruptured aneurysms of 142 patients (131 with a prior SAH) have been published. 89 were followed with conventional and/or 3D CT angiography, or at autopsy to define risk factors for aneurysm formation and growth. During 2575 person-years, 33 of the 142 patients (23%) suffered SAH, resulting in an annual incidence of 1.3% (95% CI, 0.9-1.7%). The cumulative rate of bleeding was 10.5% (95% CI, 5.3-15.8%) at 10 years, and 30.3% (21.1-39.6%) at 30 years. Independent risk factors for rupture were cigarette smoking (time-dependent relative risk, 3.04; 95% CI, 1.21-7.66), and size of aneurysm (1.14 per mm; 1.01-1.30) after adjustment for age, aneurysm group, and hypertension. In addition, current cigarette smoking at end of follow-up (age-adjusted odds ratio, 3.92; 95% CI, 1.29-11.93) and female gender 3.36 (1.11-10.22) were the only independent risk factors for aneurysm growth of > or = 1 mm but only current smoking (3.48, 1.14-10.64) was a risk factor for growth of > or = 3 mm. Probability of de novo aneurysm formation was 0.84% per year (95% CI, 0.47-1.37%). Female gender (adjusted odds ratio, 4.73; 95% CI, 1.16-19.38) and current smoking (4.07, 1.09-15.15) were the only significant (p < 0.05) independent risk factors for de novo aneurysm formation. Cessation of smoking is very important for these patients. It is recommended that unruptured aneurysms be operated on irrespective of their size and of patients' smoking status, in people aged < 50 to 60 years.

Adult↗
PubMed2001

Use of aspirin, epistaxis, and untreated hypertension as risk factors for primary intracerebral hemorrhage in middle-aged and elderly people.

BACKGROUND AND PURPOSE: The incidence of primary intracerebral hemorrhage (ICH) increases exponentially with age, but the risk factors are not well known. We investigated lifestyle factors, previous diseases, and medications as risk factors for ICH in middle-aged and elderly people. METHODS: We compared 98 consecutive patients with primary ICH between 36 and 90 years of age with 206 community-based control subjects matched for age and sex. Odds ratios (ORs) and 95% confidence intervals (CIs) after adjustment for possible confounding variables were calculated by logistic regression. RESULTS: The independent risk factors for ICH were untreated hypertension (OR, 6.95; 95% CI, 3.06 to 15.8), previous ischemic stroke (OR, 3.83; 95% CI, 1.70 to 8.63), epilepsy (OR, 13.8; 95% CI, 2.49 to 76.6), recent strenuous physical exertion (OR, 3.97; 95% CI, 1.95 to 8.10), and a history of epistaxis (OR, 2.92; 95% CI, 1.28 to 6.62). In men, treated hypertension (OR, 2.67; 95% CI, 1.03 to 6.93) was also a significant risk factor. Patients with a history of epistaxis who had used nonsteroidal anti-inflammatory drugs, especially aspirin in high doses, had an increased risk for ICH (adjusted OR of epistaxis, 2.75; 95% CI, 1.11 to 6.81; adjusted OR of aspirin use, 14.7; 95% CI, 2.03 to 106). In addition, there was a significant (P:<0.01) positive interaction between the history of epistaxis and the use of aspirin on the risk for ICH. CONCLUSIONS: Epistaxis is a risk factor for ICH in middle-aged and elderly people, both independently and combined with the use of aspirin. Other independent risk factors are untreated hypertension, previous ischemic stroke, epilepsy, and recent strenuous physical exertion. Epistaxis may be a warning sign of an increased risk for ICH in subjects using aspirin.

Adult↗
PubMed2001

Factors affecting formation and growth of intracranial aneurysms: a long-term follow-up study.

