CORK Bibliography: Substance Use and Sroke

23 citations. January 2009 to present

Prepared: June 2011

Ali WM; Zubaid M; Al-Motarreb A; Singh R; Al-Shereiqi SZ; Shehab A et al. Association of khat chewing with increased risk of stroke and death in patients presenting with acute coronary syndrome. Mayo Clinic Proceedings 85(11): 974-980, 2010. (49 refs.)

OBJECTIVE To evaluate the prevalence and significance of khat chewing in patients with acute coronary syndrome (ACS). PATIENTS AND METHODS: From January 29, 2007, through July 29, 2007, 8176 consecutive patients presenting with ACS were en roiled In a prospective, multicenter study from 6 adjacent Middle Eastern countries. RESULTS: Of the 8176 study patients, 7242 (88 6%) were non-khat chewers, and 934 (11 4%) were khat chewers, mainly of Yemeni origin Khat chewers were older (57 vs 56 years, P= 01) and more likely to be men (85 7% vs 74 5%) compared with non khat chewers Non khat chewers were more likely to have diabetes mellitus, hypertension, dyslipldemia, obesity, and prior history of coronary artery disease and revascularization. Cigarette smoking was more prevalent in khat chewers, and they were more likely to present greater than 12 hours after onset of symptoms compared with non-khat chewers. At admission, khat chewers had higher heart rate, Killlp class, and Global Registry of Acute Coronary Events risk scores. Khat chewers had a significantly higher risk of cardiogenic shock, stroke, and mortality After adjustment of baseline variables, khat chewing was an independent risk factor for in hospital mortality (odds ratio, 1 9, 95% confidence interval, 1 3-2 7, P< 001) and stroke (odds ratio, 2 7, 95% confidence interval, 135 9, P= 01). CONCLUSION: in this large cohort of patients with ACS, khat chewing was prevalent and was associated with increased risk of stroke and death in the context of increasing global migration, a greater awareness of potential widespread practices is essential

Boffetta P; Straif K. Use of smokeless tobacco and risk of myocardial infarction and stroke: Systematic review with meta-analysis. British Medical Journal 339(article b3060), 2009. (28 refs.)

Objective: To assess whether people who use smokeless tobacco products are at increased risk of myocardial infarction and stroke. Design: Meta-analysis of observational studies from Sweden and the United States. Data sources Electronic databases and reference lists. Data extraction: Quantitative estimates of the association between use of smokeless tobacco products and risk of myocardial infarction and stroke among never smokers. Review methods Both authors independently abstracted risk estimates and study characteristics. Summary relative risks were estimated on the basis of random effects models. Results 11 studies, mainly in men, were included. Eight risk estimates were available for fatal myocardial infarction: the relative risk for ever use of smokeless tobacco products was 1.13 (95% confidence 1.06 to 1.21) and the excess risk was restricted to current users. The relative risk of fatal stroke, on the basis of five risk estimates, was 1.40 (1.28 to 1.54). The studies from both the United States and Sweden showed an increased risk of death from myocardial infarction and stroke. The inclusion of non-fatal myocardial infarction and non-fatal stroke lowered the summary risk estimates. Data on dose-response were limited but did not suggest a strong relation between risk of dying from either disease and frequency or duration of use of smokeless tobacco products. Conclusion: An association was detected between use of smokeless tobacco products and risk of fatal myocardial infarction and stroke, which does not seem to be explained by chance.

Christerson S; Stromberg B. Childhood stroke in Sweden I: incidence, symptoms, risk factors and short-term outcome. Acta Paediatrica 99(11): 1641-1649, 2010. (31 refs.)

Aim: To evaluate the incidence, presenting symptoms, diagnostic delay, risk factors and short-term outcome of childhood stroke in a population-based cohort of Swedish children. Methods: We retrospectively reviewed the records of children experiencing their first stroke during a 7-year period in Uppsala-Orebro Health Care Region covering one-fifth of the Swedish population. Arterial ischaemic stroke (AIS), cerebral sinus venous stroke and nontraumatic haemorrhagic stroke (HS) in children aged > 28 days and < 18 years were included. Results: We identified 51 children (23 boys and 28 girls; median age 13). The average annual incidence of stroke was 1.8 per 100,000 children. AIS was found in 51% of the children, HS in 41% and cerebral sinus venous stroke in 8%. One-third of the children had underlying diseases, and one-third had vascular malformations. Six girls used oral contraceptives, three of these were smokers and two had iron deficiency anaemia. Two children died in the acute stage (4%), and 40/49 (82%) had some neurological dysfunction at discharge. Conclusion: The incidence of childhood stroke was 1.8 per 100,000 children and year, and the primary mortality was 4%. Risk factors of importance were oral contraceptives, smoking and anaemia in combinations.

