Pub Date : 2025-01-01DOI: 10.1016/j.arteri.2024.04.004
Kung-Hung Lin , Nuria Amigo , Pablo Ortiz , Cristina Alonso , Alexander V. Smolensky , Deven Parmar , Naga P. Chalasani , Samer Gawrieh
Background and aims
Comprehensive assessment of pharmacotherapy effects on atherogenic parameters (AP) that influence the risk of cardiovascular disease (CVD) is challenging due to interactions among a large number of parameters that modulate CVD risk.
Methods
We developed an illustrative tool, athero-contour (AC), which incorporates weighted key lipid, lipo- and glycoprotein parameters, to readily illustrate their overall changes following pharmacotherapy. We demonstrate the applicability of AC to assess changes in AP in response to saroglitazar treatment in patients with metabolic associated fatty liver disease (MAFLD) in the EVIDENCES IV study.
Results
The baseline AC of saroglitazar and placebo groups was worse than the mean of the general population. After 16-week treatment, AC improved significantly in the saroglitazar group due to alterations in very low-density lipoprotein, triglyceride, and glycoproteins.
Conclusion
Using AC, we could readily and globally evaluate and visualize changes in AP. AC improved in patients with MAFLD following saroglitazar therapy.
背景和目的：全面评估药物治疗对影响心血管疾病（CVD）风险的致动脉粥样硬化参数（AP）的影响具有挑战性，因为调节心血管疾病风险的大量参数之间存在相互作用：方法：我们开发了一种说明性工具--动脉粥样硬化轮廓（AC），它结合了加权的主要血脂、脂质和糖蛋白参数，可方便地说明药物治疗后这些参数的整体变化。我们在 EVIDENCES IV 研究中展示了 AC 的适用性，以评估代谢相关性脂肪肝（MAFLD）患者在接受沙格列扎治疗后 AP 的变化：结果：沙格列扎和安慰剂组的基线血浆浓度比一般人群的平均值低。经过16周的治疗后，由于极低密度脂蛋白、甘油三酯和糖蛋白的改变，沙格列扎尔组的AC明显改善：通过 AC，我们可以轻松、全面地评估和观察 AP 的变化。接受沙格列扎治疗后，MAFLD 患者的 AC 有所改善。
{"title":"The athero-contour: A novel tool for global and rapid assessment of atherogenic parameters. A use case in saroglitazar treatment of MAFLD patients","authors":"Kung-Hung Lin , Nuria Amigo , Pablo Ortiz , Cristina Alonso , Alexander V. Smolensky , Deven Parmar , Naga P. Chalasani , Samer Gawrieh","doi":"10.1016/j.arteri.2024.04.004","DOIUrl":"10.1016/j.arteri.2024.04.004","url":null,"abstract":"<div><h3>Background and aims</h3><div>Comprehensive assessment of pharmacotherapy effects on atherogenic parameters (AP) that influence the risk of cardiovascular disease (CVD) is challenging due to interactions among a large number of parameters that modulate CVD risk.</div></div><div><h3>Methods</h3><div>We developed an illustrative tool, athero-contour (AC), which incorporates weighted key lipid, lipo- and glycoprotein parameters, to readily illustrate their overall changes following pharmacotherapy. We demonstrate the applicability of AC to assess changes in AP in response to saroglitazar treatment in patients with metabolic associated fatty liver disease (MAFLD) in the EVIDENCES IV study.</div></div><div><h3>Results</h3><div>The baseline AC of saroglitazar and placebo groups was worse than the mean of the general population. After 16-week treatment, AC improved significantly in the saroglitazar group due to alterations in very low-density lipoprotein, triglyceride, and glycoproteins.</div></div><div><h3>Conclusion</h3><div>Using AC, we could readily and globally evaluate and visualize changes in AP. AC improved in patients with MAFLD following saroglitazar therapy.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 1","pages":"Article 100723"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.arteri.2024.10.001
Emilio Ros , Pablo Pérez-Martínez , Ramón Estruch , José López-Miranda , Cristina Soler Ferrer , Javier Delgado-Lista , Francisco Gómez-Delgado , Rosa Solà , Vicente Pascual
{"title":"Documento de recomendaciones de la Sociedad Española de Arteriosclerosis (SEA). La dieta en la prevención cardiovascular. Actualizacion 2024","authors":"Emilio Ros , Pablo Pérez-Martínez , Ramón Estruch , José López-Miranda , Cristina Soler Ferrer , Javier Delgado-Lista , Francisco Gómez-Delgado , Rosa Solà , Vicente Pascual","doi":"10.1016/j.arteri.2024.10.001","DOIUrl":"10.1016/j.arteri.2024.10.001","url":null,"abstract":"","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 1","pages":"Article 100741"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.11.001
María José Ariza Corbo , Ovidio Muñiz-Grijalvo , Agustín Blanco Echevarría , J.L. Díaz-Díaz
The development of massive sequencing techniques and guidelines for assessing the pathogenicity of variants are allowing us the identification of new cases of familial chylomicronemia syndrome (FCS) mostly in the LPL gene, less frequently in GPIHBP1 and APOA5, and with even fewer cases in LMF1 and APOC2. From the included studies, it can be deduced that, in cases with multifactorial chylomicronemia syndrome (MCS), both loss-of-function variants and common variants in canonical genes for FCH contribute to the manifestation of this other form of chylomicronemia. Other common and rare variants in other triglyceride metabolism genes have been identified in MCS patients, although their real impact on the development of severe hypertriglyceridemia is unknown. There may be up to 60 genes involved in triglyceride metabolism, so there is still a long way to go to know whether other genes not discussed in this monograph (MLXIPL, PLTP, TRIB1, PPAR alpha or USF1, for example) are genetic determinants of severe hypertriglyceridemia that need to be taken into account.
