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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
Lipoprotein (a) and cerebrovascular disease
Constantine E Kosmas1, Maria D Bousvarou2, Evangelia J Papakonstantinou3
12nd Department of Cardiology, National & Kapodistrian University of Athens, Athens, Greece.
Insights
Elevated lipoprotein (a) [Lp(a)] is linked to cerebrovascular events like stroke in adults and children. New Lp(a)-targeting therapies show promise for stroke prevention.
Area of Science:
- Cardiology
- Neurology
- Genetics
Background:
- Lipoprotein (a) [Lp(a)] is structurally similar to LDL cholesterol.
- Lp(a) is synthesized in the liver, with genetically determined plasma levels influenced by the LPA gene encoding apolipoprotein (a).
Purpose of the Study:
- To comprehensively review the role of Lp(a) in cerebrovascular disease.
- To examine the Lp(a)-cerebrovascular disease relationship from multiple perspectives.
Main Methods:
- Narrative review of pertinent studies.
- Analysis of epidemiological and Mendelian randomization data.
- Inclusion of data on pediatric patients and emerging therapies.
Main Results:
- Epidemiological studies show a positive correlation between high Lp(a) levels and cerebrovascular events, particularly ischemic strokes.
- The correlation is noted to be marginal in Mendelian randomization studies.
- Lp(a) appears significant in pediatric arterial ischemic stroke pathogenesis due to the absence of typical risk factors.
Conclusions:
- New Lp(a)-targeting agents are in Phase 3 trials for stroke risk reduction.
- Updated guidelines for Lp(a) screening and management are needed for effective primary and secondary stroke prevention.
Abstract:
The role of lipoprotein (a) [Lp(a)] in cerebrovascular disease is a topic of importance. In this narrative review, pertinent studies have been leveraged to comprehensively examine this relationship from diverse perspectives.Lp(a) shares structural traits with low-density lipoprotein cholesterol. Lp(a) is synthesized by hepatocytes, and its plasma levels are genetically determined by the LPA gene, which produces apolipoprotein (a).Numerous epidemiological studies have confirmed the positive correlation between elevated serum Lp(a) levels and the occurrence or recurrence of cerebrovascular events, especially ischemic strokes, in adults. It should be noted that the correlation strength varies among studies and is marginal in Mendelian randomization studies.Regarding pediatric patients, screening is currently limited to those with a relevant medical history. Lp(a) seems to play a significant role in the pathogenesis of arterial ischemic stroke in children because environmental thrombotic and atherogenic factors are generally not present.Phase 3 trials of novel Lp(a) targeting agents, such as pelacarsen and olpasiran, are anticipated to demonstrate their efficacy in reducing the incidence of stroke. Given the richness of the literature, new guidelines regarding Lp(a) screening and management in targeted populations are warranted to provide more effective primary and secondary prevention.
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