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Published on: October 12, 2017
Lipoprotein (a) and stroke
H J Milionis1, A F Winder, D P Mikhailidis
1Department of Molecular Pathology and Clinical Biochemistry, Royal Free and University College Medical School, University College, London, UK.
Insights
Lipoprotein (a) (Lp(a)) may predict ischemic stroke risk, but studies show conflicting results. This review explores Lp(a) mechanisms in stroke and potential therapies.
Area of Science:
- Cardiovascular Medicine
- Neurology
- Genetics
Background:
- Strokes are a leading cause of death and disability.
- Lipoprotein (a) (Lp(a)) is linked to vascular diseases like coronary artery disease.
- The association between Lp(a) and ischemic stroke is debated due to conflicting study findings.
Purpose of the Study:
- To review Lp(a)-related mechanisms in ischemic stroke pathogenesis.
- To discuss Lp(a) associations with other cardiovascular risk factors.
- To consider therapeutic strategies for lowering Lp(a) and stroke risk.
Main Methods:
- Literature review of cross-sectional and prospective studies.
- Analysis of Lp(a) related mechanisms in stroke.
- Discussion of confounding factors in existing research.
Main Results:
- Contradictory findings exist regarding Lp(a) as an ischemic stroke predictor.
- Factors like sample size, ethnicity, and statistical methods may explain discrepancies.
- Lp(a) mechanisms in stroke pathogenesis require further elucidation.
Conclusions:
- Understanding Lp(a)'s role in ischemic stroke is crucial.
- Further research is needed to clarify Lp(a) and stroke risk.
- Therapeutic lowering of Lp(a) may reduce stroke incidence.
Abstract:
Strokes are one of the most common causes of mortality and long term severe disability. There is evidence that lipoprotein (a) (Lp(a)) is a predictor of many forms of vascular disease, including premature coronary artery disease. Several studies have also evaluated the association between Lp(a) and ischaemic (thrombotic) stroke. Several cross sectional (and a few prospective) studies provide contradictory findings regarding Lp(a) as a predictor of ischaemic stroke. Several factors might contribute to the existing confusion--for example, small sample sizes, different ethnic groups, the influence of oestrogens in women participating in the studies, plasma storage before Lp(a) determination, statistical errors, and selection bias. This review focuses on the Lp(a) related mechanisms that might contribute to the pathogenesis of ischaemic stroke. The association between Lp(a) and other cardiovascular risk factors is discussed. Therapeutic interventions that can lower the circulating concentrations of Lp(a) and thus possibly reduce the risk of stroke are also considered.
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