ReviewBiomedicines2026
Lipoprotein(a) After Myocardial Infarction: Residual Risk, Measurement, and the Unresolved Therapeutic Question.
Review in Biomedicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Lipoprotein(a) [Lp(a)] is a highly heritable apoB-containing lipoprotein and a causal contributor to atherosclerotic cardiovascular disease that may contribute to residual cardiovascular risk after myocardial infarction (MI), while the clinical benefit of selective pharmacological Lp(a) lowering remains unresolved. This narrative review examines Lp(a) as a determinant of residual and recurrent cardiovascular risk after MI, integrating molecular biology, human genetics, coronary imaging, post-MI observational studies, measurement considerations, current management, and emerging therapies. Elevated Lp(a) has been associated with coronary plaque progression, high-risk plaque features, oxidized-phospholipid-related inflammatory pathways, recurrent ischemic events, and repeat revascularization, although prognostic associations vary across populations and endpoints. Because concentrations measured during acute MI may underestimate the stable Lp(a) phenotype in some patients, selective repeat measurement after clinical stabilization may be appropriate when classification could influence management or trial eligibility. Contemporary treatment remains centered on intensive control of LDL-C and other modifiable risk factors, while antisense oligonucleotides, small interfering RNAs, and oral particle-assembly inhibitors can produce profound Lp(a) reductions. According to sponsor-reported topline data released in September 2026, pelacarsen lowered Lp(a) but did not significantly reduce the prespecified primary cardiovascular endpoint in the overall Lp(a)HORIZON population; complete peer-reviewed results are not yet available. The sponsor-reported neutral HORIZON topline result raises unresolved questions regarding baseline Lp(a) and absolute reduction, timing of intervention and disease stage, and endpoint composition. Full peer-reviewed HORIZON data and ongoing cardiovascular outcome trials will be required to determine whether and under what conditions selective Lp(a) lowering translates into cardiovascular benefit.
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Registered trials
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