Inflammatory markers, cholesterol and statins: pathophysiological role and clinical importance

Statins are one of the most important medications in cardio-vascular diseases since they block cholesterol synthesis by inhibiting the 3-hydroxy-3-methylglutaryl coenzyme A reductase and thus reduce low density lipoprotein concentrations. In the last years, numerous pleiotropic properties of statins have been described, beyond their well-known lipid lowering function. In particular, they are able to modulate inflammation, which plays a pivotal role in the atherosclerotic process. Several trials have shown a direct correlation between statin therapy and lower C-reactive protein concentrations. Moreover, a large body of pathophysiological studies has demonstrated that statins lower cytokine concentrations and inhibit recruitment, migration and cell adhesion to endothelium by attenuating chemokine production. They also inhibit inflammatory pathways regulated by proteins as Ras and Rho, and increase nitric oxide production which exerts a protective effect on endothelium. In addition to reducing inflammation in coronary atherosclerosis, statins also have beneficial effects in chronic inflammatory and autoimmune diseases, such as psoriasis, and they could induce clinical improvement. Statins seem to exert benefits even in settings of infection. These results suggest that initiating and monitoring statin therapy on the basis of inflammatory markers, in particular C-reactive protein, may improve cardiovascular prevention and treatment.