BACKGROUND AND PURPOSE: We sought to investigate factors determining growth rate of unruptured intracranial aneurysms as well as formation of new (de novo) aneurysms in patients from a time period when unruptured aneurysms were not treated surgically. METHODS: Eighty-seven patients (79 had ruptured aneurysms clipped at start of follow-up) with 111 unruptured aneurysms as well as an additional 7 patients (2 with and 5 without unruptured aneurysms) who developed new aneurysms were followed from the 1950s to the 1970s until death or subarachnoid hemorrhage or until the last contact. Patients' cerebral arteries were examined later either with conventional (control) angiography (n=38) and/or, for those alive during 1996-1998, with 3-dimensional CT angiography (n=57). In addition, 10 patients were studied at neuropathological autopsy. RESULTS: Mean+/-SD duration of follow-up was 18.9+/-9.4 years (range, 1.2 to 38.9 years). Unruptured aneurysms increased in size >/=1 mm in 39 of the 87 patients (45%) and >/=3 mm in 31 (36%). New aneurysms were found in 15 of the 89 patients and in 5 without an unruptured aneurysm at the beginning of follow-up. Aneurysm rupture was associated very significantly (P:<0.001) with aneurysm growth during follow-up. Of several potential risk factors tested, only cigarette smoking (odds ratio [OR], 3.92; 95% CI, 1.29 to 11.93) and female sex (OR, 3.36; 95% CI, 1.11 to 10.22) were, after adjustment for age, significant (P:<0.05) independent risk factors for occurrence of aneurysm growth of >/=1 mm. Only cigarette smoking (OR, 3.48; 95% CI, 1.14 to 10.64; P:<0.05) was associated with growth of >/=3 mm. Age- and hypertension-adjusted risk factors for aneurysm formation were female sex (OR, 4.73; 95% CI, 1.16 to 19.38) and cigarette smoking (OR, 4.07; 95% CI, 1.09 to 15.15). CONCLUSIONS: Women and cigarette smokers are at increased risk for intracranial aneurysm formation and growth. Cigarette smoking in particular hastens aneurysm growth. Cessation of smoking is important for patients with unruptured aneurysms and possibly also for those with a prior subarachnoid hemorrhage.

Adolescent↗
PubMed2000

Risk factors for multiple intracranial aneurysms.

BACKGROUND AND PURPOSE: The presence of multiple intracranial aneurysms may be a sign of significant risk factors for aneurysm formation that differ from those factors that increase risk for aneurysm rupture. Only 2 studies concern independent risk factors for multiple aneurysms, and the results are in part controversial. This study was designed to identify independent risk factors for multiple intracranial aneurysms in patients with subarachnoid hemorrhage. METHODS: Of 266 patients with aneurysmal subarachnoid hemorrhage (139 men and 127 women, aged 15 to 60 years), 80 (30%) had multiple intracranial aneurysms. The prevalence of several health-related habits, previous diseases, and medications of these patients were compared by multiple logistic regression between those with single and those with multiple aneurysms. RESULTS: On the basis of multivariate statistics, only regular cigarette smoking at any time was a significant risk factor for the presence of multiple aneurysms. The odds ratio (OR) of smoking for multiple aneurysms was 2.10 (95% CI, 1.06 to 4.13) after adjustment for age and sex. After additional adjustment for hypertension, the risk was 2.06 (95% CI, 1. 04 to 4.07). Of other variables, only age (OR, 1.02 per year; 95% CI, 1.00 to 1.05; P=0.09) and female sex (OR, 1.60; 95% CI, 0.90 to 2. 85; P=0.11) showed a tendency to increase the risk for multiple aneurysms after adjustment for smoking. On the other hand, patients with hypertension had significantly (P=0.029) more aneurysms (1. 61+/-1.04) than did those without (1.37+/-0.68), although they did not more frequently have multiple aneurysms. CONCLUSIONS: Cigarette smoking and possibly also age and female sex seem to be risk factors for multiple intracranial aneurysms in patients of working age who have suffered a subarachnoid hemorrhage. Patients with hypertension seem to have more aneurysms than those without.

Adult↗
PubMed2000

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage.

OBJECT: The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH. METHODS: Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique. On the whole, mean plasma ET concentrations in patients with SAH (mean +/- standard error of mean, 2.1 +/- 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 +/- 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0-5, 3.1 +/- 0.8 pg/ml compared with 2.1 +/- 0.2 pg/ml; post-SAH Days 6-14, 2.5 +/- 0.4 pg/ml compared with 1.9 +/- 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0-5, 3.2 +/- 0.8 pg/ml; post-SAH Days 6-14, 2.7 +/- 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0-5, 3.1 +/- 0.8 pg/ml; post-SAH Days 6-14, 2.5 +/- 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 +/- 0.3 compared with 1.9 +/- 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others. CONCLUSIONS: Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.

