Carotid plaque, stroke pathogenesis, and CRP: Treatment of ischemic stroke

Abstract

Inflammation is receiving increased attention as a cause of atherosclerosis and stroke. Several inflammatory biomarkers, and particularly high-sensitivity C-reactive protein (hsCRP), have been identified as likely predictors of the risk of a future stroke. In clinical settings, it has been consistently observed that higher concentrations of CRP are associated with larger brain infarcts, stroke severity, neurologic disability, and future vascular events. However, there is still controversy over the degree of risk conferred by elevated CRP concentrations. Some studies reported that the predictive value of CRP is moderate compared with classical risk factors and is only weakly related to cardiovascular damage after adjustment for traditional cardiovascular risk factors. CRP like many other hemostatic factors is an acute-phase protein and, therefore, it is not always clear whether its association with cerebrovascular disease reflects its contribution to atherothrombosis, its acute-phase condition, or both. Furthermore, the value of single measurements of CRP in patients with concurrent infection or other inflammatory conditions has not been established and reported data should be interpreted cautiously. Several drugs, especially hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), have been demonstrated to reduce hsCRP levels independently of their effects on plasma cholesterol. Recently, emerging therapies have been aimed at the control of blood pressure and inflammation in stroke patients. Whether a reduction of hsCRP levels could be beneficial to stroke patients remains to be clarified, and it is also unclear whether other drugs may be useful to lower hsCRP levels. More studies are needed before hsCRP becomes a routine part of the evaluation of stroke patients. This should also prompt the search for new agents directly blocking CRP actions.