Response to Athyros and Colleagues: Inflammation and LDL Reduction

Abstract

Atyros has discussed the role of statins in different clinical scenarios, doses, and timing of application. In response to your interesting observations, we would like to comment that statins have indeed changed the natural history of atherosclerotic disease in patients with hyperlipaemia and inflammation. Even in patients without hyperlipidemia, and with low-grade systemic inflammation data, studies such as JUPITER [1] demonstrated that statins reduce the risk of major cardiovascular events. In recent years, the use of these lipid-lowering drugs has been extended to patients whose cardiovascular risk is determined by an increased baseline inflammatory rate, such as patients infected with human immunodeficiency virus [2, 3], rheumatoid arthritis [4], systemic lupus erythematosus [5], and heart transplant recipients [6]. As mentioned in our review article [7], innate immunity represents an interesting field of study in the diagnosis and treatment of cardiovascular disease. In fact, innate immunity mechanisms, such as activation of monocytes, T-lymphocytes and platelets, strengthen the local inflammatory response, which contribute to the rupture of the atherosclerotic plaque [8]. These physiopathological events finally lead to acute thrombus formation, the major cause of acute coronary syndromes [9, 10]. The stability of atherosclerotic plaque mainly depends on immune and antiinflammatory pathways [11]. Contemporary studies in stable and unstable coronary artery disease, such as the CANTOS study [12], the COLCOT [13], the LODOCO2 [14], and the OXI trial [15], have supported the inflammatory hypothesis of atherosclerosis. The majority of these studies have demonstrated that the coronary residual inflammatory risk, a crucial prognostic factor of cardiovascular events, could be successfully decreased by inhibition of different proinflammatory interleukins [16]. In conclusion, the horizon in the treatment for atherosclerosis is the prevention of cardiovascular events by targeting the systemic low-grade inflammation and the innate immune response.