Abstract
Inflammation is recognized as an important component of atherosclerosis resulting in an increased risk of myocardial infarction and stroke. Studies, conducted as early as the 1960s, involving drugs targeting different pathways of inflammation linked to cardiovascular (CV) disease have produced inconsistent results. Drugs such as the statins with mechanisms of action beyond an anti-inflammatory effect have clear benefit in reducing CV risk. Other drugs such as the broad-spectrum anti-inflammatory agents (corticosteroids, lipoprotein-associated phospholipase A2 inhibitors, methotrexate) have been found to have no benefit in reducing CV risk. More specific anti-inflammatory agents which target the NLRP3 inflammasome, interleukin (IL)-1β and/or IL-6, and high-sensitivity C-reactive protein have been associated with therapeutic benefit. Despite favorable outcome data and FDA-approval for one of these agents (colchicine), a recent study has created uncertainty concerning the routine use of this agent for CV risk reduction. Multiple studies with a variety of anti-cytokine related agents are on-going in efforts to further reduce residual CV risk. Compared to other common CV risk factors such as hypertension and dyslipidemia, our understanding and management of inflammation is poorly understood. Due to the complexities of the inflammatory process, targeted approaches that can markedly reduce inflammatory markers are likely needed to demonstrate clinically relevant reductions in major adverse cardiovascular events.