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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
From LDL-C to lipoprotein(a) - those who fail to learn from history are doomed to repeat it
Ashish Sarraju1,2, Steve E Nissen1,2
1Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH 44195, USA.
Insights
Suboptimal use of LDL-C therapies persists despite their importance in managing atherosclerotic cardiovascular disease (ASCVD). Lessons learned can guide future strategies for residual ASCVD risk reduction, including novel lipoprotein (a) therapies.
Area of Science:
- Cardiology
- Pharmacology
- Public Health
Background:
- Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of mortality globally.
- Despite available therapies like statins, achieving low-density lipoprotein cholesterol (LDL-C) goals is suboptimal.
- Residual ASCVD risk persists even with LDL-C lowering, necessitating alternative strategies.
Purpose of the Study:
- To review lessons from suboptimal LDL-C therapy implementation.
- To inform future strategies for residual ASCVD risk reduction.
- To highlight the potential of novel therapies targeting lipoprotein (a) (Lp(a)).
Main Methods:
- Literature review of LDL-C therapy implementation.
- Analysis of factors contributing to residual ASCVD risk.
- Examination of emerging Lp(a)-lowering therapies and clinical trials.
Main Results:
- Suboptimal attainment of LDL-C goals impacts ASCVD risk management.
- Lipoprotein (a) (Lp(a)) is a key target for novel therapies.
- Ongoing trials are evaluating the efficacy of Lp(a)-lowering agents on ASCVD events.
Conclusions:
- Lessons from LDL-C therapy implementation are crucial for future residual risk strategies.
- Effective implementation of novel Lp(a) therapies could significantly reduce ASCVD events.
- Future research and clinical practice should focus on comprehensive ASCVD risk reduction beyond LDL-C.
Abstract:
Reducing plasma low-density lipoprotein cholesterol (LDL-C) levels is a critical component of managing atherosclerotic cardiovascular disease (ASCVD) risk. However, LDL-C goal attainment and the use of LDL-C lowering therapies, which include cost-effective statins and multiple non-statin therapies, have remained suboptimal. In this setting, ASCVD remains the leading cause of morbidity and mortality in the US and globally. Due to persistent ASCVD risk despite LDL-C lowering, there has been strong interest in approaches to identify factors contributing to residual ASCVD risk beyond LDL-C levels. In particular, lipoprotein (a) [Lp (a)] has emerged as a leading target for multiple ongoing development programs of novel, potent pharmacologic agents that decrease Lp (a) levels, with ongoing clinical trials evaluating their effects on ASCVD events. This review outlines key lessons learned from the suboptimal implementation of LDL-C therapies that may be relevant to better implementation of future residual ASCVD risk reduction strategies, particularly for Lp (a) therapies that may be proven in clinical trials and approved by regulatory authorities in the future.
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