Lipid-Lowering Therapy after Acute Coronary Syndrome.

PCSK9-inhibitor acute coronary syndrome bempedoic acid cardiovascular disease ezetimibe inclisiran lipid-lowering therapy secondary prevention statins

Journal

Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588

Informations de publication

Date de publication:
01 Apr 2024
Historique:
received: 05 03 2024
revised: 27 03 2024
accepted: 30 03 2024
medline: 13 4 2024
pubmed: 13 4 2024
entrez: 13 4 2024
Statut: epublish

Résumé

Achieving guideline-recommended low-density lipoprotein cholesterol (LDL-C) targets remains a significant challenge in clinical practice. This review assesses the barriers to reaching LDL-C goals and explores the potential solutions to these issues. When aiming for the recommended LDL-C goal, strategies like "lower is better" and "strike early and strong" should be used. The evidence supports the safety and efficacy of intensive lipid-lowering therapy post-acute coronary syndrome (ACS), leading to improved long-term cardiovascular health and atherosclerotic plaque stabilization. Despite the availability of effective lipid-lowering therapies, such as high-intensity statins, ezetimibe, the combination of both, bempedoic acid, and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, a substantial proportion of patients do not meet their LDL-C targets. Contributing factors include systemic healthcare barriers, healthcare provider inertia, patient non-adherence, and statin intolerance. Statin intolerance, often rather statin reluctance, is a notable obstacle due to perceived or expected side effects, which can lead to discontinuation of therapy. In conclusion, while there are obstacles to achieving optimal LDL-C levels post-ACS, these can be overcome with a combination of patient-centric approaches, clinical vigilance, and the judicious use of available therapies. The safety and necessity of reaching lower LDL-C goals to improve outcomes in patients post-ACS are well-supported by current evidence.

Identifiants

pubmed: 38610808
pii: jcm13072043
doi: 10.3390/jcm13072043
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Auteurs

Edita Pogran (E)

3rd Medical Department for Cardiology and Intensive Care Medicine, Klinik Ottakring, 1160 Vienna, Austria.
Medical Faculty, Sigmund Freud University, 1020 Vienna, Austria.

Achim Leo Burger (AL)

3rd Medical Department for Cardiology and Intensive Care Medicine, Klinik Ottakring, 1160 Vienna, Austria.
Medical Faculty, Sigmund Freud University, 1020 Vienna, Austria.

David Zweiker (D)

3rd Medical Department for Cardiology and Intensive Care Medicine, Klinik Ottakring, 1160 Vienna, Austria.

Christoph Clemens Kaufmann (CC)

3rd Medical Department for Cardiology and Intensive Care Medicine, Klinik Ottakring, 1160 Vienna, Austria.
Medical Faculty, Sigmund Freud University, 1020 Vienna, Austria.

Marie Muthspiel (M)

3rd Medical Department for Cardiology and Intensive Care Medicine, Klinik Ottakring, 1160 Vienna, Austria.
Medical Faculty, Sigmund Freud University, 1020 Vienna, Austria.

Gersina Rega-Kaun (G)

5th Medical Department with Endocrinology, Rheumatology and Acute Geriatrics, Klinik Ottakring, 1160 Vienna, Austria.

Alfa Wenkstetten-Holub (A)

5th Medical Department with Endocrinology, Rheumatology and Acute Geriatrics, Klinik Ottakring, 1160 Vienna, Austria.

Johann Wojta (J)

Ludwig Boltzmann Institute for Cardiovascular Research, 1090 Vienna, Austria.
Core Facilities, Medical University of Vienna, 1090 Vienna, Austria.

Heinz Drexel (H)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Carinagasse 47, 6800 Feldkirch, Austria.

Kurt Huber (K)

3rd Medical Department for Cardiology and Intensive Care Medicine, Klinik Ottakring, 1160 Vienna, Austria.
Medical Faculty, Sigmund Freud University, 1020 Vienna, Austria.
Ludwig Boltzmann Institute for Cardiovascular Research, 1090 Vienna, Austria.

Classifications MeSH