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Changes in lipoprotein(a) concentrations in patients with acute coronary syndrome
Joanna Satała1, Anna Witkowska2, Agnieszka Pawlos2
1Department of Internal Diseases and Clinical Pharmacology, Laboratory of Tissue Immunopharmacology, Medical University of Lodz, Łódź, Poland. Joanna.satala@umed.lodz.pl
Insights
Lipoprotein(a) levels increase significantly 3 months after acute coronary syndrome (ACS). This suggests ACS is a non-genetic factor influencing lipoprotein(a) concentration, impacting cardiovascular risk assessment.
Area of Science:
- Cardiology
- Biochemistry
- Clinical Medicine
Background:
- Lipoprotein(a) (Lp[a]) is an independent cardiovascular disease risk factor.
- Lp[a] levels, once thought to be solely genetic, may change over time.
- Current guidelines recommend Lp[a] measurement for cardiovascular risk stratification.
Purpose of the Study:
- To compare changes in Lp[a] concentration in acute coronary syndrome (ACS) patients.
- To assess Lp[a] levels at the time of ACS and 3 months post-event.
Main Methods:
- Forty ACS patients were categorized into STEMI and NSTEMI+UA groups.
- Routine laboratory methods and ELISA were used to measure Lp(a) and other biomarkers.
- Lp(a) levels were assessed at ACS onset and 3 months later.
Main Results:
- Elevated Lp(a) levels (>75 nmol/l) were found in 22.5% of ACS patients, higher in STEMI.
- All ACS patients exhibited significantly higher serum Lp(a) levels 3 months post-ACS.
- Significant differences in Lp(a) levels were observed at 3 months compared to ACS onset in STEMI, NSTEMI+UA, and overall ACS groups.
Conclusions:
- Lp[a] concentration increases 3 months after ACS.
- Measuring Lp(a) solely at the time of ACS may be insufficient for diagnosis and treatment.
- Acute coronary syndrome is identified as a non-genetic factor influencing Lp(a) levels.
Introduction:
Recently, interest has been growing in lipoprotein(a) (Lp[a]) as an independent risk factor for cardiovascular diseases. European Society of Cardiology recommends a single measurement of Lp(a) concentration as a guide to determine cardiovascular risk group and appropriate treatment. Although initially assumed to be genetically determined, a growing number of reports indicate that Lp(a) concentration may change over time.
Objectives:
The aim of the study was to compare changes in the concentration of Lp(a) in patients with acute coronary syndrome (ACS) at the moment of ACS and 3 months later.
Patients And Methods:
Forty patients with ACS were enrolled and divided into ST‑segment elevation myocardial infarction (STEMI) and non‑STEMI (NSTEMI) + unstable angina (UA) groups. The levels of lipids, C‑reactive protein, high‑sensitivity troponin T, N-terminal pro-B-type natriuretic peptide, and Lp(a) were determined using routine laboratory methods, with interleukin‑33 levels measured using an enzyme‑linked immunosorbent assay.
Results:
Among all ACS patients, 9 (22.5%) had elevated Lp(a) levels (>75 nmol/l). This proportion was higher in the STEMI (n = 8; 35%) than NSTEMI+UA (n = 2; 13%) patients. All patients with ACS showed significantly higher serum Lp(a) levels 3 months after ACS. The Lp(a) level at the moment of ACS and 3 months later differed markedly in the STEMI patients (P = 0.03), all patients with ACS (P = 0.003), and NSTEMI+UA individuals (P = 0.003).
Conclusion:
Measuring Lp(a) level during ACS may be insufficient for accurate diagnosis and effective treatment, as its concentration increases 3 months post‑ACS. Therefore, ACS may be regarded as another nongenetic factor influencing Lp(a) concentration.
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