Evidence map›Paper›PMID 42893181›Full record

ArticleAmerican journal of preventive cardiology2027

Temporal changes in lipoprotein(a) after acute coronary syndrome.

Christelle Lattouf, Mark Atallah, Nadim Nasrallah, Tarek Harb, Gary Gerstenblith, Thorsten M Leucker

Abstract read
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Article in American journal of preventive cardiology, 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Christelle LattoufDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Mark AtallahDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Nadim NasrallahDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Tarek HarbDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Gary GerstenblithDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Thorsten M LeuckerDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and aims: Lipoprotein(a) [Lp(a)] is an established independent risk factor for atherosclerotic cardiovascular disease and is traditionally considered stable. Its behavior following acute coronary syndrome (ACS) and clinical implications remain unclear. This study aimed to characterize the temporal trajectory of Lp(a) following ACS, evaluate whether baseline levels predict longitudinal changes, and assess the stability of clinically relevant Lp(a) risk categories. Methods: In this prospective study, 225 patients with ACS underwent serial Lp(a) measurements during hospitalization and at follow-up (≥6 months). Longitudinal changes were assessed using linear mixed-effects models. Associations between baseline Lp(a) and changes over time were evaluated using Spearman correlation. Stability of Lp(a) threshold risk categories (<50, 50-105, ≥105 nmol/L) was assessed by examining transitions across categories. Results: Lp(a) increased following ACS (p < 0.001), peaking at Days 4-7 (+30.0 %, p = 0.0001) and remaining elevated at Day 30 (+15.0 %, p = 0.0042), before returning to baseline at follow-up. Among individuals with increases in Lp(a), baseline Lp(a) was the strongest determinant of trajectory, with higher levels associated with greater increases at all timepoints (ρ 0.37-0.63, all p < 0.05). Categories for those evels in the low (<50 nmol/L) and high (≥105 nmol/L) categories remained stable with minimal reclassification. Variability was confined to levels in the intermediate range (50-105 nmol/L), where 37.5 % transitioned to ≥105 nmol/L. Conclusions: Lp(a) rises transiently after ACS and returns to baseline over time. Levels in the high and low risk categories remain in those categories, while variability is limited to the intermediate range. A single Lp(a) measurement obtained during ACS may be sufficient for individuals with clearly low or markedly elevated Lp(a) levels, whereas repeat testing after clinical stabilization may be considered for patients with intermediate or borderline baseline levels.

Indexed as

Acute coronary syndromeBiomarkersLipoprotein(a)Myocardial infarctionRisk stratificationTrajectory

Identifiers

PMID42893181
PMCPMC13676056

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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.