Novel Targets and Strategies Addressing Residual Cardiovascular Risk in Post-acute Coronary Syndromes Patients

Transl Med UniSa. 2024 Aug 28;26(2):99-110. doi: 10.37825/2239-9747.1058. eCollection 2024.

Abstract

Despite the advancement in secondary cardiovascular prevention strategies for post-acute coronary syndrome (ACS) patients, the development of new drugs addressing dyslipidemia and the personalization of dual antiplatelet therapies (DAPT), these patients continue to suffer a significant incidence of recurrent ischemic events. Therefore, novel targets that can be tackled to reduce cardiovascular risk are needed to improve the outcome of this very high-risk population. The role of chronic inflammation and inflammasome in the development and progression of atherosclerosis has been broadly investigated in patients with established coronary artery disease (CAD) and recent randomized trials have highlighted the possibility to manage these targets with specific drugs such as colchicine and monocolonal antibodies with a significant improvement of cardiovascular outcomes in post-ACS patients. Lipoprotein(a) [Lp(a)] is the most promising non-traditional risk factor and has shown to predict worse outcome in post-ACS patients. Lowering Lp(a) through PCSK9 inhibitors and specific targeted therapies has shown positive results in reducing adverse cardiovascular events in patients with established CAD. The effect of microbiome and its alteration in gut dysbiosis seems to actively participate in residual cardiovascular risk of CAD patients; however, the risk-modifying effect of targeted-microbiome therapies hasn't been yet investigated in large population-based studies. Long-term outcome of post-ACS patients is a complex puzzle of multiple factors. In this minireview, we summarize the emerging risk factors that may interplay in the residual risk of post-ACS patients and their possible prognostic and therapeutic implications.

Keywords: Acute coronary syndrome; Coronary artery disease; Emerging therapies; Inflammasome; Inflammation; Lipoprotein(a); Microbiota; Secondary prevention.

Publication types

  • Review