Physicians' Academy for Cardiovascular Education

More evidence for association between higher Lp(a) levels and calcific aortic valve disease

Lipoprotein(a) and calcific aortic valve disease initiation and progression: a systematic review and meta-analysis

Literature - Pantelidis P, Oikonomou E, Lampsas S, et al. - Cardiovasc Res. 2023 Jul 6;119(8):1641-1655. doi: 10.1093/cvr/cvad062

Introduction and methods


Calcific aortic valve stenosis (AVS) is one of the most common age-related valvulopathies [1,2]. Recently, Lp(a) has emerged as a new risk factor for calcific aortic valve disease (CAVD), thereby mediating aortic valve calcification (AVC) and AVS [3,4]. Although there is evidence linking Lp(a) to CAVD [5], this association is still unclear, particularly with regard to demographic, genetic, and other interfering factors.

Aim of the study

The authors examined the existing evidence for the relationship between Lp(a) and the onset and progression of AVC and AVS.


In this systematic review and meta-analysis, a systematic search of 8 literature databases was performed (up to February 2023) to identify observational studies comparing high versus normal to low Lp(a) plasma levels with AVC or AVS as outcomes and studies exploring the association between relevant genetic risk factors and AVC or AVS.

A total of 44 studies (n=163,139) were included in the systematic review of the association between Lp(a) levels and CAVD. The overall quality was high for 33 studies (75%) and moderate for the remaining 11 (25%). After exclusion of outlying and influential studies, 11 studies (n=26,191) were included in the meta-analysis. In the systematic review of Lp(a)-related genetic risk and CAVD, 17 studies were included, 8 of which were eligible for meta-analysis.

Main results

Association between Lp(a) levels and aortic valve stenosis

//Association between Lp(a) levels and aortic valve calcification//

Association between genetic risk factors and aortic valve stenosis


This systematic review and meta-analysis showed higher Lp(a) levels were associated with the onset, progression, and serious adverse outcomes of CAVD. Both age and sex were significant predictors of the Lp(a) difference between AVS and non-AVS patients, with a stronger association seen in younger individuals and male-dominant populations. In addition, genetic variations in LPA loci were related to increased AVS risk. The authors believe their findings support the early onset of Lp(a)-related subclinical lesions before they become clinically evident.


Show references

Find this article online at Cardiovasc Res.

Share this page with your colleagues and friends: