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Infections precipitate acute ischaemic stroke

Jairia Dela Cruz
09 Jul 2019

Catching any type of infection, including those that affect the urinary and respiratory tracts and sepsis, could increase the chances of having subsequent acute ischaemic stroke (AIS), according to a recent study.

“The greatest magnitude of association was seen with urinary tract infection (UTI), which was associated with a more than threefold increased risk of AIS within 30 days,” the investigators said. “We also observed a gradient of decreasing magnitudes of association with longer time periods, across various infection types and stroke subtypes, supporting the concept of infection as a trigger of these events with a greater potential influence over a shorter time window.”

The investigators sourced data from the New York State Inpatient Databases and Emergency Department Databases, analysing the relationship of 152,356 index AIS, 27,257 intracerebral haemorrhage (ICH) and 11,853 subarachnoid haemorrhage (SAH) episodes to emergency department visits and hospitalizations for infection (skin, urinary tract infection, septicaemia, abdominal and respiratory). They used conditional regression models to test the relationship of the stroke subtypes to exposure to infection within progressively longer case periods (7, 14, 30, 60, 90 and 120 days before index stroke event) vs control periods exactly 1 year before the case period.

Results revealed that every infection type was associated with an increased likelihood of AIS, with the greatest risk estimates seen for UTI within the 1-month window before stroke (7 days: odds ratio [OR], 5.32; 14 days: OR, 4.54; 30 days: OR, 3.24; 60 days: OR, 2.65; 90 days: OR, 2.32; 120 days: OR, 2.13; p<0.0001 for all). [Stroke 2019;doi:10.1161/STROKEAHA.119.025872]

UTI was also implicated in ICH, although the association was of lesser magnitude, with ORs of 1.80 (95 percent CI, 1.04–3.11; p=0.0351) in the 14-day exposure period and 1.54 (1.23–1.94; p=0.0002) in the 120-day period.

With respect to other infection types, ORs for AIS ranged 1.36–1.52 with skin infection, 2.29–2.63 with septicaemia, 1.63–3.00 with abdominal infection, and 1.95–3.20 with respiratory infection. ORs for ICH varied between 2.86 and 3.25 with septicaemia, and 1.52 and 2.11 with respiratory infection.

Finally, only respiratory infection showed an association with SAH, with ORs of 3.67 (1.49–9.04; p=0.0048) in the 14-day exposure window and 1.95 (1.44–2.64; p<0.0001) in the 120-day window.

“There are several mechanisms by which infection can trigger stroke,” the investigators noted.

Among those that were enumerated included circulating leukocyte proliferations contributing to atherogenesis and thrombogenesis; increased platelet activation; elevated risk of deep vein thrombosis because of immobilization, causing paradoxical embolism; and increased fibrinogen, leukocytes, clotting factor, and cytokines, and metabolism and function of endothelial cells and macrophages favouring atherosclerosis and thrombosis formation. [Stroke 2011;42:1851-1856; Stroke 2004;35:1147-1152]

“More research is … needed on potential interventions, such as vaccination or antibiotic regimens, or intensive antithrombotic treatments, to not only treat the infection but also potentially reduce thrombotic and bleeding risk,” the investigators said.

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Roshini Claire Anthony, 30 Nov 2019

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