Abstract
Acute coronary syndrome (ACS) is a major cause of acute death worldwide. Both innate and adaptive immunity regulate atherosclerosis progression, plaque stability, and thrombus formation. Immune and inflammation dysfunction have been indicated in the pathogenesis of ACS. The imbalance in the proatherogenic and antiatherogenic immune networks promotes the transition of plaques from a stable to unstable state and results in the occurrence of acute coronary events. The residual inflammatory risk (RIR) has received increasing attention in recent years, and lowering RIR has been expected to improve the outcomes of ACS patients. The CANTOS, COLCOT, and LoDoCo trials verified the benefits of reducing cardiovascular events using anti-inflammation therapies; however, most of the other studies focusing on lowering RIR produced negative or contradicting results. Therefore, restoring the balance in autoimmune regulation is essential because proatherogenic and antiatherogenic immunomodulatory effects are equally important in the complex human immune network. In this review, we summarized the recent evidence of the roles of proatherogenic and antiatherogenic immune networks in the pathogenesis of ACS and discussed how immune and inflammation contribute to atherosclerosis progression, plaque instability, and adverse cardiovascular events. We also provide a “from bench to bedside” perspective of a novel and promising personalized strategy in RIR intervention and therapeutic approaches for the treatment of ACS.
Highlights
Acute coronary syndrome (ACS) refers to a complex clinical syndrome that includes a spectrum of entities including unstable angina, ST segment elevation myocardial infarction (STEMI), and non-ST segment elevation myocardial infarction (NSTEMI)
60% of ACS patients have a high level of high-sensitivity C-reactive protein (>2.0 mg/L), a biomarker of systemic inflammation and a predictive factor of high cardiovascular mortality, which is defined as the residual inflammatory risk (RIR) in these patients [3]
This study demonstrated that coronary RIR could be successfully treated by inhibiting IL-1β with canakinumab and raised a potential implication of anti-inflammatory therapy in ACS patients
Summary
Acute coronary syndrome (ACS) refers to a complex clinical syndrome that includes a spectrum of entities including unstable angina, ST segment elevation myocardial infarction (STEMI), and non-ST segment elevation myocardial infarction (NSTEMI). The accumulating evidence has implicated an inflammatory process in the pathogenesis of ACS that involves local immune cells in coronary arteries generating inflammatory factors that promote thrombus formation [1, 2]. Systemic or local inflammation promotes coronary thrombus formation. Both innate and adaptive immune responses contribute to atherosclerosis and its thrombotic complications in ACS. Journal of Immunology Research through complex interactions between atherosclerosis, innate immunity, and inflammation [5]. The CANTOS trial (The Canakinumab Anti-inflammatory Thrombosis Outcomes Study) targeted interleukin-1β (IL-1β) innate immunity with canakinumab in patients with a history of ACS and hsCRP ≥ 2:0 mg/L and reported significantly attenuated systemic inflammation indicated by hsCRP and improved clinical outcomes independent of lipid metabolism [6]. This article reviews recent advances in the understanding of immune-mediated inflammation in the pathogenesis of ACS and discusses its implications for ACS management strategies
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