Djousse L; Himali JJ; Beiser A; Kelly-Hayes M; Wolf PA. Apolipoprotein E, alcohol consumption, and risk of ischemic stroke: The Framingham Heart Study revisited. Journal of Stroke & Cerebrovascular Diseases 18(5): 384-388, 2009. (35 refs.)

Background: Data on the association between alcohol consumption and ischemic stroke have been inconsistent. It is not known whether allele epsilon(4) of the apolipoprotein E (apoE) gene modifies the alcohol-stroke association. We sought to examine whether epsilon(4) allele of the apoE gene influences the association between alcohol consumption and ischemic stroke or high-density lipoprotein (HDL) cholesterol. Methods: We examined a cohort of 7676 person-observations of the Framingham Heart Study. Incident stroke was ascertained by standardized methods. We used Cox proportional hazard model to estimate hazard ratios of ischemic stroke. Results: The average age at baseline was 63 years and 55% of the participants were women. During a mean follow-up of 7.4 years, 222 new cases of ischemic stroke occurred (56 embolic and 166 atherothrombotic events). Comparing current drinkers with nondrinkers, multivariable adjusted hazard ratio (95% confidence interval) for ischemic stroke was 0.50 (0.24-1.07) in the absence Of epsilon(4) allele and 0.70 (0.24-2.05) in the presence Of epsilon(4) allele (P for interaction = .64) for those younger than 65 years. Similarly, we did not observe a statistically significant interaction between epsilon(4) allele and alcohol consumption on the risk of stroke among people aged 65 years and older (P for interaction = .17). Alcohol consumption was positively associated with HDL cholesterol independent of epsilon(4) allele and age. Conclusions: Our data do not provide evidence for an interaction between epsilon(4) allele and alcohol consumption on the risk of ischemic stroke in this population. Furthermore, apoE polymorphism did not influence the alcohol-HDL relation.

Galimanis A; Mono ML; Arnold M; Nedeltchev K; Mattle HP. Lifestyle and stroke risk: A review. (review). Current Opinion in Neurology 22(1): 60-68, 2009. (82 refs.)

Purpose of review: In recent years, many epidemiological studies have given new insights into old and new lifestyle factors that influence the risk of cerebrovascular events. In this review, we refer especially those important to the most important articles to highlight recent advances, for stroke prevention. Recent findings: This review focuses on the most recent studies that show the association of environmental factors, nutrition, alcohol, tobacco, education, lifestyle and behavior with the risk of vascular disease, including ischemic stroke and cerebral hemorrhage. The link between air pollution and stroke risk has become evident. Low education levels and depression are established as risk factors. This is also true for heavy alcohol consumption, although moderate drinking may be protective. Active and passive smoking are independent risk factors, and a smoking ban in public places has already reduced cardiovascular events in the short term. Physical activity reduces stroke risk; overweight increases it. However, clinical trials to assess the effect of weight reduction on stroke risk are still lacking. Fruits, vegetables, fish, fibers, low-fat dairy products, potassium and low sodium consumption are known and recommended to reduce cardiovascular risk. Data on omega 3 fatty acid, folic acid and B vitamins are inconsistent, and antioxidants are not recommended. Summary: Stroke can be substantially reduced by an active lifestyle, cessation of smoking and a healthy diet. Both public and professional education should promote the awareness that a healthy lifestyle and nutrition have the potential to reduce the burden of stroke.

Ho EL; Josephson SA; Lee HS; Smith WS. Cerebrovascular complications of methamphetamine abuse. Neurocritical Care 10(3): 295-305, 2009. (44 refs.)

