Background and Purpose - Acute triggers for ischemic stroke, which may include infection, are understudied, as is whether background cardiovascular disease (CVD) risk modifies such triggering. We hypothesized that infection increases acute stroke risk, especially among those with low CVD risk. Methods - Hospitalized strokes and infections were identified in the Atherosclerosis Risk in Communities (ARIC) cohort. A case-crossover design and conditional logistic regression were used to compare hospitalized infections among patients with stroke (14, 30, 42, and 90 days before stroke) with corresponding control periods 1 year and 2 years before stroke. Background CVD risk was assessed at both visit 1 and the visit most proximal to stroke, with risk dichotomized at the median. Results - A total of 1008 adjudicated incident ischemic strokes were included. Compared with control periods, hospitalized infection was more common within 2 weeks before stroke (14-day odds ratio [OR], 7.7; 95% CI, 2.1-27.3); the strength of association declined with increasing time in the exposure window before stroke (30-day OR, 5.7 [95% CI, 2.3-14.3]; 42-day OR, 4.5 [95% CI, 2.0-10.2]; and 90-day OR, 3.6 [95% CI, 2.1-6.5]). Stroke risk was higher among those with low compared with high CVD risk, with this interaction reaching statistical significance for some exposure periods. Conclusions - These results support the hypothesis that hospitalized infection is a trigger of ischemic stroke and may explain some cryptogenic strokes. Infection control efforts may prevent strokes. CVD preventive therapies may prevent strokes if used in the peri-infection period, but clinical trials are needed.
Bibliographical noteFunding Information:
Sources of Funding: The ARIC study was supported by National Heart, Lung, and Blood Institute (NHLBI) contracts HHSN268201100005C, HHSN 268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN2682011 00011C, and HHSN268201100012C. L.T.C. is supported by an NHLBI training grant T32 HL007779. A.A. is supported by grant R01 HL122200 from the National Institutes of Health and 16EIA2641001 from the American Heart Association.
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