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Study Title and Description

Coffee and acute ischemic stroke onset: the Stroke Onset Study.



Key Questions Addressed
1 For [population], is caffeine intake above [exposure dose], compared to intakes [exposure dose] or less, associated with adverse effects on cardiovascular outcomes?
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Primary Publication Information
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TitleData
Title Coffee and acute ischemic stroke onset: the Stroke Onset Study.
Author E Mostofsky,G Schlaug,KJ Mukamal,WD Rosamond,MA Mittleman,
Country
Year 2010
Numbers

Secondary Publication Information
There are currently no secondary publications defined for this study.


Extraction Form: Cardiovascular Design
Design Details
Question... Follow Up Answer Follow-up Answer
What outcome is being evaluated in this paper? Cardiovascular
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What is the objective of the study (as reported by the authors)? We hypothesized that caffeine intake is associated with a transiently increased risk of ischemic stroke.
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Provide a general description of the methods as reported by the authors. Information should be extracted based on relevance to the SR (i.e., caffeine related methods) Study design: The Stroke Onset Study used a case-crossover design, a variation of a case-control design that is appropriate when a brief exposure (caffeinated coffee consumption) causes a transient change in the risk of an acute outcome (ischemic stroke). We compared a subject’s coffee consumption in the hour prior to onset of stroke symptoms (the case period) with the same subject’s usual frequency of coffee consumption in the prior year (the control period). Because control information for each subject is based on his or her own past exposure experience, self-matching eliminates confounding by risk factors that are constant within individuals over the sampling period but often differ between study subjects. Study population: The Stroke Onset Study was conducted in 3 medical centers (Beth Israel Deaconess Medical Center, Boston, MA; University of North Carolina Hospitals, Chapel Hill, NC; Vancouver Island Health Authority, Victoria, BC) between January 2001 and November 2006. Trained research staff identified eligible subjects by reviewing admission logs and charts of subjects admitted to each hospital’s stroke service. Additionally, subjects with new onset of an acute neurologic syndrome compatible with stroke were screened upon admission to emergency departments. Presumed stroke etiology was determined according to an abbreviated Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification system. Across all sites, 43% of patients with confirmed ischemic stroke met all inclusion criteria. Of these, 83% agreed to participate, 5.5% refused, and the remaining 12.5% were discharged from the hospital before the interviewers were able to approach them. The final sample includes 390 subjects (209 men and 181 women) who were interviewed a median of 3 days (range 0–14) after sustaining an acute ischemic stroke. To be eligible, subjects were required to have a neurologist-confirmed diagnosis of acute ischemic stroke, either by clinical diagnosis or appropriate imaging studies, to be English-speaking, and to be free of dementia prior to the index event. Subjects were excluded if they were unable to complete the structured interview because they were cognitively impaired, had poor memory around the time of the stroke, could not identify the time of onset of their stroke symptoms, experienced aphasia, or were too ill to complete the structured interview that lasted 30 to 45 minutes. Coffee consumption: Interviewers used a structured questionnaire and asked subjects if they had consumed any coffee in the year preceding their stroke. Subjects who reported any coffee consumption were also asked to report the last time that they had consumed a serving of coffee and their usual frequency of coffee consumption over the prior year. The portion size for 1 serving of coffee was defined as 8 ounces or 1 cup of caffeinated coffee. Similar questions were asked about consumption of caffeinated tea and cola. Subjects were also asked to report the timing of their last exposure to other potential triggers and usual frequency of these factors in the year preceding the onset of stroke symptoms. Other information collected from the interview included medication use and symptoms on the day of the stroke. Reliability of the questionnaire: The test-retest reliability of the Stroke Onset Study questionnaire was assessed in a subgroup of 25 subjects who were re-interviewed up to 6 days after their initial interview and asked again about their coffee consumption patterns in the past year as well as the time of their last drink before the onset of their stroke symptoms. The intraclass correlation for the usual frequency of coffee consumption was found to be excellent, and there was high agreement for reporting of any coffee consumption during the past year and during the hour preceding stroke onset.
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How many outcome-specific endpoints are evaluated? 1
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What is the (or one of the) endpoint(s) evaluated? (Each endpoint listed separately) Acute ischemic stroke
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List additional health endpoints (separately). 2
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List additional health endpoints (separately).3
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List additional health endpoints (separately).4
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List additional health endpoints (separately).5
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List additional health endpoints (separately).6
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Clinical, physiological, other Clinical
