Laboratory-confirmed respiratory infections as triggers for acute myocardial infarction and stroke: a self-controlled case series analysis of national linked datasets from Scotland

Literature - Warren-Gash C, Blackburn R, Whitaker H, et al. - Eur Respir J 2018; 51: 1701794

Introduction and methods

Acute respiratory tract infections are associated with a short-term increase in the risk of acute CV events [1]. Influenza virus and S. pneumoniae have direct myocardial effects and may exacerbate underlying atherosclerotic disease, however the effects of specific organisms is not clear [2]. A meta-analysis of data comparing influenza vaccine versus placebo in people with existing CVD shows a 36% reduction in the risk of major adverse cardiovascular events associated with influenza vaccination [3]. Moreover, the receipt of pneumococcal vaccine was associated with a modest cardio-protective effect [4].

In this study, the association between laboratory-confirmed respiratory bacteria or virus infections and risk of first myocardial infarction (MI) or stroke was quantified, using self-controlled case series analysis of anonymized linked electronic health records from Scotland in the UK.

For this purpose, the following data sources were used:

• the general/acute hospital inpatient data from the Scottish Morbidity Record (SMR01), a large national dataset with more than 1.4 million records per year
• the Electronic Communication of Surveillance in Scotland (ECOSS) dataset, with information on all identifications of organisms or infections of clinical and public health significance

All individuals aged ≥40 years, with a hospital admission for MI or stroke from 2004-2014 were identified in the SMR01. All linked ECOSS records were searched for positive tests for influenza virus, parainfluenza virus, rhinovirus, respiratory syncytial virus, human meta-pneumo-virus or S. pneumoniae during the same study period. Individuals with a record of first MI or stroke and a record of at least one laboratory-confirmed respiratory infection were included in the analysis (N=1989).

Main results

• The adjusted IR for first MI was significantly increased in the first 1–3 days after both respiratory bacterial and viral infections (IR for S. pneumoniae: 5.98; 95%CI: 2.47–14.4; P<0.001; IR for viruses: 5.59; 95%CI: 1.77–17.6; P=0.003), and persisted for approximately 1 week.
• The adjusted IR for first stroke was 12.3 for S. pneumoniae (95%CI: 5.48–27.7; P<0.001) and 6.79 for viruses (95%CI: 1.67–27.5; P=0.007) for days 1–3. Elevated rates of stroke following both bacterial and viral infections persisted to 28 days (P<0.001).
• Influenza virus infections were associated with higher IRs for both MI and stroke compared with all other respiratory viruses combined.
• The MI adjusted day 1–3 IR for influenza virus was 9.80 (95%CI: 2.37–40.5) and for other respiratory viruses it was 2.81 (95%CI: 0.39–20.3).
• The stroke adjusted day 1–3 IR after influenza virus was 7.82 (95%CI: 1.07–56.9) and for other respiratory viruses it was 4.86 (95%CI: 0.67–35.4).
• Individuals aged <65 years tended to have higher adjusted IRs for MI and stroke after respiratory bacteria and virus infections than those aged ≥65 years, although CIs were overlapping.

Conclusion

References

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