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Influenza as a trigger for cardiovascular disease: An investigation of serotype, subtype and geographic location.

Influenza as a trigger for cardiovascular disease: An investigation of serotype, subtype and geographic location.
Author Information (click to view)

Pearce DC, McCaw JM, McVernon J, Mathews JD,


Pearce DC, McCaw JM, McVernon J, Mathews JD, (click to view)

Pearce DC, McCaw JM, McVernon J, Mathews JD,

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Environmental research 2017 05 05156() 688-696 pii S0013-9351(16)31182-3
Abstract
BACKGROUND
Seasonal peaks of influenza and cardiovascular disease tend to coincide. Many excess deaths may be triggered by influenza, and the severity of this effect may vary with the virulence of the circulating influenza strain and host susceptibility. We aimed to explore the association between hospital admissions for influenza and/or pneumonia (IP) and acute myocardial infarction (AMI) or ischaemic heart disease (IHD) in Queensland, Australia, taking into account temporal and spatial variation of influenza virus type and subtype in 2007, 2008 and 2009.

METHODS
This ecological study at Statistical Subdivision level (SSD, n=38) used linked patient-level data. For each study year, Standardized Morbidity Ratios (SMRs) were calculated for hospital admissions with diagnoses of IP, AMI and IHD. We investigated the associations between IP and AMI or IHD using spatial autoregressive modelling, adjusting for socio-demographic factors.

RESULTS
Spatial autocorrelation was detected in SMRs, possibly reflecting underlying social and behavioural risk factors, but consistent with infectious disease spread. SMRs for IP were consistently predictive of SMRs for AMI and IHD when adjusted for socioeconomic status, population density and per cent Indigenous population (coefficient: 0.707, 95% confidence interval (CI): 0.318 – 1.096; 0.553, 0.222 – 0.884; 0.598, 0.307 – 0.888 and 1.017, 0.711 – 1.323; 0.650, 0.342 – 0.958; 1.031, 0.827 – 1.236) in 2007, 2008 and 2009, respectively.

CONCLUSIONS
This ecological study provides further evidence that severe respiratory infections may trigger the onset of cardiovascular events, implicating the influenza virus as a contributing factor.

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