Adult↗
PubMed2000

Natural history of unruptured intracranial aneurysms: probability of and risk factors for aneurysm rupture.

OBJECT: The authors conducted a study to investigate the long-term natural history of unruptured intracranial aneurysms and the predictive risk factors determining subsequent rupture in a patient population in which surgical selection of cases was not performed. METHODS: One hundred forty-two patients with 181 unruptured aneurysms were followed from the 1950s until death or the occurrence of subarachnoid hemorrhage or until the years 1997 to 1998. The annual and cumulative incidence of aneurysm rupture as well as several potential risk factors predictive of rupture were studied using lifetable analyses and Cox's proportional hazards regression models including time-dependent covariates. The median follow-up time was 19.7 years (range 0.8-38.9 years). During 2575 person-years of follow up, there were 33 first-time episodes of hemorrhage from previously unruptured aneurysms, for an average annual incidence of 1.3%. In 17 patients, hemorrhage led to death. The cumulative rate of bleeding was 10.5% at 10 years, 23% at 20 years, and 30.3% at 30 years after diagnosis. The diameter of the unruptured aneurysm (relative risk [RR] 1.11 per mm in diameter, 95% confidence interval [CI] 1-1.23, p = 0.05) and patient age at diagnosis inversely (RR 0.97 per year, 95% CI 0.93-1, p = 0.05) were significant independent predictors for a subsequent aneurysm rupture after adjustment for sex, hypertension, and aneurysm group. Active smoking status at the time of diagnosis was a significant risk factor for aneurysm rupture (RR 1.46, 95% CI 1.04-2.06, p = 0.033) after adjustment for size of the aneurysm, patient age, sex, presence of hypertension, and aneurysm group. Active smoking status as a time-dependent covariate was an even more significant risk factor for aneurysm rupture (adjusted RR 3.04, 95% CI 1.21-7.66, p = 0.02). CONCLUSIONS: Cigarette smoking, size of the unruptured intracranial aneurysm, and age, inversely, are important factors determining risk for subsequent aneurysm rupture. The authors conclude that such unruptured aneurysms should be surgically treated regardless of their size and of a patient's smoking status, especially in young and middle-aged adults, if this is technically possible and if the patient's concurrent diseases are not contraindications. Cessation of smoking may also be a good alternative to surgery in older patients with small-sized aneurysms.

Adolescent↗
PubMed2000

Natural history of unruptured intracranial aneurysms: probability and risk factors for aneurysm rupture.

OBJECT: The authors conducted a study to investigate the long-term natural history of unruptured intracranial aneurysms and the predictive risk factors determining subsequent rupture in a patient population in which surgical selection of cases was not performed. METHODS: We followed 142 patients with 181 unruptured aneurysms from the 1950s until death or the occurrence of subarachnoid hemorrhage, or until the years 1997 to 1998. The annual and cumulative incidence of aneurysm rupture as well as several potential risk factors predictive of rupture were studied using life-table analyses and the Cox's proportional hazards regression models including time-dependent covariates. The median follow-up time was 19.7 years (range 0.8-38.9 years). During 2575 person years of follow up, there were 33 first-time episodes of hemorrhage from a previously unruptured aneurysm, giving an average annual incidence of 1.3%. In seventeen of these cases, hemorrhages led to the patients' deaths. The cumulative rate of bleeding was 10.5% at 10 years, 23.0% at 20 years, and 30.3% at 30 years after diagnosis. The diameter of the unruptured aneurysm(relative risk [RR] 1.11 per mm in diameter, 95% confidence interval [CI] 1.00-1.23, p = 0.05) and patient age at diagnosis inversely (RR 0.97 per year, 95% CI 0.93-1.00, p = 0.05) were significant independent predictors for a subsequent aneurysm rupture after adjustment for sex, hypertension, and aneurysm group. Active smoking status at the time of diagnosis was a significant risk factor for aneurysm rupture (RR 1.46, 95% CI 1.04-2.06, p = 0.033) after adjustment for the size of the aneurysm, age, sex, presence of hypertension, and aneurysm group. Active smoking status asa time-dependent covariate was an even more significant risk factor for aneurysm rupture (adjusted RR 3.04, 95% CI 1.21-7.66, p = 0.020). CONCLUSIONS: Cigarette smoking, size of the unruptured intracranial aneurysm, and age, inversely, are important factors determining risk for subsequent aneurysm rupture. The authors conclude that such unruptured aneurysms should be surgically treated irrespective of their size and of patients' smoking status, especially in young and middle-aged adults, if this is technically possible and if the patient's concurrent diseases are not contraindications. Cessation of smoking may also be a good alternative to surgery in older patients with small-sized aneurysms.

