Key result
Elevated Lp(a) over 30 mg/dL is linked to over threefold higher odds of aortic valve calcification.
Why the study?
Is elevated Lp(a) >30 mg/dl associated with an increased risk of early aortic valve calcification in individuals under 65 without prior cardiovascular disease?
Observational (n=228)
Is elevated Lp(a) >30 mg/dl associated with an increased risk of early aortic valve calcification in individuals under 65 without prior cardiovascular disease?
Odds Ratio: 3.25
Absolute Event Rate: 38% vs 15.8%
p-value: p=0.015
Elevated Lp(a) >30 mg/dl is independently associated with early aortic valve calcification in individuals under 65 without prior cardiovascular disease, suggesting a role in the early pathogenesis of aortic stenosis.
Introduction High liproprotein (Lp) (a) levels have been linked with atherosclerosis, significantly impacting the cardiovascular system. The aortic valve is no exception. Elevated Lp(a) levels have been associated with the development of severe aortic stenosis. However, it is still unknown if its pro-inflammatory and atherogenic properties are key to initial aortic valve calcification. Objective Determine if elevated Lp(a) levels are associated with aortic valve calcification. Methods Aortic valve calcification (AVC) was measured in 228 individuals under 65 years with no prior diagnosis of cardiovascular disease. AVC score was calculated by CT angiography and reported in Agatston units. The population was divided into two groups: AVC=0 and AVC>0. Patients with likely severe aortic stenosis were excluded (Men>2000 A.U; Women>1200 A.U). According to current evidence, an Lp(a) was considered elevated>30 mg/dl. Bivariate and multivariate analyses were conducted to understand the influence of Lp(a) levels on AVC after adjusting for traditional risk factors. Results Individuals with elevated Lp(a) levels (>30 mg/dl) were more likely to have AVC, 38.0%, when compared with the ones with lower Lp(a) levels (≤30 mg/dl), being 15.8% (p<0.01). Traditional risk factors, such as older age, obesity, male sex and hypertension, were significant in the bivariate analysis. After multivariate analysis, it was clear that Lp(a) >30 mg/dl remained an independent risk factor for AVC (p=0.015; OR=3.25) along with obesity (p=0.039; OR=2.62), male sex (p= 0.029; OR=2.58) and older age (p<0.0001; OR=1.18). Conclusion Levels of Lp(a) higher than 30 mg/dl were associated with early aortic valve calcification, supporting its role in the early stages of the development of aortic stenosis. Future studies might shed a light on whether Lp(a) level control through medication could prevent the progression of aortic stenosis.
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Sousa et al. (2025) conducted an observational in Aortic valve calcification (n=228). Elevated Lipoprotein(a) (>30 mg/dl) vs. Lower Lipoprotein(a) (≤30 mg/dl) was evaluated on Aortic valve calcification (AVC > 0) (OR 3.25, p=0.015). Elevated Lipoprotein(a) levels (>30 mg/dl) were independently associated with early aortic valve calcification compared to lower levels (38.0% vs 15.8%; OR 3.25, p=0.015).
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