In post-ACS patients, vulnerable non-culprit lesions, increased thrombotic state, residual dyslipidemia (especially high LDL-C), and inflammation have been identified as risk factors for future ischemic events. (IMAGE)

Chinese Medical Journals Publishing House Co., Ltd.

In post-ACS patients, vulnerable non-culprit lesions, increased thrombotic state, residual dyslipidemia (especially high LDL-C), and inflammation have been identified as risk factors for future ischemic events.

Caption

The anatomical and functional characteristics of non-culprit lesions can be assessed using intracoronary imaging modalities and fractional flow reserve to implement precision revascularization strategies. ACS patients are recommended to receive 1 year of standard DAPT, followed by a de-escalating regimen (eg, extended monotherapy) to balance ischemia and bleeding. High levels of cholesterol (especially elevated LDL-C) increase the risk of atherogenic coronary events. Statins, ezetimibe, PCSK9i, and siRNA therapy have been used alone or in combination to reach LDL-C targets with earlier, more intensive, and longerduration lowering. High-dose EPA may be a worthwhile add-on treatment, especially in statin-treated post-ACS patients with elevated TG levels. Lp(a) lowering agents will be part of future prevention. Inflammation is a common pathway in cardiovascular diseases, and anti-inflammatory treatment has emerged as a novel therapy. Abundant evidence has been accumulated on the effects of colchicine, but little on IL-1β or IL-6 inhibitors. Immune modulation with Treg-based treatment and alterations in gut microbiome profiling show promising results for managing residual risk post-ACS. ACS: Acute coronary syndrome; DAPT: Dual antiplatelet therapy; EPA: Eicosapentaenoic acid; hsCRP: High-sensitivity C-reactive protein; IL: Interleukin; LDL-C: Low-density lipoprotein cholesterol; Lp(a): Lipoprotein (a); PCSK9i: Proprotein convertase subtilisin/kexin type 9 inhibitor; QFR: Quantitative flow ratio; RIPK3: Receptor-interacting protein kinase 3; siRNA: Small interfering RNA; TG: Triglyceride.

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Cardiology Discovery

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