Adolescent↗
PubMed1999

Effects of nonsteroidal anti-inflammatory drugs on hemostasis in patients with aneurysmal subarachnoid hemorrhage.

Platelet function is impaired by nonsteroidal anti-inflammatory drugs (NSAIDs) with prominent anti-inflammatory properties. Their safety in patients undergoing intracranial surgery is under debate. Patients with aneurysmal subarachnoid hemorrhage (SAH) were randomized to receive either ketoprofen, 100 mg, three times a day (ketoprofen group, n = 9) or a weak NSAID, acetaminophen, 1 g, three times a day (acetaminophen group, n = 9) starting immediately after the diagnosis of aneurysmal SAH. Treatment was continued for 3 days postoperatively. Test blood samples were taken before treatment and surgery as well as on the first, third, and fifth postoperative mornings. Maximal platelet aggregation induced by 6 microM of adenosine diphosphate decreased after administration of ketoprofen. Aggregation was lower (P < .05) in the ketoprofen group than in the acetaminophen group just before surgery and on the third postoperative day. In contrast, maximal platelet aggregation increased in the acetaminophen group on the third postoperative day as compared with the pretreatment platelet aggregation results (P < .05). One patient in the ketoprofen group developed a postoperative intracranial hematoma. Coagulation (prothrombin time [PT], activated partial thromboplastin time [APPT], fibrinogen concentration, and antithrombin III [AT III]) was comparable between the two groups. Ketoprofen but not acetaminophen impaired platelet function in patients with SAH. If ketoprofen is used before surgery on cerebral artery aneurysms, it may pose an additional risk factor for hemorrhage.

Acetaminophen↗
PubMed1999

Recent heavy drinking of alcohol and embolic stroke.

BACKGROUND AND PURPOSE: Epidemiological evidence suggests that heavy alcohol consumption increases the risk for ischemic stroke, whereas light-to-moderate alcohol intake decreases the risk, but the role of different drinking patterns has remained unclear. We investigated recent light, moderate, and heavy alcohol drinking and former heavy drinking as risk factors for acute ischemic brain infarction by etiological subtype of stroke. METHODS: We compared 212 consecutive patients aged between 16 and 60 years, who were completely evaluated for the etiology of their ischemic stroke, with 274 control subjects admitted to the emergency unit of the same hospital. ORs, as estimates of multivariate relative risks (RRs), and 95% CIs after adjustment for possible confounding variables were calculated by logistic regression. The ORs were adjusted for age, sex, body mass index, hypertension, diabetes, hyperlipemia, current smoking, and history of migraine. RESULTS: Recent heavy drinking but not former heavy drinking was an independent risk factor for stroke (RR 1.82, 95% CI 1.08 to 3.05). Consumption of 151 to 300 g and >300 g alcohol within the week preceding the onset of stroke significantly increased the risk for cardioembolic and cryptogenic stroke. Consumption of >40 g alcohol within the preceding 24 hours increased the risk for cardiogenic embolism to the brain among those who had a high-risk source (RR 4.75, 95% CI 1.23 to 18.4), the risk for tandem embolism among those who had prominent large-artery atherosclerosis (RR 7.68, 95% CI 1.82 to 32.3), and the risk for cryptogenic stroke (RR 3.84, 95% CI 1.69 to 8.71). Light drinking did not increase the risk for stroke. CONCLUSIONS: We conclude that acute drinking of intoxicating amounts of alcohol may trigger the onset of embolic stroke among subjects who have a source of thrombus in the heart or the large arteries.

Adolescent↗
PubMed1999

Alcohol intake and the risk of stroke.

