Inflammation, atherosclerosis, and stroke

Inflammation has received increasing attention in recent years as a cause of atherosclerosis, coronary artery disease, and stroke. Basic and animal research has implicated inflammatory mechanisms in the pathogenesis and progression of atherosclerosis, as well as in clinical events related to plaque rupture and other atherothrombotic events.

The literature on the association of inflammatory markers with risk of stroke was reviewed and a clinical example provided. Several inflammatory biomarkers, and particularly high-sensitivity C-reactive protein (hsCRP), have been identified as likely predictors of the risk of a future stroke. Medications, particularly hydroxymethylglutaryl coenzyme A reductase inhibitors, or statins, have been demonstrated to reduce levels of inflammatory markers independently of effects on cholesterol. Most recently, the ability of these agents to reduce risk of myocardial infarction and other coronary events in patients with acute coronary artery disease has been demonstrated to correlate with their ability to lower levels of hsCRP. Whether reduction of hsCRP would have similar benefits in stroke patients remains unsettled, as does whether other drugs may be similarly used to lower hsCRP levels.

Inflammatory biomarkers, especially hsCRP, may allow improved prediction of the risk of stroke in primary and secondary stroke prevention. Modalities to reduce inflammation are becoming available that may help to modify this risk. Further studies, however, are needed before inflammatory markers become a routine part of the evaluation of stroke patients.