ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background and Purpose—Psychological distress is common after stroke, but little is known about its etiologic importance, although the general public often ascribes stroke to the experience of stress. Therefore, we examined whether psychological distress leads to an increased risk of ischemic stroke and transient ischemic attack (TIA).Methods—The association between the 30-item General Health Questionnaire (GHQ), a measure of psychological distress, and the incidence of nonfatal and fatal ischemic stroke and TIA was measured by Cox regression modeling in a prospective observational study of 2201 men aged 45 to 59 years in phase II of the Caerphilly cohort. Hazard ratios comparing those with high (≥5) and normal GHQ scores were calculated with adjustment for age and other covariates.Results—Twenty-two percent of men suffered from psychological distress, indicated by a score of ≥5 on the GHQ. There were 130 incident strokes recorded, of which 17 were fatal and 113 nonfatal. The relative risk of incident ischemic stroke was 1.45 (95% CI, 0.98 to 2.14) for those who showed symptoms of psychological distress compared with those who did not. For fatal stroke the relative risk was 3.36 (95% CI, 1.29 to 8.71) and for nonfatal stroke 1.25 (95% CI, 0.82 to 1.92). The relative risk of TIA for the distressed group was 0.63 (95% CI, 0.26 to 1.53). The results were unchanged after adjustment for body mass index, systolic blood pressure, smoking, heavy drinking, social class, and marital status. However, additionally controlling for previously diagnosed ischemic heart disease, diabetes, respiratory disease, and retirement due to ill health attenuated the relative risks, but not markedly. For fatal strokes the relative risk decreased to 2.56 (95% CI, 0.97 to 6.75) when all confounding variables were included in the model. There was a graded association between degree of psychological distress and risk of fatal ischemic stroke.Conclusions—Psychological distress is a predictor of fatal ischemic stroke but not of nonfatal ischemic stroke or TIA. Further work examining the mechanisms of this association is required.

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background and Purpose—This study examined the relation between trait anger and incident stroke risk among participants without a history of stroke at the first follow-up examination of the Atherosclerosis Risk in Communities (ARIC) study.Methods—The study sample included 13 851 black and white men and women, aged 48 to 67 years, who completed the Spielberger Trait Anger Scale. Median follow-up time was 77.3 months.Results—In the full cohort, Cox proportional hazards regression analyses showed a modest increase in the risk for stroke among individuals with high trait anger, though the association did not remain statistically significant after multivariate adjustment. Participants ≤60 years of age who reported having high trait anger had a 2.82 (95% CI, 1.65 to 4.80) times greater risk for hemorrhagic and ischemic strokes combined (any) and a 2.93 (95% CI, 1.64 to 5.22) times greater risk for ischemic strokes alone than their counterparts who reported having low trait anger (hazard rate ratios adjusted for sex and race/ethnicity). Similarly, among participants with HDL cholesterol levels >47, the risk for any stroke was 2.86 (95% CI, 1.56 to 5.25) times greater for those who reported having high trait anger, whereas the risk for ischemic strokes alone was 2.98 (95% CI, 1.58 to 5.61) times greater (hazard rate ratios adjusted for age, sex, and race/ethnicity). These associations remained strong and statistically significant after further adjustment for several established biological and sociodemographic risk factors for stroke and were absent among older participants and those with lower HDL cholesterol values.Conclusions—Trait anger was associated with an increased risk for incident stroke in the ARIC study among younger participants and those with higher HDL cholesterol levels.

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background and Purpose—Silent brain infarcts are commonly seen on magnetic resonance imaging (MRI) both in patients with a first stroke and in healthy elderly persons. These infarcts seem associated with an increased risk of stroke. It is unclear whether risk factors for silent infarcts differ from those for symptomatic stroke. We investigated the prevalence of, and cardiovascular risk factors for, silent brain infarcts.Methods—The Rotterdam Scan Study is a population-based cohort study among 1077 participants 60 to 90 years of age. Participants underwent cerebral MRI. We assessed cardiovascular risk factors by interview and physical examination. Associations between risk factors and presence of infarcts were analyzed by logistic regression and adjusted for age, sex, and relevant confounders.Results—For 259 participants (24%) 1 or more infarcts on MRI were seen; 217 persons had only silent and 42 had symptomatic infarcts. The prevalence odds ratio (OR) of both silent and symptomatic infarcts increased with age by 8% per year (95% CI, 1.06 to 1.10 and 1.04 to 1.13, respectively). Silent infarcts were more frequent in women (age-adjusted OR, 1.4; 95% CI, 1.0 to 1.8). Hypertension was associated with silent infarcts (age- and sex-adjusted OR, 2.4; 95% CI, 1.7 to 3.3), but diabetes mellitus and smoking were not.Conclusions—Silent brain infarcts are 5 times as prevalent as symptomatic brain infarcts in the general population. Their prevalence increases with age and seems higher in women. Hypertension is associated with silent infarcts, but other cardiovascular risk factors are not.