Alcohol consumption has been reported to have both beneficial and harmful effects on the incidence of stroke. Different drinking habits may explain the diversity of the observations, but this is still unclear. We reviewed recent clinical and epidemiological studies to find out whether alcohol intake could increase or decrease the risk for stroke. By a systematic survey of literature published from 1989 to 1997, we identified 14 case-control studies addressing alcohol as a risk factor for haemorrhagic and ischaemic stroke morbidity and fulfilling the following criteria: the type of stroke was determined by a head computerised tomography scan on admission or at autopsy; and alcohol consumption was verified using structured questionnaires or by personal interviews. In some studies, adjustment for hypertension abolished the independent role of alcohol as a risk factor. On the other hand, the studies covering even recent alcohol intake showed in many cases that heavy drinking is an independent risk factor for most stroke subtypes, and that the risk may decrease relatively rapidly after the cessation of alcohol abuse. In some studies, regular light to moderate drinking seemed to be associated with a decreased risk for ischaemic stroke of atherothrombotic origin. In conclusion, recent heavy alcohol intake seems to be an independent risk factor for all major subtypes of stroke. The ultimate mechanisms leading to the increased risk are unclear. The significance of alcohol as a risk factor has been demonstrated in young subjects because they are more often heavy drinkers than the elderly. Several factors to explain the beneficial effect of light to moderate drinking have been proposed.

Alcohol Drinking↗
PubMed1998

Mechanisms of alcohol-related strokes.

Epidemiological investigations have shown a linear positive correlation between the risk of haemorrhagic stroke and level of alcohol consumption. Ischaemic stroke shows a weaker relationship, which is J-shaped, suggesting that regular light-to-moderate alcohol consumption may carry a decreased risk. Case reports and case-control studies indicate that heavy recent drinking, but not heavy former drinking, increases the risk for both types of stroke. Larger amounts of alcohol are needed to trigger aneurysmal subarachnoid haemorrhage than spontaneous intracerebral haemorrhage. The increased risk caused by recent heavy drinking may be partly due to elevated systolic blood pressure, but alcohol may also provoke cerebral arterial vasospasm, as observed in animal experiments. Alcohol-induced fluctuation in haemostatic and fibrinolytic factors has not been proved to precipitate alcohol-related strokes, but may contribute to both an increase and a decrease of the risk. Subtypes of ischaemic stroke associate differently with alcohol consumption. A recent series of patients with ischaemic brain infarction showed that of the victims having a high and medium risk for cardiogenic embolism, 50% and 45% were intoxicated, respectively. This suggests that cardiogenic embolism is a significant mechanism leading to ischaemic stroke during heavy drinking of alcohol.

Adult↗
PubMed1997

Lifestyle-associated risk factors for acute brain infarction among persons of working age.

BACKGROUND AND PURPOSE: This study was designed to identify whether cigarette smoking, alcohol drinking, obesity, and use of oral contraceptives are independent risk factors for brain infarction among persons of working age. METHODS: Health habits and previous diseases of 506 patients (366 men and 140 women aged 16 to 60 years) with acute first-ever symptomatic brain infarction were compared with those of 345 hospitalized control patients (219 men and 126 women) who did not differ from case subjects in respect to day of onset of symptoms or acuteness of disease onset. With the use of stepwise logistic regression, the variables for which the simultaneous risks of acute brain infarction were tested by sex were age, amount of alcohol consumed within 24 hours and 1 week before the illness, heavy drinking, smoking status, current smoking, cardiac disease, hypertension, diabetes, hyperlipemia, migraine, body mass index, and, in women, current use of oral contraceptives. RESULTS: Intake of > 40 g ethanol within the 24 hours preceding the onset of illness increased the risk for acute brain infarction both among men (P < .001) and women (P < .01) independently from other risk factors. Other significant independent risk factors for brain infarction among men were hypertension (P < .001), cardiac disease (P < .01), current smoking (P < .01), diabetes (P < .05), and history of migraine (P < .05) and among women, current use of oral contraceptives (P < .01) and current smoking (P < .05). CONCLUSIONS: Recent heavy drinking of alcohol, hypertension, cardiac disease, current smoking, diabetes, and history of migraine among men, and recent heavy drinking of alcohol, current use of oral contraceptives, and current smoking among women, seem to be independent risk factors for acute brain infarction.

Adolescent↗
PubMed1997

Hemostasis and fibrinolysis activation after subarachnoid hemorrhage.

