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Study Title and Description

Caffeine does not increase the risk of atrial fibrillation: a systematic review and meta-analysis of observational studies.



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 Caffeine does not increase the risk of atrial fibrillation: a systematic review and meta-analysis of observational studies.
Author D Caldeira,C Martins,LB Alves,H Pereira,JJ Ferreira,J Costa,
Country
Year 2013
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)? The association between caffeine exposure and AF is currently unknown, although a positive association has been suggested in the literature. To further evaluate this putative association, we performed a systematic review and meta-analysis of observational studies.
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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) Randomised controlled trials, prospective or retrospective cohorts and case–control studies evaluating exposure to caffeine (whether as coffee, tea, chocolate or caffeinated beverages) and risk of AF (or atrial flutter) were eligible. Studies addressing the effects of short-term exposure to caffeine (ie, <6 months) as well as studies evaluating caffeine exposure in patients already in AF were excluded. Studies that met inclusion criteria were not excluded a priori on the basis of weakness of design or data quality. For primary analysis, we performed random-effects meta-analysis weighted by the inverse variance method to estimate pooled ORs and 95% CIs. For this purpose, in case studies that did not report a single estimate for consumers versus non-consumers, but expressed multiple levels of exposure, we pooled these estimates against the lowest quintile to derive an overall OR for that study, which was then used for pooled analysis. When different risk estimates for the same strata were available in the same publication, we considered for analysis those reflecting the greatest degree of control for potential confounders, or the most comprehensive assessment of caffeine intake using these criteria sequentially.
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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) Atrial fibrillation
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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? Meta-analysis
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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 This systematic review had PRISMA and MOOSE guidelines as standards for reporting data. Reporting quality was independently evaluated by two investigators (DC and JC) using a qualitative classification according to risk of bias (high, unclear or low risk). We used a five-item classification system based on MOOSE, QATSO and STROBE adapted from previous published quality assessment instruments. The following items were taken into consideration: (1) participants, if the population was adequate and the study reported appropriate inclusion and exclusion criteria; (2) exposure, if caffeine exposure use was adequately assessed through food questionnaires; (3) outcome, if AF was assessed by clinical, ECG methods or through database codes, and not exclusively based on self-report; (4) specific outcome adjustments, for both age and at least one of cardiovascular disease, alcohol intake or smoking; (5) other adjustments.
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Caffeine (general)
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Coffee, Chocolate, energy drink, gum, medicine/supplement, soda, tea, other? Coffee, Chocolate, 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.) The exposure categories were <350 mg/day (low), 350-699 mg/day (moderate), and >/= 700 mg/day (high). While the <350 mg/day category appears high, six of the seven studies had comparator/reference group of 0 cups per day to up to a mean of 23 mg/day. The study of Frost and Vestergaard (2006) that was included had a reference group with a mean caffeine intake of 248 +/- 91 mg/day, but none of the RRs from this study were above unity.
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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) We used a random-effects model independently of the existence of statistical heterogeneity because we combined studies with different designs and populations. We presented the results stratified according to study design (cohort and case–control) in order to explore differences in the outcome estimate. Statistical heterogeneity was assessed with the I2 test, which measures the percentage of total variation between studies due to heterogeneity. If significant heterogeneity was found, we planned to perform a sensitivity analysis excluding studies of poorer quality to explore the impact of the study quality on the results. We planned to conduct three subgroup analyses: (1) to explore the effect of the level of caffeine exposure on AF risk; (2) to explore the effect of the source of caffeine on AF risk; (3) to explore the effect of the length of follow-up. For the first analysis, we considered three levels of caffeine intake: low, moderate and high. The highest category of exposure reported in each study was considered for the group of high caffeine intake, independently of the cut-off value used in that study. We considered low intake to be <350 mg, moderate intake 350–699 mg and high intake ≥700 mg. Many factors contribute to the caffeine content of beverages and food and differences exist in caffeine content of a given caffeine source (in particular coffee) between, and even within, countries.24 25 For the purpose of this study, when cups of coffee were provided as a measure of caffeine intake, we considered each cup to have an amount of caffeine according to the geographic region of the study; UK/Northern Europe 140 mg; Southern Europe 50 mg; USA 85 mg.25 When a study’s interval for caffeine consumption crossed two of the above mentioned categories, we considered for analysis the mean value of caffeine intake. For the second subgroup analysis, we considered only studies that took coffee consumption as the sole source of caffeine exposure because this beverage was the main source of caffeine. In the third subgroup evaluation, we assessed pooled estimates according to follow-up, using the value of 10 years as the threshold (<10 vs ≥10 years).
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What conflicts of interest were reported? No conflicts were noted.
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Refid 24009307
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What were the sources of funding? Not discussed.
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Results & Comparisons

No Results found.