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Association of Lipoprotein(a) With Major Adverse Cardiovascular Events Across hs-CRP: A Systematic Review and
Pamela L Alebna1, Chin Yip Han2, Mathew Ambrosio3
1Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia, USA.
Insights
Elevated Lipoprotein(a) [Lp(a)] increases the risk of major adverse cardiovascular events (MACE) regardless of high-sensitivity C-reactive protein (hs-CRP) levels. This association holds true for both primary and secondary cardiovascular prevention strategies.
Area of Science:
- Cardiology
- Biochemistry
- Epidemiology
Background:
- Lipoprotein(a) [Lp(a)] is recognized as an independent risk factor for atherosclerotic cardiovascular disease.
- The interplay between Lp(a) and major adverse cardiovascular events (MACE) in relation to high-sensitivity C-reactive protein (hs-CRP) levels is not fully understood, with prior research yielding conflicting outcomes.
Purpose of the Study:
- To conduct a systematic review and meta-analysis to elucidate the association between Lp(a) and MACE risk across varying hs-CRP levels.
- To evaluate this association in both primary and secondary cardiovascular prevention cohorts.
Main Methods:
- A comprehensive systematic review of multiple databases (MEDLINE, Embase, Cochrane CENTRAL, Web of Science) was performed up to February 2024.
- Meta-analyses utilized random-effects models to calculate pooled hazard ratios (HRs) for MACE based on hs-CRP levels (<2 mg/L and ≥2 mg/L).
- Subgroup analyses were conducted for primary and secondary prevention populations.
Main Results:
- The meta-analysis included 11 studies with 562,301 participants. Elevated Lp(a) was significantly associated with increased MACE risk in both low (HR: 1.26) and high (HR: 1.33) hs-CRP groups.
- In primary prevention, HRs for low and high hs-CRP groups were 1.33 and 1.43, respectively.
- In secondary prevention, HRs for low and high hs-CRP groups were 1.13 and 1.31, respectively.
Conclusions:
- Elevated Lp(a) is consistently linked to a higher risk of MACE.
- This association is independent of hs-CRP levels.
- The findings apply to both individuals undergoing primary and secondary cardiovascular prevention.
Background:
Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease. The relationship between Lp(a) and major adverse cardiovascular events (MACE) in the context of high-sensitivity C-reactive protein (hs-CRP) levels remains controversial due to conflicting results from previous studies.
Objectives:
This systematic review and meta-analysis aimed to clarify the association between Lp(a) and risk of MACE across different hs-CRP levels in both primary and secondary prevention settings.
Methods:
We performed a systematic review by searching MEDLINE (PubMed), Embase (Ovid), Cochrane CENTRAL (Wiley), and Web of Science (Clarivate) from their inception to February 2024. Eligible studies reported the association of Lp(a) with MACE stratified by hs-CRP level. Data extraction and quality assessment were systematically conducted. Meta-analyses used random-effects models to compute pooled HRs for individuals with low (<2 mg/L) and high (≥2 mg/L) hs-CRP levels. Subgroup analyses were performed in primary and secondary prevention populations.
Results:
Nine publications encompassing 11 studies that involved 562,301 participants met the inclusion criteria. The mean proportion of females was 39.9% and the weighted mean age for the entire cohort was 61.2 years. Elevated Lp(a) was significantly associated with MACE risk in both low and high hs-CRP groups, with pooled HR of 1.26 (95% CI: 1.11-1.42) and 1.33 (95% CI: 1.20-1.47), respectively. In the primary prevention group, the pooled HR for low and high hs-CRP groups was 1.33 (95% CI: 1.06-1.66) and 1.43 (95% CI: 1.13-1.82), respectively (subgroup difference, P = 0.65). The corresponding HRs for the secondary prevention population were 1.13 (95% CI: 1.00-1.27) and 1.31 (95% CI: 1.12-1.52), respectively (subgroup difference P = 0.13).
Conclusion:
Elevated Lp(a) is associated with an increased risk of MACE independent of hs-CRP levels in both primary and secondary prevention populations.
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