Methamphetamine is a stimulant widely abused in the United States. The objective of this study was to demonstrate an association of methamphetamine use and ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage and to further reveal the underlying vascular pathology using neuroimaging and pathology. This was a retrospective study based on medical chart review of admissions to the neurovascular service of a tertiary care medical center from January 2003 to July 2007. Cases included patients who used methamphetamine as documented by history or urine toxicology screening. From 1,574 records, 30 cases were identified. The mean age of patients was 43 years and the discharge diagnoses included ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. All subarachnoid hemorrhages were aneurysmal with the majority of the aneurysms located in the anterior circulation. The majority of strokes were located in the anterior circulation. In many cases, radiologic imaging confirmed arterial stenoses in the vascular distribution of the stroke. One patient who presented with ischemic stroke had severe atherosclerosis of bilateral common, internal, and external carotid arteries. On pathology, there was no evidence of inflammation or necrosis to suggest vasculitis as a possible etiology. Methamphetamine use is associated with ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage, especially among young patients. We showed no evidence that the ischemic stroke associated with methamphetamine use is due to an inflammatory etiology but may be due to a process of accelerated atherosclerosis.

Hsu WY; Chiu NY; Liao YC. Rhabdomyolysis and brain ischemic stroke in a heroin-dependent male under methadone maintenance therapy. Acta Psychiatrica Scandinavica 120(1): 76-79, 2009. (25 refs.)

Objective: There are several complications associated with heroin abuse, some of which are life-threatening. Methadone may aggravate this problem. Method: A clinical case description. Results: A 33-year-old man presented with rhabdomyolysis and cerebral ischemic stroke after intravenous heroin. He had used heroin since age 20, and had used 150 mg methadone daily for 6 months. He was found unconsciousness at home and was sent to our hospital. In the ER, his opiate level was 4497 ng/ml. In the ICU, we found rhabdomyolysis, acute renal failure and acute respiratory failure. After transfer to an internal ward, we noted aphasia and weakness of his left limbs. After MRI, we found cerebral ischemic infarction. Conclusion: Those using methadone and heroin simultaneously may increase risk of rhabdomyolysis and ischemic stroke. Patients under methadone maintenance therapy should be warned regarding these serious adverse events. Hypotheses of heroin-related rhabdomyolysis and stroke in heroin abusers are discussed. Note: There is commentary in the same issue by Somala (pages 76-79).

Jarraya B; Brugieres P; Tani N; Hodel J; Grandjacques B; Fenelon G et al. Disruption of cigarette smoking addiction after posterior cingulate damage. Journal of Neurosurgery 113(6): 1219-1221, 2010. (12 refs.)

The authors describe the case of a 35-year-old woman with a history of an addiction to cigarette smoking who presented with an intracerebral hemorrhage from a ruptured arteriovenous malformation. The patient reported an immediate and complete disruption of her addiction to cigarette smoking following her stroke. Structural MR imaging revealed a lesion of the posterior cingulate cortex. Neuropsychological tests showed intact cognitive functioning. This observation suggests that the posterior cingulate cortex may play a role in the addiction to cigarette smoking.

Jochum T; Reinhard M; Boettger MK; Piater M; Bar KJ. Impaired cerebral autoregulation during acute alcohol withdrawal. Drug and Alcohol Dependence 110: 240-246 110(3): 240-246, 2010. (67 refs.)

Heavy alcohol consumption increases the risk for all major types of stroke and is associated with autonomic dysfunction during alcohol withdrawal syndrome (AWS). Cerebral autoregulation is the mechanism by which cerebral perfusion is maintained stable, representing an intrinsic protective system of the cerebral circulation. Here, we aimed to analyze the influence of acute AWS on cerebral hemodynamics in alcohol-dependent patients. We investigated 20 men in the unmedicated acute state of AWS and repeated the investigation 24h after initiation of clomethiazole treatment. Dynamic cerebral autoregulation (dCA) was assessed by the correlation coefficient index and transfer function analysis (phase and gain) from oscillations of arterial blood pressure and cerebral blood flow velocity (CBFV). The vasomotor reserve (VMR) was measured by the CO2-reactivity test. In addition, we assessed autonomic modulation by means of heart rate variability and baroreflex sensitivity. We observed impaired dynamic autoregulation as shown by a multivariate analysis of variance (p < 0.038) including all parameters of dCA. Similar results were found for VMR at admission (p < 0.05). Pair-wise comparison between baseline and treatment with clomethiazole revealed a significant improvement for the systolic correlation coefficient index (Sx; p < 0.001). Furthermore, we found a strong association of autonomic dysfunction and impaired autoregulation indicated by a correlation between the LF/HF ratio and Sx (p < 0.001). In conclusion, cerebral autoregulation and VMR are disturbed during acute AWS. Influences of autonomic dysbalance and mental state during withdrawal are suggested. The finding of an affected autoregulation during acute withdrawal might indicate an increased risk for cerebro-vascular disease.

