The influence of lipoprotein(a) on aortic valve calcification in patients undergoing transcatheter aortic valve replacement

Background: Elevated levels of lipoprotein(a) (Lp[a]) have been recognized as substantial risk factors for cardiovascular disease and aortic stenosis (AS). However, the specific role of Lp(a) in promoting aortic valve calcification (AVC) and influencing mortality in elderly, multimorbid patients undergoing transcatheter aortic valve replacement (TAVR) remains unclear and warrants further investigation.

Methods: A retrospective analysis was conducted on all consecutive patients who underwent TAVR between August 2019 and June 2020 at our clinic. Patients with missing data or prior aortic valve replacement were excluded. The study cohort was stratified based on an Lp(a) threshold of 60 mg/dl according to guidelines for lipoprotein apheresis in UK and Germany.^1,2 RESULTS: In total, 454 patients were included into the analysis. Mean age was 81 ± 6 years and patients presented with a notable cardiovascular risk profile. Lp(a) values ≥ 60 mg/dl were detected in 102 (22.5%) patients, while 352 (77.5%) had Lp(a) values < 60 mg/dl. The median calcium volume of the total cohort was 894.5 [570.8; 1,382.8] mm². No significant difference was observed between the groups (p = 0.83). Furthermore, Lp(a) did not emerge as a statistically significant predictor of calcium levels before TAVR. Notably, male gender (B = 404.11, p < 0.001) and mean trans-valvular pressure gradient (B = 15.64, p < 0.001) were identified as the strongest coefficients within the robust regression analysis. Log-rank tests indicated no prognostic utility of Lp(a) for 30-day all-cause mortality (p = 0.30) or 40 months long-term all-cause mortality (p = 0.60).

Conclusion: Lp(a) might not exert a significant effect on calcification levels or all-cause mortality in patients undergoing TAVR. Despite the study's highly selected population, these results align with current research, supporting the assumption that the influence of Lp(a) may be confined to the early stages of AS and its progression.