Lipoprotein(a) elevation independently associates with incident atrial fibrillation irrespective of inflammatory status
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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Le Li1, Sheng Su1, Zhicheng Hu1
1Arrhythmia Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Insights
Elevated lipoprotein(a) (Lp[a]) is an independent risk factor for atrial fibrillation (AF), even when systemic inflammation, measured by high-sensitivity C-reactive protein (hs-CRP), is not elevated. This finding highlights Lp[a] as a key predictor for AF development.
Area of Science:
- Cardiovascular Medicine
- Epidemiology
- Biomarkers
Background:
- Atrial fibrillation (AF) poses significant risks for stroke, heart failure, and mortality.
- Elevated lipoprotein(a) (Lp[a]) is a suspected contributor to AF pathogenesis.
- The interplay between Lp(a) and systemic inflammation (hs-CRP) in AF development is not well understood.
Purpose of the Study:
- To determine if the association between Lp(a) and AF is independent of baseline inflammatory status.
- To investigate the role of Lp(a) as a risk factor for incident AF, considering hs-CRP levels.
Main Methods:
- Retrospective cohort study of 365,899 UK Biobank participants without baseline AF.
- Lp(a) analyzed continuously and categorically (≥125 nmol/L); systemic inflammation defined as hs-CRP ≥2 mg/L.
- Multivariable Cox proportional hazards and Fine-Gray competing risk models used to estimate AF risk.
Main Results:
- Over 13.5 years, 25,048 incident AF cases were recorded.
- Elevated Lp(a) and hs-CRP were individually associated with higher incident AF rates.
- Higher Lp(a) levels independently predicted increased AF risk, irrespective of hs-CRP status (e.g., hs-CRP ≥2 mg/L: HR 1.12; hs-CRP <2 mg/L: HR 1.09).
Conclusions:
- Lipoprotein(a) is confirmed as an independent risk factor for atrial fibrillation.
- This independence holds true regardless of baseline systemic inflammatory status, as indicated by hs-CRP levels.
- Lp(a) emerges as a crucial, inflammation-independent predictor for AF development.
Background:
Atrial fibrillation (AF) significantly increases stroke, heart failure, and mortality risk. Elevated lipoprotein(a) (Lp[a]) is implicated in AF pathogenesis, but its relationship with systemic inflammation (assessed by high-sensitivity C-reactive protein [hs-CRP]) remains unclear.
Objective:
We investigated whether the Lp(a)-AF association is independent of baseline inflammatory status.
Methods:
In this retrospective cohort study, we analyzed 365,899 United Kingdom (UK) Biobank participants without baseline AF. Lp(a) was modeled as a continuous exposure (per 50 nmol/L increase) and categorically (≥125 nmol/L). Systemic inflammation was defined as hs-CRP ≥2 mg/L. Multivariable Cox proportional hazards models (adjusted for age, sex, cardiovascular risk factors, and comorbidities) and Fine-Gray competing risk analyses estimated adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident AF.
Results:
Over a median 13.5-year follow-up, 25,048 (6.8%) incident AF cases occurred. Elevated Lp(a) (7.44% vs 6.77%, log-rank P < .001) and hs-CRP (8.49% vs 5.96%, log-rank P < .001) were associated with higher incident AF. Cox proportional hazard model adjusted for covariates, higher Lp(a) (≥125 nmol/L) was associated with increased AF risk regardless of hs-CRP levels for AF (hs-CRP ≥2 mg/L: HR, 1.12; 95% CI, 1.06-1.19; P < .001; hs-CRP <2 mg/L: HR, 1.09; 95% CI, 1.04-1.15; P = .001). Results remained consistent in propensity score matched cohorts and sensitivity analyses.
Conclusion:
Lp(a) is an independent risk factor for AF, irrespective of baseline inflammatory status, as measured by hs-CRP.
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