Context: While the effects of weather and, in particular, ambient temperature on overall mortality are well documented, the strength of the evidence base for the effects on acute myocardial infarction (MI) are less clear.
Objective: To systematically review studies specifically focusing on the effects of temperature on MI.
Data sources: Medline, Embase, and GeoBase publication databases, as well as reference lists, and the websites of a number of relevant public organisations.
Study selection: Studies of original data in which ambient temperature was an exposure of interest and MI a specific outcome were selected.
Data extraction: The reported effects of ambient temperature on the risk of MI, including effect sizes and confidence intervals, where possible, were recorded. Methodological details were also extracted, including study population, location and setting, ascertainment of MI events, adjustment for potential confounders and consideration of lagged effects.
Results: 19 studies were identified, of which 14 considered the short-term effects of temperature on a daily timescale, the remainder looking at longer-term effects. Overall, 8 of the 12 studies which included relevant data from the winter season reported a statistically significant short-term increased risk of MI at lower temperatures, while increases in risk at higher temperatures were reported in 7 of the 13 studies with relevant data. A number of differences were identified between studies in the population included demographics, location, local climate, study design and statistical methodology.
Conclusion: A number of studies, including some that were large and relatively well controlled, suggested that both hot and cold weather had detrimental effects on the short-term risk of MI. However, further research with consistent methodology is needed to clarify the magnitude of these effects and to show which populations and individuals are vulnerable.
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▸ An additional table and references are published online only at http://heart.bmj.com/content/vol95/issue21
Funding This study was funded through grants from the British Heart Foundation and the Garfield Weston Foundation. LS is supported by a Wellcome Trust Senior Research Fellowship in Clinical Science. SH is funded by a Wellcome Trust Research Career Development Fellowship (076583/Z/05/Z).
Competing interests None declared.
Role of funding sources: The British Heart Foundation, the Garfield Weston Foundation and the Wellcome Trust had no role in the design or conduct of this review, or in the preparation, review, or approval of the manuscript.
Provenance and Peer review Not commissioned; externally peer reviewed.