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Published on: February 4, 2021
Association Between Lipoprotein(a) and Calcific Aortic Valve Disease: A Systematic Review and Meta-Analysis
Qiyu Liu1,2, Yanqiao Yu1,2, Ruixi Xi1
1National Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Insights
High lipoprotein(a) [lp(a)] levels, specifically 50 mg/dL or greater, significantly increase the risk of calcific aortic valve disease (CAVD). This finding clarifies the association between elevated lp(a) and CAVD risk.
Area of Science:
- Cardiovascular Medicine
- Clinical Biochemistry
- Epidemiology
Background:
- Preliminary research suggested a link between elevated lipoprotein(a) [lp(a)] and calcific aortic valve disease (CAVD).
- The precise clinical association between plasma lp(a) levels and CAVD risk remained inconclusive prior to this study.
Approach:
- A systematic review and meta-analysis were conducted, searching major databases for relevant studies.
- Eight studies with 52,931 participants were included, analyzing incidence of CAVD and plasma lp(a) concentrations.
- Pooled risk ratios and confidence intervals were calculated using a random-effects model, with subgroup analyses and publication bias assessments.
Key Points:
- Plasma lp(a) levels of 50 mg/dL or higher were associated with a 1.76-fold increased risk of CAVD.
- Elevated lp(a) levels of 30 mg/dL were not significantly associated with CAVD risk (RR, 1.28; 95% CI, 0.98-1.68).
- Cohort studies indicated that lp(a) levels ≥50 mg/dL (RR, 1.70) and ≥30 mg/dL (RR, 1.38) showed a positive association with CAVD.
Conclusions:
- High plasma lp(a) levels (≥50 mg/dL) are significantly associated with an increased risk of developing calcific aortic valve disease (CAVD).
- This meta-analysis provides robust evidence supporting lp(a) as a risk factor for CAVD.
Background:
Preliminary studies indicated that enhanced plasma levels of lipoprotein(a) [lp(a)] might link with the risk of calcific aortic valve disease (CAVD), but the clinical association between them remained inconclusive. This systematic review and meta-analysis were aimed to determine this association.
Methods:
We comprehensively searched PubMed, Embase, Web of Science, and Scopus databases for studies reporting the incidence of CAVD and their plasma lp(a) concentrations. Pooled risk ratio (RR) and 95% confidence interval (95% CI) were calculated to evaluate the effect of lp(a) on CAVD using the random-effects model. Subgroup analyses by study types, countries, and the level of adjustment were also conducted. Funnel plots, Egger's test and Begg's test were conducted to evaluate the publication bias.
Results:
Eight eligible studies with 52,931 participants were included in this systematic review and meta-analysis. Of these, four were cohort studies and four were case-control studies. Five studies were rated as high quality, three as moderate quality. The pooled results showed that plasma lp(a) levels ≥50 mg/dL were associated with a 1.76-fold increased risk of CAVD (RR, 1.76; 95% CI, 1.47-2.11), but lp(a) levels ≥30 mg/dL were not observed to be significantly related with CAVD (RR, 1.28; 95% CI, 0.98-1.68). We performed subgroup analyses by study type, the RRs of cohort studies revealed lp(a) levels ≥50 mg/dL and lp(a) levels ≥30 mg/dL have positive association with CAVD (RR, 1.70; 95% CI, 1.39-2.07; RR 1.38; 95% CI, 1.19-1.61).
Conclusion:
High plasma lp(a) levels (≥50 mg/dL) are significantly associated with increased risk of CAVD.
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