Key result
Elevated Lp(a) is linked to increased ischemic stroke risk via proatherogenic, proinflammatory, and prothrombotic properties.
Why the study?
Therapeutic interventions targeting Lp(a) are in development, and understanding the link between Lp(a) and ischemic stroke could improve ischemic stroke management and clinical awareness.
Does elevated Lipoprotein(a) increase the risk of ischemic stroke?
This review highlights the emerging evidence linking elevated Lipoprotein(a) to an increased risk of ischemic stroke, emphasizing its potential as a therapeutic target.
Lp(a) testing may refine stroke risk stratification; leaves open whether targeted lowering reduces events.
Lipoprotein(a) [Lp(a)], a particle similar to low-density lipoprotein, has been consistently identified as a significant risk factor for cardiovascular disease (CVD). Emerging data from epidemiological observation and genetic studies have demonstrated that elevated levels of Lp(a), primarily influenced by genetic variation, are associated with an increased risk of ischemic strokes (IS). This association may be attributed to the proatherogenic, proinflammatory, and prothrombotic properties of Lp(a). Although therapeutic interventions specifically aimed at reducing Lp(a) levels are still under development, understanding the relationship of Lp(a) and IS could aid in the management of IS. This review aims to present the clinical evidence, pathophysiological mechanisms, and potential implications linking Lp(a) to IS, with the goal of raising awareness of Lp(a) in real-world clinical practice for IS prevention and treatment.
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Yang et al. (2024) conducted a review in Ischemic stroke. Elevated Lipoprotein(a) was evaluated on Ischemic stroke. Elevated levels of Lipoprotein(a) are associated with an increased risk of ischemic stroke due to its proatherogenic, proinflammatory, and prothrombotic properties.
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