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What is the study design? Case-Control
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Randomized or Non-Randomized?
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What were the diagnostics or methods used to measure the outcome? Objective
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Optional: Name of Method or short description Trained research staff identified eligible subjects by reviewing admission logs and charts of subjects admitted to each hospital’s stroke service. Additionally, subjects with new onset of an acute neurologic syndrome compatible with stroke were screened upon admission to emergency departments. Presumed stroke etiology was determined according to an abbreviated Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification system.
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Caffeine (general)
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Coffee, Chocolate, energy drink, gum, medicine/supplement, soda, tea, other? Coffee, soda, tea
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Measured or self reported? Self-report
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Children, adolescents, adults, or pregnant included? Adults
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What was the reference, comparison, or control group(s)? (e.g. high vs low consumption, number of cups, etc.) "We compared a subject’s coffee consumption in the hour prior to onset of stroke symptoms (the case period) with the same subject’s usual frequency of coffee consumption in the prior year (the control period). Because control information for each subject is based on his or her own past exposure experience, self-matching eliminates confounding by risk factors that are constant within individuals over the sampling period but often differ between study subjects."
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What were the listed confounders or modifying factors as stated by the authors? (e.g. multi-variable components of models.  Copy from methods) Each subject in a case-crossover study forms his or her own stratum and thus is his or her own control. The ratio of the observed exposure frequency in the case period to the expected frequency based on control information about coffee consumption in the previous year was used to calculate estimates of the rate ratio as a measure of relative risk (RR). We multiplied the usual annual frequency of coffee consumption by the hypothesized window of its physiologic effect (1 hour in the primary analysis) to estimate the amount of person-time exposed to coffee. The unexposed person-time was calculated by subtracting this value from the number of hours in 1 year. The data were analyzed using methods for cohort studies with sparse data in each stratum. Similar analyses were conducted for caffeinated tea and caffeinated cola. To estimate the length of time from coffee consumption to the onset of ischemic stroke, RRs were calculated for each 1-hour period before stroke onset. We stratified by sex, age (<65, 65– 75, and >75 years), smoking status (never, former, current), habitual moderate or vigorous physical activity (3 or more times per week vs fewer than 3 times per week), and stroke etiology and compared the RRs by means of a test for homogeneity. Thirty-two subjects were excluded from the analysis stratified by stroke etiology because it was not determined at 1 center. We stratified by intake of coffee in the past week (up to 1 cup per day, more than 1 to 3 cups per day, more than 3 cups per day) and conducted a test for trend. Because there is a circadian peak of stroke onset in the morning hours and people tend to drink more coffee in the morning than during the rest of the day, we conducted a sensitivity analysis which we restricted to subjects experiencing strokes between 6 AM and 9 AM. We made the conservative assumption that all coffee in the past year is only consumed during that time of day, which should result in a conservative estimate of the RR. To evaluate whether potential triggers could account for the observed association, we conducted a sensitivity analysis excluding subjects simultaneously exposed to other potential triggers (e.g., vigorous physical exertion, alcohol, marijuana, and anger) in the hour preceding their stroke and a sensitivity analysis excluding subjects reporting a stroke or myocardial infarction (MI) within the year preceding the index event. In another sensitivity analysis, we used the number of servings of coffee consumed in the week preceding the stroke as the control information.
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What conflicts of interest were reported? Disclosure information reported: E. Mostofsky receives research support from the NIH/NIAID (T32-A1007535-11). Dr. Schlaug receives research support from the NIH/NIDCD (1RO1 DC008796 [PI], R01 DC009823-01[PI], and 3R01DC008796-02S1 [PI]). Dr. Mukamal serves on the editorial board of Nutrition; has received institutional research support from Martek Corporation; and receives research support from the NIH (HL094555 [PI], HL091874 [PI], and AA016110 [PI]) and from Harvard Medical School. Dr. Rosamond receives research support from the CDC (NCDHHS 01602-05 [subcontract, PI]) and the NIH (N01-HC-55015 [coinvestigator]). Dr. Mittleman served on the editorial board of Epidemiology and serves on the editorial board of Environmental Health Perspectives; and has received/receives research support from the NIH (ES009825 [Project PI], ES017125 [PI], AA016567 [PI], AA016110 [coinvestigator], HL091874 [coinvestigator], DK071083 [coinvestigator], and UL1RR025758 [coinvestigator]), the CDC/NIOSH, and the American Heart Association.
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Refid 20881275
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What were the sources of funding? Supported by the American Heart Association (0140219N to M.A.M.) and the NIH/NIAID (T32-A1007535-11 to E.M.).
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Results & Comparisons

No Results found.