The authors assessed hemostasis and fibrinolysis serially: on admission and on the 1st and 7th days after surgery for subarachnoid hemorrhage (SAH), examining the complications of aneurysm rupture and its surgical repair. Of 32 patients, 25 with SAH were compared with seven control patients who underwent surgery for an unruptured intracranial aneurysm. On admission, patients with SAH had higher thrombin-antithrombin III complex (TAT) levels (13.3 +/- 3.8 vs. 3.8 +/- 0.6 ng/ml, p = 0.01), fibrin degradation product, D-dimer levels (1310 +/- 220 vs. 556 +/- 89 ng/ml, p = 0.0001), and leukocyte counts (14.6 +/- 0.7 vs. 10.6 +/- 1.8 x 10(9) cells/L, p < 0.05) than did control patients. Postoperative D-dimer values (p = 0.007) remained higher in the SAH group. Furthermore, admission D-dimer levels were higher in the patients in poor clinical condition than in those in good condition (2017 +/- 377 vs. 934 +/- 208 ng/ml, p = 0.007), and D-dimer levels were associated with the outcome at 3 months after admission. Additionally, thrombin generation and fibrinolytic markers measured on admission were related to clinical grade, amount of subarachnoid blood seen on computerized tomography (CT) scanning, and patient fatality. Patients with hypodense lesions verified on follow-up CT scanning or with persistent neurological deficits at 3 months had higher prothrombin fragments 1 and 2, TAT, D-dimer, and plasminogen activator inhibitor-1 values on the 1st day postoperatively than did patients without such lesions. In short, in patients with SAH, activation of coagulation and fibrinolysis was strongly associated with clinical state, patient fatality, and outcome at 3 months, and postoperatively this activation correlated with the development of brain infarction.

Adult↗
PubMed1996

Prevalence of risk factors in spontaneous intracerebral hemorrhage and aneurysmal subarachnoid hemorrhage.

OBJECTIVE: To evaluate whether differences exist in the occurrence of modifiable risk factors between aneurysmal subarachnoid hemorrhage and spontaneous intracerebral hemorrhage, since these stroke subtypes have frequently been combined in epidemiological studies and labeled hemorrhagic stroke. DESIGN: Cross-sectional survey. SETTING: Helsinki University Central Hospital in Helsinki, Finland. PATIENTS: One hundred fifty-six consecutive patients with spontaneous intracerebral hemorrhage aged 16 to 60 years (96 males and 60 females) and 281 patients with aneurysmal subarachnoid hemorrhage (145 males and 136 females) who were admitted to an emergency department. MAIN OUTCOME MEASURES: Prevalence of several health habits, previous diseases, and medication of patients with spontaneous intracerebral hemorrhage were compared with that of patients with subarachnoid hemorrhage using multiple logistic regression. RESULTS: Hypertension (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.6-4.3), diabetes mellitus (OR, 26.4; 95% CI, 3.1-221.6), alcohol intake within the preceding week (for 1-150 g of alcohol: OR, 2.0; 95% CI, 1.1-3.6; for 151-300 g of alcohol: OR, 1.7; 95% CI, 0.8-3.8; and for > 300 g of alcohol: OR, 4.4; 95% CI, 2.1-9.1), and anticoagulant treatment (OR, 21.8; 95% CI, 2.3-207.3) were all significantly more common, but current cigarette smoking (OR, 0.3; 95% CI, 0.2-0.5) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage simultaneously after adjustment for sex, age, and body mass index. In males, hypertension (OR, 2.3; 95% CI, 1.1-4.5) and alcohol intake (for > 300 g/wk: OR, 5.8; 95% CI, 2.2-15.7) were more common, but current smoking (OR, 0.2; 95% CI, 0.1-0.4) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage after adjustment for age, body mass index, and diabetes mellitus. In females, hypertension (OR, 2.9; 95% CI, 1.4-5.8) and anticoagulant treatment (OR, 10.0; 95% CI, 1.0-100.2) were more common in patients with intracerebral hemorrhage after adjustment for age and body mass index. In univariate statistics, patients with intracerebral hemorrhage were also older, more often had previous symptoms of cerebral ischemia, and had higher values for body mass index and gamma-glutamyltransferase than did those with subarachnoid hemorrhage. CONCLUSIONS: Hypertension, diabetes mellitus, anticoagulant treatment, and amount of alcohol taken within 1 week seem more commonly to be associated with intracerebral hemorrhage than with subarachnoid hemorrhage, which is, however, associated more frequently with cigarette smoking.

Adolescent↗