{"title":"Bases genéticas de las hipertrigliceridemias","authors":"María José Ariza Corbo , Ovidio Muñiz-Grijalvo , Agustín Blanco Echevarría , J.L. Díaz-Díaz","doi":"10.1016/j.arteri.2024.11.001","DOIUrl":"10.1016/j.arteri.2024.11.001","url":null,"abstract":"<div><div>The development of massive sequencing techniques and guidelines for assessing the pathogenicity of variants are allowing us the identification of new cases of familial chylomicronemia syndrome (FCS) mostly in the LPL gene, less frequently in GPIHBP1 and APOA5, and with even fewer cases in LMF1 and APOC2. From the included studies, it can be deduced that, in cases with multifactorial chylomicronemia syndrome (MCS), both loss-of-function variants and common variants in canonical genes for FCH contribute to the manifestation of this other form of chylomicronemia. Other common and rare variants in other triglyceride metabolism genes have been identified in MCS patients, although their real impact on the development of severe hypertriglyceridemia is unknown. There may be up to 60 genes involved in triglyceride metabolism, so there is still a long way to go to know whether other genes not discussed in this monograph (MLXIPL, PLTP, TRIB1, PPAR alpha or USF1, for example) are genetic determinants of severe hypertriglyceridemia that need to be taken into account.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S3-S12"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.11.002
Carlos Lahoz, Xavier Pintó
{"title":"Nuevos horizontes en el tratamiento de la hipercolesterolemia","authors":"Carlos Lahoz, Xavier Pintó","doi":"10.1016/j.arteri.2024.11.002","DOIUrl":"10.1016/j.arteri.2024.11.002","url":null,"abstract":"","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S1-S2"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.10.005
José Luis Díaz Díaz
{"title":"Hipertrigliceridemias graves: lo necesario y lo suficiente","authors":"José Luis Díaz Díaz","doi":"10.1016/j.arteri.2024.10.005","DOIUrl":"10.1016/j.arteri.2024.10.005","url":null,"abstract":"","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S1-S2"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.10.004
Carlos Guijarro
The role of cholesterol associated to low density lipoproteins (LDL) as a causal agent of arteriosclerosis is scientifically consolidated. A number of seminal clinical trials of the highest scientific quality (randomized, controlled, double-blind versus placebo) in the last 40 years have confirmed that lipid lowering therapy with progressively ambitious therapeutic goals is associated with reductions in cardiovascular complications in the absence of major side effects at least up to the range of 30 mg/dL of LDL cholesterol. Drugs that have demonstrated these effects act by reducing circulating LDL cholesterol by upregulating the LDL receptor, independently of their primary action: inhibition of synthesis (statins, bempedoic acid), or absorption of cholesterol (ezetimibe) and promoting recycling of the LDL receptor via proprotein conversin subtilisine kexin 9 blockade. The early reduction of LDL cholesterol and its maintenance over time reinforce the protective effect of these drugs. Additional efforts are needed to improve the LDL control of high-risk patients to reduce their cardiovascular complications.