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background and Purpose—Although white matter lesions (WMLs) on brain MRI in older persons are common, the mechanisms are unclear. Besides the associations with advanced age and high blood pressure (BP), variability in systolic BP (SBP) and the resulting changes in blood flow to the deep arteries of the brain may be contributing factors.Methods—Japanese-American men in Hawaii have participated in a long-term study of cardiovascular disease, including midlife BP measurements at 3 clinical examinations in the period from 1965 to 1974. In the period from 1991 to 1993, dementia status was added to the fourth examination, and a brain MRI was completed in a fifth examination, which was from 1994 to 1996, on a subset of 575 men, who averaged 82 years. WMLs and ventricular atrophy were determined as the upper fifth in a standardized semiquantitative measure. Excess SBP variability was defined as greater than average increases in BP measurements from up to 3 examinations over 6 years. Logistic regression was used for the association of this variability with WMLs and atrophy, controlling for age, apolipoprotein E4 status, dementia diagnosis, and history of stroke.Results—There were significant (2-fold) increased risks for WMLs among those with moderate and high SBP variability (third and fifth quintiles compared with the lowest quintile). Those in the highest SBP variability category (the fifth quintile) also had significantly more atrophy.Conclusions—These SBP variability–MRI relationships suggest that variation in SBP in midlife may be a contributing factor to the development of WMLs and ventricular atrophy in late life.

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background and Purpose—Recent evidence suggests that atherosclerosis is an inflammatory condition. Serum levels of inflammatory markers may serve as measures of the severity of atherosclerosis and risk of stroke. We sought to determine whether tumor necrosis factor-&agr; (TNF-&agr;) and TNF receptor levels are associated with carotid plaque thickness.Methods—The Northern Manhattan Stroke Study is a community-based study of stroke risk factors. For this cross-sectional analysis, inflammatory marker levels, including TNF-&agr; and TNF receptors 1 and 2, were measured by immunoassay in stroke-free community subjects undergoing carotid duplex Doppler ultrasound. Maximal carotid plaque thickness (MCPT) was measured for each subject. Analyses were stratified by age <70 and ≥70 years. Simple and multiple linear regression analyses were used to calculate the association between marker levels and MCPT. Multiple logistic regression was used to calculate odds ratios and 95% CIs for the association of inflammatory markers with MCPT ≥1.5 mm (>75th percentile), after adjustment for demographic and potential medical confounding factors.Results—The mean age of the 279 subjects was 67.6±8.5 years; 49% were men; 63% were Hispanic, 17% black, and 17% white. Mean values for TNF-&agr; and its receptors were as follows: TNF-&agr;, 1.88±3.97 ng/mL; TNF receptor 1, 2.21±0.99 ng/mL; and TNF receptor 2, 4.85±2.23 ng/mL. Mean MCPT was elevated in those in the highest quartiles compared with lowest quartiles of TNF receptor 1 and 2 (1.24 versus 0.79 mm and 1.23 versus 0.80 mm, respectively). Among those aged <70 years, TNF receptor 1 and 2 were associated with an increase in MCPT (mean difference=0.36 mm,P=0.01 for TNF receptor 1 and mean difference=0.10 mm,P=0.04 for TNF receptor 2). After adjustment for sex, race-ethnicity, hypertension, diabetes mellitus, LDL cholesterol, smoking, and body mass index, associations remained (mean difference=0.36 mm,P=0.001 for TNF receptor 1 and mean difference=0.09 mm,P=0.051 for TNF receptor 2). There was no association for TNF receptors in those aged ≥70 years old and no association for TNF-&agr; in either age group. Among those aged <70 years, each unit increase in TNF receptor level increased the odds of the participant’s having MCPT ≥1.5 mm (adjusted odds ratio=4.7; 95% CI, 1.7 to 15.4 for TNF receptor 1; odds ratio=1.9; 95% CI, 1.3 to 2.9 for TNF receptor 2).Conclusions—Relative elevation in TNF receptor levels, but not TNF-&agr;, is associated with carotid atherosclerosis among individuals aged <70 years in this multiethnic, urban population. Chronic subclinical infection or inflammation may account for this association, and modification of these inflammatory pathways may provide a novel approach to stroke prevention.

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background and Purpose—There are limited prospective cohort studies of the well-known association between stroke events and serum lipids for the Taiwanese population, in whom stroke is the second most common cause of death.Methods—This report describes the effect of dyslipidemia on the risk of stroke in a community-based cohort consisting of 3602 adults aged ≥35 years, established in 1990 in the Chin-Shan community in Taipei County, Taiwan.Results—As of the end of 1998, 97 stroke incidence cases were identified from medical records and death certificates (53 in men and 44 in women). The female-to-male stroke event rates increased from 0.42 in the youngest group (aged 35 to 44 years) to 1.38 in the oldest (aged ≥75 years). Multiple Cox proportional hazard regression models controlling for age and sex revealed that individuals with serum apolipoprotein A-I (apoA-I) at the highest quartile were more likely to have a stroke event than those at the lowest quartile level (relative risk [RR]=2.02,Pfor trend=0.010). The corresponding risk of stroke predicted by apolipoprotein B (apoB) was also significant (RR=1.88,Pfor trend=0.020). After adjustment for age, sex, hypertension, and diabetes status, the interaction between hypertension and apoA-I level remained significant in predicting stroke events in men but not in women (RR=1.71,P=0.033 in men; RR=2.29,P=0.071 in women).Conclusions—We conclude that apoA-I but not apoB levels may serve as an effect modifier of hypertension for the risk of stroke events.

ISSN:0039-2499    

出版商:OVID    

年代:2002

数据来源: OVID