bb MacIntyre 2013.
Methods | Case‐control study investigating the protective effect of influenza vaccination against acute myocardial infarction | |
Participants | Cases (n = 275): patients aged ≥ 40 years of age admitted with an acute myocardial infarction, evolving or recent myocardial infarction to the cardiology unit during the influenza season. Eligible respondents were those able to provide samples within 72 hours of the acute myocardial infarction event, residing in Sydney, Australia, available for follow‐up, and provided informed consent. Cases reporting a previous cardiovascular event were eligible. A diagnosis of acute myocardial infarction was defined as a typical rise and gradual fall in troponin or more rapid rise and fall in creatine kinase‐MB biochemical markers of myocardial necrosis, with 1 or more of the following: ischaemic symptoms (chest or arm pain, nausea/vomiting, sweating, shortness of breath); development of pathological Q waves on ECG; ECG changes indicative of ischaemia (ST segment elevation or depression); coronary artery intervention; or pathological findings of an acute myocardial infarction. Participants were recruited into the study between 27 June and 20 October 2008; 18 May and 23 October 2009; and 21 June and 28 October 2010. Controls (n = 284): controls were people aged ≥ 40 years of age attending the orthopaedic or ophthalmic outpatient clinics during the same time period. Respondents residing in Sydney, available for follow‐up, and able to provide informed consent were eligible. Controls were unmatched, except for the same age cut‐off and recruitment period, to ensure similar level of exposure to circulating influenza. Controls were excluded if they reported a history of acute myocardial infarction, transient ischaemic attack, or stroke in the previous 12 months. Stable angina was permissible if there had been no worsening of angina or acute myocardial infarction episodes or hospital admissions in the last year. Controls were recruited into the study between 30 June and 31 October 2008; 19 May and 26 October 2009; and 23 June and 29 October 2010. |
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Interventions | Influenza vaccination status was validated for current and previous influenza seasons from hospital and GP records, with GPs contacted via facsimile or telephone. If discrepancies arose between GP and self report, GP‐reported vaccination status was considered correct. Self reported vaccination status was considered sufficient in those individuals whose GP could not be contacted. Type and characteristics of the administered vaccines are not provided. | |
Outcomes | ||
Notes | Funding source ‐ industry This work was supported by a grant from GlaxoSmithKline, Belgium. Dr Iman Ridda and Dr Holly Seale are supported by Australian National Health and Medical Research Council Training Fellowships. |
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Risk of bias | ||
Bias | Authors' judgement | Support for judgement |
CC ‐ case selection All outcomes | Low risk | Consecutive series of cases (patients admitted to the cardiology unit during the influenza season) |
CC ‐ control selection All outcomes | Unclear risk | Community controls (patients attending orthopaedic or ophthalmic outpatient clinics during the same period without history of disease) |
CC ‐ comparability All outcomes | Unclear risk | Unmatched |
CC ‐ exposure All outcomes | Low risk | Vaccination certificate, GP records |
Summary assessment | Unclear risk | Unclear risk of bias |