{"title":"El control estricto del colesterol aterogénico en la prevención de las enfermedades cardiovasculares","authors":"Carlos Guijarro","doi":"10.1016/j.arteri.2024.10.004","DOIUrl":"10.1016/j.arteri.2024.10.004","url":null,"abstract":"<div><div>The role of cholesterol associated to low density lipoproteins (LDL) as a causal agent of arteriosclerosis is scientifically consolidated. A number of seminal clinical trials of the highest scientific quality (randomized, controlled, double-blind versus placebo) in the last 40 years have confirmed that lipid lowering therapy with progressively ambitious therapeutic goals is associated with reductions in cardiovascular complications in the absence of major side effects at least up to the range of 30<!--> <!-->mg/dL of LDL cholesterol. Drugs that have demonstrated these effects act by reducing circulating LDL cholesterol by upregulating the LDL receptor, independently of their primary action: inhibition of synthesis (statins, bempedoic acid), or absorption of cholesterol (ezetimibe) and promoting recycling of the LDL receptor via proprotein conversin subtilisine kexin 9 blockade. The early reduction of LDL cholesterol and its maintenance over time reinforce the protective effect of these drugs. Additional efforts are needed to improve the LDL control of high-risk patients to reduce their cardiovascular complications.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S9-S14"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.10.006
Agustín Blanco Echevarría , María José Ariza Corbo , Ovidio Muñiz-Grijalvo , José Luis Díaz-Díaz
Familial chylomicronemia syndrome (FCS) is a very rare, underdiagnosed disorder that can cause abdominal pain and recurrent pancreatitis from childhood —potentially life-threatening— and chronic complications such as diabetes mellitus and exocrine pancreatic insufficiency. FCS affects the quality of life and mental health of those who suffer from it, aspects that must be taken into account in its treatment, based on a strict low-fat diet, which is difficult to adhere to and persist. People with FCS lack the lipolytic capacity to hydrolyze triglycerides (TG) and have a minimal or null response to conventional lipid-lowering treatments. ApoCIII antagonists, specifically volanesorsen, olezarsen and ARO-APOC3, are the most promising drugs to reduce TG concentrations in patients with FCS. Anti-ANGPTL3 therapies appear to be less effective. More clinical trials and new pharmacological treatments are needed to improve the quality of life and prognosis of people with FCS.
{"title":"Quilomicronemia familiar: nuevas perspectivas","authors":"Agustín Blanco Echevarría , María José Ariza Corbo , Ovidio Muñiz-Grijalvo , José Luis Díaz-Díaz","doi":"10.1016/j.arteri.2024.10.006","DOIUrl":"10.1016/j.arteri.2024.10.006","url":null,"abstract":"<div><div>Familial chylomicronemia syndrome (FCS) is a very rare, underdiagnosed disorder that can cause abdominal pain and recurrent pancreatitis from childhood —potentially life-threatening— and chronic complications such as diabetes mellitus and exocrine pancreatic insufficiency. FCS affects the quality of life and mental health of those who suffer from it, aspects that must be taken into account in its treatment, based on a strict low-fat diet, which is difficult to adhere to and persist. People with FCS lack the lipolytic capacity to hydrolyze triglycerides (TG) and have a minimal or null response to conventional lipid-lowering treatments. ApoCIII antagonists, specifically volanesorsen, olezarsen and ARO-APOC3, are the most promising drugs to reduce TG concentrations in patients with FCS. Anti-ANGPTL3 therapies appear to be less effective. More clinical trials and new pharmacological treatments are needed to improve the quality of life and prognosis of people with FCS.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S18-S24"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.07.001
Juan Pedro-Botet , Elisenda Climent , David Benaiges
Atherosclerosis is a chronic disease that begins in early childhood, and without intervention, progresses throughout life, and inevitably worsens over time, sometimes rapidly. LDL cholesterol, beyond being a cardiovascular risk factor, is a causal agent of atherosclerosis. Without LDL cholesterol there is no atherosclerosis, so the evolution of the disease is modifiable, and even reversible.
{"title":"El colesterol LDL como agente causal de la aterosclerosis","authors":"Juan Pedro-Botet , Elisenda Climent , David Benaiges","doi":"10.1016/j.arteri.2024.07.001","DOIUrl":"10.1016/j.arteri.2024.07.001","url":null,"abstract":"<div><div>Atherosclerosis is a chronic disease that begins in early childhood, and without intervention, progresses throughout life, and inevitably worsens over time, sometimes rapidly. LDL cholesterol, beyond being a cardiovascular risk factor, is a causal agent of atherosclerosis. Without LDL cholesterol there is no atherosclerosis, so the evolution of the disease is modifiable, and even reversible.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S3-S8"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141753080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.07.003
José López-Miranda
Hypercholesterolemia is a causal factor of atherosclerotic cardiovascular disease (ASCVD), which is one of the main causes of morbidity and mortality in Spain. The reduction of LDL cholesterol (LDL-C) decreases the risk of ASCVD and adverse cardiovascular events. Targeted therapy for the proprotein convertase subtilisin/kexin type 9 (PCSK-9) has emerged as a novel tool for the treatment of hyperlipidemia. Inclisiran is a small double-stranded small interfering RNA that acts by blocking PCSK-9 transcription in hepatocytes, leading to a marked and sustained reduction in circulating LDL-C levels. In contrast to other lipid-lowering therapies such as statins, ezetimibe and monoclonal antibodies PCSK-9 inhibitors, Inclisiran proposes an infrequent dosing regimen of twice times a year. Its prolonged effect represents an advantage over non-compliance of the treatment, which is one of the main reasons why LDL-C goals are not achieved with standard therapy. This review aims to present and discuss current scientific data regarding the efficacy, tolerability and safety of Inclisiran in the treatment of hypercholesterolemia. Inclisiran has been shown to provide significant long-term reductions in LDL-C levels associated with notable decreases in levels of PCSK9 and other atherogenic lipoproteins with a highly favourable side effect profile similar to placebo. The convenience of a twice-yearly dosing regimen promotes adherence to therapy and facilitates achievement of LDL-C goals. Results from ongoing trials designed to determine its effect on cardiovascular events are expected to provide further information about the cardiovascular benefit of inclisiran in patients with ACVD and in patients at high cardiovascular risk.