Johnson JYM; Rowe BH; Villeneuve PJ. Ecological analysis of long-term exposure to ambient air pollution and the incidence of stroke in Edmonton, Alberta, Canada26. Stroke 41(7): 1319-1325, 2010. (26 refs.)

Background and Purpose: Long-term air pollution effects on stroke incidence have not been examined extensively. We investigated the associations between ambient pollution and the incidence of stroke, as well as stroke subtypes, in a northern Canadian city surrounded by energy-sector pollution sources. Methods-Stroke data from an administrative database from 2003 through 2007 were used to estimate annual incidence rates within small geographic regions within Edmonton, Canada. Air pollution levels for each region were estimated from continuous fixed-site monitoring stations in and around Edmonton. We fit models estimating stroke risk in relation to pollution levels; risks were adjusted for age, sex, income, social deprivation, and other factors. Results-Between 2003 and 2007, the average 5-year concentration of NO2 and CO was positively associated with the incidence of stroke, particularly for hemorrhagic and nonhemorrhagic stroke subtypes (NO2: hemorrhagic stroke relative risk=1.46; 95% CI, 1.19-1.80; nonhemorrhagic stroke relative risk=1.36; 95% CI, 1.19-1.56). However, these estimates of risk diminished after controlling for the ecological measures of income and deprivation. Adjustment for ecologically derived indices of smoking, hypertension, and body mass index did not alter the estimates of risk in any meaningful way. Conclusions-Although long-term NO2 and CO levels were positively associated with a higher incidence of stroke in the entire study area, the risk estimates were strongly attenuated by household income levels. Further research that incorporates individual-level risk factor data would improve our understanding of the relation of longer-term exposures to ambient air pollution and stroke outcomes.

Johnston SC; Mendis S; Mathers CD. Global variation in stroke burden and mortality: estimates from monitoring, surveillance, and modelling. Lancet Neurology 8(4): 345-354, 2009. (55 refs.)

Background Recent improvements in the monitoring and modelling of stroke have led to more reliable estimates of stroke mortality and burden worldwide. However, little is known about the global distribution of stroke and its relations to the prevalence of cardiovascular disease risk factors and sociodemographic and economic characteristics. Methods National estimates of stroke mortality and burden (measured in disability-adjusted life years [DALYs]) were calculated from monitoring vital statistics, a systematic review of studies that report disease surveillance, and modelling as part of the WHO Global Burden of Disease programme. Similar methods were used to generate standardised measures of the national prevalence of cardiovascular risk factors. Risk factors other than diabetes and disease burden estimates were age-adjusted and sex-adjusted to the WHO standard population. Findings There was a ten-fold difference in rates of stroke mortality and DALY loss between the most-affected and the least-affected countries. Rates of stroke mortality and DALY loss were highest in eastern Europe, north Asia, central Africa, and the south Pacific. National per capita income was the strongest predictor of mortality and DALY loss rates (p<0.0001) even after adjustment for cardiovascular risk factors (p<0.0001). Prevalences of cardiovascular risk factors measured at a national level were generally poor predictors of national stroke mortality rates and burden, although raised mean systolic blood pressure (p=0.028) and low body-mass index (p=0.017) predicted stroke mortality, and greater prevalence of smoking predicted both stroke mortality (p=0.041) and DALY-loss rates (p=0.034). Interpretation Rates of stroke mortality and burden vary greatly among countries, but low-income countries are the most affected. Current measures of the prevalence of cardiovascular risk factors at the population level poorly predict overall stroke mortality and burden and do not explain the greater burden in low-income countries.

Logroscino G; Kurth T. Ischemic stroke: Coffee may pull the trigger. (editorial). Neurology 75(18): 1576-1577, 2010. (13 refs.)

