RESUMEN
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.
RESUMEN
Over the last decades, bioprosthetic heart valves (BHV) have been increasingly implanted instead of mechanical valves in patients undergoing surgical aortic valve replacement (SAVR). Structural valve deterioration (SVD) is a common issue at follow-up and can justify the need for a reintervention. In the evolving landscape of interventional cardiology, valve-in-valve transcatheter aortic valve replacement (ViV TAVR) has emerged as a remarkable innovation to address the complex challenges of patients previously treated with SAVR and has rapidly gained prominence as a feasible technique especially in patients at high surgical risk. On the other hand, the expanding indications for TAVR in progressively younger patients with severe aortic stenosis pose the crucial question on the long-term durability of transcatheter heart valves (THVs), as patients might outlive the bioprosthetic valve. In this review, we provide an overview on the role of ViV TAVR for failed surgical and transcatheter BHVs, with a specific focus on current clinical evidence, pre-procedural planning, procedural techniques, and possible complications. The combination of integrated Heart Team discussion with interventional growth curve makes it possible to achieve best ViV TAVR results and avoid complications or put oneself ahead of time from them.
RESUMEN
Current research on cardiovascular prevention predominantly focuses on risk-stratification and management of patients with coronary artery disease (CAD) to optimize their prognosis. Several basic, translational and clinical research efforts aim to determine the etiological mechanisms underlying CAD pathogenesis and to identify lifestyle-dependent metabolic risk factors or genetic and epigenetic parameters responsible for CAD occurrence and/or progression. A log-linear association between the absolute exposure of LDL cholesterol (LDL-C) and the risk of atherosclerotic cardio-vascular disease (ASCVD) was well documented over the year. LDL-C was identified as the principal enemy to fight against, and soluble proprotein convertase subtilisin kexin type 9 (PCSK9) was attributed the role of a powerful regulator of blood LDL-C levels. The two currently available antibodies (alirocumab and evolocumab) against PCSK9 are fully human engineered IgG that bind to soluble PCSK9 and avoid its interaction with the LDLR. As documented by modern and dedicated "game-changer" trials, antibodies against soluble PCSK9 reduce LDL-C levels by at least 60 percent when used alone and up to 85 percent when used in combination with high-intensity statins and/or other hypolipidemic therapies, including ezetimibe. Their clinical indications are well established, but new areas of use are advocated. Several clues suggest that regulation of PCSK9 represents a cornerstone of cardiovascular prevention, partly because of some pleiotropic effects attributed to these newly developed drugs. New mechanisms of PCSK9 regulation are being explored, and further efforts need to be put in place to reach patients with these new therapies. The aim of this manuscript is to perform a narrative review of the literature on soluble PCSK9 inhibitor drugs, with a focus on their indications and clinical impact.