{"title":"Eficacia, beneficio y seguridad de inclisiran","authors":"José López-Miranda","doi":"10.1016/j.arteri.2024.07.003","DOIUrl":"10.1016/j.arteri.2024.07.003","url":null,"abstract":"<div><div>Hypercholesterolemia is a causal factor of atherosclerotic cardiovascular disease (ASCVD), which is one of the main causes of morbidity and mortality in Spain. The reduction of LDL cholesterol (LDL-C) decreases the risk of ASCVD and adverse cardiovascular events. Targeted therapy for the proprotein convertase subtilisin/kexin type 9 (PCSK-9) has emerged as a novel tool for the treatment of hyperlipidemia. Inclisiran is a small double-stranded small interfering RNA that acts by blocking PCSK-9 transcription in hepatocytes, leading to a marked and sustained reduction in circulating LDL-C levels. In contrast to other lipid-lowering therapies such as statins, ezetimibe and monoclonal antibodies PCSK-9 inhibitors, Inclisiran proposes an infrequent dosing regimen of twice times a year. Its prolonged effect represents an advantage over non-compliance of the treatment, which is one of the main reasons why LDL-C goals are not achieved with standard therapy. This review aims to present and discuss current scientific data regarding the efficacy, tolerability and safety of Inclisiran in the treatment of hypercholesterolemia. Inclisiran has been shown to provide significant long-term reductions in LDL-C levels associated with notable decreases in levels of PCSK9 and other atherogenic lipoproteins with a highly favourable side effect profile similar to placebo. The convenience of a twice-yearly dosing regimen promotes adherence to therapy and facilitates achievement of LDL-C goals. Results from ongoing trials designed to determine its effect on cardiovascular events are expected to provide further information about the cardiovascular benefit of inclisiran in patients with ACVD and in patients at high cardiovascular risk.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S24-S30"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.arteri.2024.07.004
Lluís Masana, Daiana Ibarretxe
Despite the various therapeutic tools available, many patients do not achieve therapeutic goals, and cardiovascular diseases remain a significant cause of death in our setting. Furthermore, even in patients who manage to reduce their LDL-C levels to the recommended targets, cardiovascular events continue to occur.
The therapeutic challenge and the persistent risk have led to active research into new drugs targeting novel therapeutic pathways in the field of lipoprotein metabolism disorders. The therapeutic approach involves new pharmacological mechanisms, ranging from small molecules and monoclonal antibodies to RNA interference, with inclisiran being the first drug approved for clinical use in the cardiovascular domain.
In this review, we aim to provide a comprehensive overview of the new therapeutic targets and pharmacological mechanisms under development, as well as their potential clinical impact.
{"title":"Nuevos fármacos para tratar las dislipemias. De las pequeñas moléculas a los ARN pequeños de interferencia","authors":"Lluís Masana, Daiana Ibarretxe","doi":"10.1016/j.arteri.2024.07.004","DOIUrl":"10.1016/j.arteri.2024.07.004","url":null,"abstract":"<div><div>Despite the various therapeutic tools available, many patients do not achieve therapeutic goals, and cardiovascular diseases remain a significant cause of death in our setting. Furthermore, even in patients who manage to reduce their LDL-C levels to the recommended targets, cardiovascular events continue to occur.</div><div>The therapeutic challenge and the persistent risk have led to active research into new drugs targeting novel therapeutic pathways in the field of lipoprotein metabolism disorders. The therapeutic approach involves new pharmacological mechanisms, ranging from small molecules and monoclonal antibodies to RNA interference, with inclisiran being the first drug approved for clinical use in the cardiovascular domain.</div><div>In this review, we aim to provide a comprehensive overview of the new therapeutic targets and pharmacological mechanisms under development, as well as their potential clinical impact.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"36 ","pages":"Pages S15-S23"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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