In this issue of Neurology, Mostofsky and colleagues 5 challenge the idea of coffee being safe. They test the hypothesis that coffee intake is associated with a transient increase in risk of ischemic stroke. In a multicenter case-crossover study, they studied 390 subjects after an acute ischemic stroke event. Each subject's coffee consumption in the hour before stroke symptoms was compared with their usual consumption over the prior year. Coffee consumption was associated with a 2-fold increase in risk of ischemic stroke in the subsequent hour when compared to the risk during periods without coffee consumption. The increased risk returned to baseline within a 2-hour window, strengthening the plausibility of a causal relationship. This study provides new information that may be useful in stroke prevention and is concordant with what we know of the physiologic effects of coffee. Even if coffee contains other substances that may be responsible for the observed effect, caffeine is the most likely candidate for pulling the trigger. The peak plasma concentration of caffeine is usually less than 2 hours following oral intake and has several systemic effects including rapidly increasing epinephrine release, blood pressure, and insulin sensitivity. Caffeine has both systemic and cerebral vasoconstrictive effects. Volunteers taking oral caffeine (250-500 mg) demonstrate a rapid reduction in cerebral perfusion within 30 to 90 minutes. Partial tolerance of the effects of coffee on the cardiovascular system develops after only 1 week. Mostofsky et al. found attenuation of the acute risk of ischemic stroke following consumption of caffeinated coffee among those reporting higher levels of habitual coffee consumption similar to previously reported data on risk of myocardial infarction.9 Thus, coffee may increase the risk of stroke in na�ve coffee drinkers but not in long-term users

Lopez-Garcia E; Rodriguez-Artalejo F; Rexrode KM; Logroscino G; Hu FB; van Dam RM. Coffee consumption and risk of stroke in women. Circulation 119(8): 1116-1123, 2009. (38 refs.)

Background: Data on the association between coffee consumption and risk of stroke are sparse. We assessed the association between coffee consumption and the risk of stroke over 24 years of follow-up in women. Methods and Results: We analyzed data from a prospective cohort of 83 076 women in the Nurses' Health Study without history of stroke, coronary heart disease, diabetes, or cancer at baseline. Coffee consumption was assessed first in 1980 and then repeatedly every 2 to 4 years, with follow-up through 2004. We documented 2280 strokes, of which 426 were hemorrhagic, 1224 were ischemic, and 630 were undetermined. In multivariable Cox regression models with adjustment for age, smoking status, body mass index, physical activity, alcohol intake, menopausal status, hormone replacement therapy, aspirin use, and dietary factors, the relative risks (RRs) of stroke across categories of coffee consumption (<1 cup per month, 1 per month to 4 per week, 5 to 7 per week, 2 to 3 per day, and >= 4 per day) were 1, 0.98 (95% CI, 0.84 to 1.15), 0.88 (95% CI, 0.77 to 1.02), 0.81 (95% CI, 0.70 to 0.95), and 0.80 (95% CI, 0.64 to 0.98) (P for trend=0.003). After further adjustment for high blood pressure, hypercholesterolemia, and type 2 diabetes, the inverse association remained significant. The association was stronger among never and past smokers (RR for >= 4 cups a day versus <1 cup a month, 0.57; 95% CI, 0.39 to 0.84) than among current smokers (RR for >= 4 cups a day versus <1 cup a month, 0.97; 95% CI, 0.63 to 1.48). Other drinks containing caffeine such as tea and caffeinated soft drinks were not associated with stroke. Decaffeinated coffee was associated with a trend toward lower risk of stroke after adjustment for caffeinated coffee consumption (RR for >= 2 cups a day versus <1 cup a month, 0.89; 95% CI, 0.73 to 1.08; P for trend=0.05). Conclusions: Long-term coffee consumption was not associated with an increased risk of stroke in women. In contrast, our data suggest that coffee consumption may modestly reduce risk of stroke.

Mazzone P; Tierney W; Hossain M; Puvenna V; Janigro D; Cucullo L. Pathophysiological impact of cigarette smoke exposure on the cerebrovascular system with a focus on the blood-brain barrier: Expanding the awareness of smoking toxicity in an underappreciated area. (review). International Journal of Environmental Research and Public Health 7(12): 4111-4126, 2010. (98 refs.)

Recent evidence has indicated that active and passive cigarette smoking are associated, in a dose-dependent manner, with dysfunction of normal endothelial physiology. Tobacco smoke (TS) may predispose individuals to atherogenic and thrombotic problems, significantly increasing the risk for ischemic manifestations such as acute coronary syndrome and stroke. Despite the strong evidence for an association between smoking and vascular impairment, the impact of TS exposure on the blood-brain barrier (BBB) has only been marginally addressed. This is a major problem given that the BBB is crucial in the maintenance of brain homeostasis. Recent data have also shown that chronic smokers have a higher incidence of small vessel ischemic disease (SVID), a pathological condition characterized by leaky brain microvessels and loss of BBB integrity. In the brain TS increases the risk of silent cerebral infarction (SCI) and stroke owing to the pro-coagulant and atherogenic effects of smoking. In this article we provide a detailed review and analysis of current knowledge of the pathophysiology of tobacco smoke toxicity at the cerebrovascular levels. We also discuss the potential toxicity of recently marketed "potential-reduced exposure products".

