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Review
. 2010 Oct;41(10 Suppl):S3-8.
doi: 10.1161/STROKEAHA.110.594945.

Inflammatory mechanisms of stroke

Mitchell S V Elkind  1
Affiliations
Review

Inflammatory mechanisms of stroke

Mitchell S V Elkind. Stroke. 2010 Oct.

Abstract

Basic and clinical research provides evidence that inflammatory mechanisms play a central role in the pathogenesis and progression of atherosclerosis, plaque rupture, thrombosis, and stroke. Inflammatory biomarkers such as high-sensitivity C-reactive protein have been identified as predictors of first stroke and prognosis after stroke. The value of high-sensitivity C-reactive protein and other markers may depend on the characteristics of the study population; their utility may be less among populations with high vascular risk. A recent randomized, clinical trial suggests that the use of rosuvastatin therapy in otherwise healthy patients with high-sensitivity C-reactive protein >2 mg/dL can reduce the risk of a first stroke by 50%. The prognostic role of high-sensitivity C-reactive protein among patients after stroke, however, is less clear, and other biomarkers, including lipoprotein-associated phospholipase A(2), may provide complementary information about the risk of stroke recurrence. Infections, moreover, may contribute to inflammation and stroke risk. Although no single infectious organism is likely to be identified as the direct cause of atherosclerosis, summary measures of multiple chronic infectious exposures, or "infectious burden," have been associated with the risk of stroke and atherosclerosis affecting the carotid arteries. Acute infections have also been found to serve as stroke triggers in epidemiologic studies. Recommendations to vaccinate patients with cardiovascular disease against influenza represent the first specific anti-infective strategy to be used in vascular prophylaxis. Further studies are needed to determine the role of treatment of inflammation and infection in stroke prevention.

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Figures

Figure 1
Figure 1
HsCRP levels and risk of ischemic stroke (A) and myocardial infarction (B) in the Northern Manhattan Study (N=2240; reference group hsCRP<1 mg/L)
Figure 1
Figure 1
HsCRP levels and risk of ischemic stroke (A) and myocardial infarction (B) in the Northern Manhattan Study (N=2240; reference group hsCRP<1 mg/L)
Figure 2
Figure 2
Mechanism of the Effect of Infectious Burden on Atherosclerosis and Stroke
See this image and copyright information in PMC

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