Evidence map›Paper›PMID 41843791›Full record

ReviewAnatolian journal of cardiology2026

Managing Progressive Atherosclerotic Cardiovascular Disease in a Patient with Elevated Lipoprotein(a).

Ece Yurtseven, Lale Tokgözoğlu

Abstract readReview
In one paragraph

Review in Anatolian journal of cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Ece YurtsevenDepartment of Cardiology, Koç University School of Medicine, İstanbul, Türkiye.
Lale TokgözoğluDepartment of Cardiology, Hacettepe University Faculty of Medicine, İstanbul, Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein(a) [Lp(a)] is a genetically determined, proatherogenic, and prothrombotic lipoprotein associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Elevated Lp(a) levels are associated with progressive ASCVD even when guideline-recommended low-density lipoprotein cholesterol (LDL-C) targets are achieved under optimal lipid-lowering therapy. There is currently no approved pharmacological therapy specifically targeting Lp(a) reduction in routine clinical practice; therefore, current management strategies for patients with elevated Lp(a) primarily focus on aggressive control of modifiable cardiovascular risk factors and intensive LDL-C lowering. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors provide a modest reduction in Lp(a) levels and have been associated with greater cardiovascular benefit in patients with high baseline Lp(a); however, this degree of reduction is often insufficient in individuals with markedly elevated Lp(a) levels and progressive ASCVD. At present, lipoprotein apheresis remains the only therapeutic option capable of achieving substantial and sustained reductions in Lp(a) concentrations and is recommended in selected high-risk patients with progressive ASCVD despite optimal medical therapy. Meanwhile, Lp(a)-specific therapies, including antisense oligonucleotides and small interfering RNA agents, are in advanced clinical development and have shown marked reductions in Lp(a) levels in early phase trials. These emerging therapies are expected to significantly change future treatment strategies for patients with Lp(a)-driven residual cardiovascular risk.

Identifiers

PMID41843791
PMCPMC13176596

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.