Mostofsky E; Schlaug G; Mukamal KJ; Rosamond WD; Mittleman MA. Coffee and acute ischemic stroke onset: The Stroke Onset Study. Neurology 75(18): 1583-1588, 2010. (26 refs.)

Objective: Prior research suggests an acutely elevated risk of myocardial infarction and sudden cardiac death in the hour after coffee intake. However, the risk of ischemic stroke associated with transient exposure to coffee remains unclear. We hypothesized that caffeine intake is associated with a transiently increased risk of ischemic stroke. Methods: In this multicenter case-crossover study, we interviewed 390 subjects (209 men, 181 women) between January 2001 and November 2006 a median of 3 days after acute ischemic stroke. Each subject's coffee consumption in the hour before stroke symptoms was compared with his or her usual frequency of consumption in the prior year. Results: Of the 390 subjects, 304 (78%) drank coffee in the prior year, 232 within 24 hours and 35 within 1 hour of stroke onset. The relative risk (RR) of stroke in the hour after consuming coffee was 2.0 (95% confidence interval [CI], 1.4-2.8; p < 0.001). There was no apparent increase in risk in the hour following consumption of caffeinated tea (RR = 0.9, 95% CI 0.4-2.0; p = 0.85) or cola (RR = 1.0, 95% CI 0.4-2.4; p = 0.95). The association between ischemic stroke in the hour after coffee consumption was only apparent among those consuming a cup per day but not for patients who consumed coffee more regularly (p for trend = 0.002). Relative risks remained similar when the sample was restricted to those who were not simultaneously exposed to other potential triggers and the results remained significant after stratifying by time of day. Conclusion: Coffee consumption transiently increases the risk of ischemic stroke onset, particularly among infrequent drinkers.

Nilsson PM; Cederholm J; Eeg-Olofsson K; Eliasson B; Zethelius B; Fagard R et al. Smoking as an independent risk factor for myocardial infarction or stroke in type 2 diabetes: A report from the Swedish National Diabetes Register. European Journal of Cardiovascular Prevention & Rehabilitation 16(4): 506-512, 2009. (36 refs.)

Background Few earlier studies have analysed smoking as a risk factor for myocardial infarction NO or stroke in type 2 diabetic patients. Design and methods A longitudinal study involved 13087 female and male patients with type 2 diabetes from the Swedish National Diabetes Register with no previous M I or stroke at baseline, aged 30-74 years, and with data available for all analysed variables, followed up for mean 5.7 years. Results Adjusted hazard ratios (HRs) for smoking and first-incident fatal/nonfatal MI, stroke and total mortality were 1.7 [95% confidence interval (CI): 1.4-2.0; P<0.001], 1.3 (95% CI: 1.1-1.6; P=0.006) and 1.8 (95% CI: 1.5-2.2; P<0.001), respectively, by Cox regression analysis, adjusted for age, sex, diabetes duration, hypoglycaemic treatment, haemoglobin A(1c), blood pressure, body mass index, microalbuminuria, antihypertensive and lipid-lowering drugs. Adjusted HR was higher for fatal MI, 2.1 (95% CI: 1.7-2.7; P<0.001), than for nonfatal MI, 1.4 (95% CI: 1.2-1.7; P<0.001). The highest HRs were observed in more frequently smoking (22%), middle-aged patients (age <60 years) for fatal/nonfatal MI, 2.3 (95% CI: 1.8-3.1; P<0.001) and for total mortality, 2.5 (95% CI: 1.6-3.8, P<0.001), whereas lower HRs were observed in older and less smoking patients. With predicted cessation of smoking in patients aged below 60 years, 24% (95% CI: 15-33%) of cases of fatal/nonfatal MI and 24% (11-37%) of cases of total mortality may have been prevented. Conclusion The risk for MI and total mortality associated with smoking is high in type 2 diabetes, especially in more frequently smoking, middle-aged patients, and was higher for MI than for stroke, and also higher for fatal than for nonfatal events. Smoking cessation would strongly affect risk reduction.

Patra J; Taylor B; Irving H; Roerecke M; Baliunas D; Mohapatra S et al. Alcohol consumption and the risk of morbidity and mortality for different stroke types: A systematic review and meta-analysis. BMC Public Health 10: article 258, 2010. (69 refs.)

