Why the study?
To investigate the potential causal association of lipoprotein(a) levels with pulse wave velocity.
Are genetically predicted Lipoprotein(a) levels causally associated with pulse wave velocity?
Are genetically predicted Lipoprotein(a) levels causally associated with pulse wave velocity?
Mendelian randomization analysis does not support a causal relationship between Lipoprotein(a) levels and arterial stiffness as measured by pulse wave velocity.
MR evidence does not support Lp(a) causing arterial stiffness; leaves open alternative pathways for its cardiovascular effects.
BACKGROUND: In this study we used Mendelian randomization (MR) to investigate the potential causal association of lipoprotein (a) [Lp(a)] levels with pulse wave velocity (PWV). METHODS: Genetic variants associated with Lp(a) were retrieved from the UK Biobank GWAS (N = 290,497). A non- overlapping GWAS based on a European cohort (N = 7,000) was used to obtain genetic associations with PWV (outcome) and utilized two different measures for the same trait, brachial-ankle (baPWV) and carotid-femoral (cfPWV) PWV. We applied a two-sample MR using the inverse variance weighting method (IVW) and a series of sensitivity analyses for 170 SNPs that were selected as instrumental variables (IVs). RESULTS: (cfPWV) = -.006, p = .16]. The above findings were consistent across sensitivity analyses including weighted median, mode-based estimation, MR-Egger regression and MR-PRESSO. CONCLUSION: We did not find evidence indicating that Lp(a) is causally associated with PWV, the gold standard marker of arterial stiffness.
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Simistiras et al. (2024) studied this question.
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