Background: Observational studies have suggested a complex relationship between alcohol consumption and stroke, dependent on sex, type of stroke and outcome (morbidity vs. mortality). We undertook a systematic review and a meta-analysis of studies assessing the association between levels of average alcohol consumption and relative risks of ischemic and hemorrhagic strokes separately by sex and outcome. This meta-analysis is the first to explicitly separate morbidity and mortality of alcohol-attributable stroke and thus has implications for public health and prevention. Methods: Using Medical Subject Headings (alcohol drinking, ethanol, cerebrovascular accident, cerebrovascular disorders, and intracranial embolism and thrombosis and the key word stroke), a literature search of MEDLINE, EMBASE, CINAHL, CABS, WHOlist, SIGLE, ETOH, and Web of Science databases between 1980 to June 2009 was performed followed by manual searches of bibliographies of key retrieved articles. From twenty-six observational studies (cohort or case-control) with ischemic or hemorrhagic strokes the relative risk or odds ratios or hazard ratios of stroke associated with alcohol consumption were reported; alcohol consumption was quantified; and life time abstention (manually estimated where data for current abstainers were given) was used as the reference group. Two reviewers independently extracted the information on study design, participant characteristics, level of alcohol consumption, stroke outcome, control for potential confounding factors, risk estimates and key criteria of study quality using a standardized protocol. Results: The dose-response relationship for hemorrhagic stroke had monotonically increasing risk for increasing consumption, whereas ischemic stroke showed a curvilinear relationship, with a protective effect of alcohol for low to moderate consumption, and increased risk for higher exposure. For more than 3 drinks on average/day, in general women had higher risks than men, and the risks for mortality were higher compared to the risks for morbidity. Conclusions: These results indicate that heavy alcohol consumption increases the relative risk of any stroke while light or moderate alcohol consumption may be protective against ischemic stroke. Preventive measures that should be initiated are discussed.

Putaala J; Curtze S; Hiltunen S; Tolppanen H; Kaste M; Tatlisumak T. Causes of death and predictors of 5-year mortality in young adults after first-ever ischemic stroke: The Helsinki young stroke registry. Stroke 40(8): 2698-2703, 2009. (26 refs.)

Background and Purpose: Data on mortality and its prognostic factors after an acute ischemic stroke in young adults are scarce and based on relatively small heterogeneous patient series. Methods: We analyzed 5-year mortality data of all consecutive patients aged 15 to 49 with first-ever ischemic stroke treated at the Department of Neurology, Helsinki University Central Hospital, from January 1994 to September 2003. We followed up the patients using data from the mortality registry of Statistics Finland. We used life table analyses for calculating mortality risks. Kaplan-Meier method allowed comparisons of survival between clinical subgroups. We used the Cox proportional hazard model for identifying predictors of mortality. Stroke severity was measured using the National Institutes of Health Stroke Scale and the Glasgow Coma Scale. Results: Among the 731 patients (mean age, 41.5 +/- 7.4 years; 62.8% males) followed, 78 died. Cumulative mortality risks were 2.7% (95% CI, 1.5% to 3.9%) at 1 month, 4.7% (3.1% to 6.3%) at 1 year, and 10.7% (9.9% to 11.5%) at 5 years with no gender difference. Those >= 45 years of age had lower probabilities of survival. Among the 30-day survivors (n = 711), stroke caused 21%, cardioaortic and other vascular causes 36%, malignancies 12%, and infections 9% of the deaths. Malignancy, heart failure, heavy drinking, preceding infection, type 1 diabetes, increasing age, and large artery atherosclerosis causing the index stroke independently predicted 5-year mortality adjusted for age, gender, relevant risk factors, stroke severity, and etiologic subtype. Conclusions: Despite the overall low mortality after an ischemic stroke in young adults, several recognizable subgroups had substantially increased risk of death in the long term.

Sienkiewicz-Jarosz H; Zatorski P; Baranowska A; Ryglewicz D; Bienkowski P. Predictors of smoking abstinence after first-ever ischemic stroke: A 3-month follow-up. Stroke 40(7): 2592-2593, 2009. (15 refs.)

Background and Purpose-Predictors of smoking abstinence in stroke survivors remain largely unexplored. The present study addressed the relationship between degrees of nicotine dependence and smoking abstinence 3 months after ischemic stroke. Methods-One hundred smokers with first-ever ischemic stroke were prospectively enrolled to the study. Correlates of nicotine dependence as well as sociodemographic and clinical characteristics were assessed during hospitalization. Smoking status was determined at 3-month follow-up. Results-Significant predictors of smoking abstinence at follow-up included: the Fagerstrom Test for Nicotine Dependence score, the Barthel Index, the number of smoking household members, and the Geriatric Depression Scale score. Conclusions-Our results suggest that smoking cessation after ischemic stroke can be determined by the interplay of psychobiological and environmental factors.

Thanvi BR; Treadwell SD. Cannabis and stroke: is there a link? (review). Postgraduate Medical Journal 85(1000): 80-83, 2009. (41 refs.)

Stroke associated with drug abuse has been frequently reported, particularly in young patients. The most commonly implicated drugs include cocaine, heroine, and amphetamines. Despite its widespread abuse, cannabis associated stroke is only infrequently reported. The cause and effect association between cannabis use and stroke is not firmly established. Presuming that cannabis may cause stroke, potential pathophysiologic mechanisms are not known. In this paper, we shall review the literature linking cannabis use and stroke and possible mechanisms supporting this link.

Toossi S; Hess CP; Hills NK; Josephson SA. Neurovascular complications of cocaine use at a tertiary stroke center. Journal of Stroke & Cerebrovascular Diseases 19(4): 273-278, 2010. (29 refs.)

Objective: An association between cocaine use and stroke has been reported, but few studies have examined cocaine-related neurovascular disease using modern stroke diagnostic techniques. We describe a large cohort of patients with cocaine-related stroke to define the pathophysiology and manifestations of cocaine-related neurovascular disease. Methods: All adult admissions to a tertiary neurovascular service from July 1, 1998 to July I, 2008 were screened for evidence of current or previous cocaine use. Patients included underwent thorough review of medical records including diagnostic procedure, laboratory, and imaging results. Results: A total of 5142 records were screened and 96 patients were identified; 45 (47%) were given the diagnosis of ischemic stroke/transient ischemic attack (TIA), 26 (27%) with intracerebral hemorrhage (ICH), and 25 (26%) with subarachnoid hemorrhage. In all, 61(63.5%) patients were categorized as active and 35 (36.5%) as previous cocaine users. Stroke type differed significantly between active and prior users (P = .004), with active users more likely to have ICH compared with previous users (37.7% v 8.6%) and less likely to have ischemic stroke or TIA (36.1% v 65.7%). The most common stroke/TIA cause was large artery atherosclerosis in 20 (44%) patients. Of the 25 subarachnoid hemorrhage cases, 22 (88%) were aneurysmal. Conclusion: Ischemic stroke/TIA is a common neurovascular presentation in patients with a remote history of cocaine use, often as a result of atherosclerotic disease; neither vasculitis nor vasospasm was a common cause of stroke in this cohort. ICH is more common in those currently using cocaine perhaps because of acute spikes in blood pressure. Further prospective trials are needed to confirm these results.

Woodward M; Fang X; Gu DF; Huxley R; Imai Y; Lam TH et al. Impact of cigarette smoking on the relationship between body mass index and coronary heart disease: A pooled analysis of 3264 stroke and 2706 CHD events in 378,579 individuals in the Asia Pacific region. BMC Public Health 9(article 294), 2009. (28 refs.)

Background: Elevated levels of body mass index (BMI) and smoking are well established lifestyle risk factors for coronary heart disease (CHD) and stroke. If these two risk factors have a synergistic relationship, rigorous lifestyle modification may contribute to greater reduction in cardiovascular burden than previously expected. Methods: A pooled analysis of individual participant data from 38 cohorts, involving 378,579 participants. Hazards ratios (HRs) and 95% confidence intervals (CIs) for BMI by cigarette smoking status were estimated using Cox proportional hazard models. Results: During a mean follow-up of 3.8 years, 2706 CHD and 3264 strokes were recorded. There was a log-linear, positive relationship of BMI with CHD and stroke in both smokers and nonsmokers with evidence of a synergistic effect of smoking on the association between BMI and CHD only: HRs (95% CIs) associated with a 2 kg/m(2) higher BMI were 1.13 (1.10 - 1.17) in current smokers and 1.09 (1.06 - 1.11) in non-smokers (p-value for interaction = 0.04). Conclusion: Smoking amplifies the positive association between BMI and CHD but not stroke. If confirmed, these results suggest that effective strategies that target smoking cessation and weight loss are likely to have a greater impact than anticipated on reducing the burden of CHD.