Related Experiment Video
Updated: Jun 5, 2025
Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
Published on: February 4, 2021
The influence of lipoprotein(a) on aortic valve calcification in patients undergoing transcatheter aortic valve
Johanna Bormann1, Felix Rudolph1, Maximilian Miller
1Clinic for General and Interventional Cardiology/Angiology, Herz- und Diabeteszentrum Nordrhein-Westfalen, Ruhr-Universität Bochum, Georgstraße 11, 32545, Bad Oeynhausen, Germany.
Insights
Lipoprotein(a) (Lp[a]) does not significantly impact aortic valve calcification or mortality in patients undergoing transcatheter aortic valve replacement (TAVR). These findings suggest Lp[a] may primarily influence early stages of aortic stenosis.
Area of Science:
- Cardiology
- Biomarkers
- Aortic Stenosis
Background:
- Elevated Lipoprotein(a) (Lp[a]) is a known cardiovascular disease risk factor.
- Its specific role in aortic valve calcification (AVC) and mortality in TAVR patients is unclear.
Purpose of the Study:
- To investigate the association between Lp[a] levels and AVC.
- To determine the prognostic value of Lp[a] for mortality in elderly, multimorbid TAVR patients.
Main Methods:
- Retrospective analysis of 454 TAVR patients (August 2019 - June 2020).
- Stratification based on Lp[a] threshold of 60 mg/dl.
- Analysis of calcium volume and all-cause mortality (30-day and 40-month).
Main Results:
- No significant difference in calcium volume between Lp[a] groups (≥60 mg/dl vs. <60 mg/dl).
- Lp[a] was not a significant predictor of pre-TAVR calcium levels.
- Lp[a] showed no prognostic utility for 30-day or 40-month all-cause mortality.
Conclusions:
- Lp[a] may not significantly affect calcification or mortality in TAVR patients.
- Findings suggest Lp[a]'s influence might be limited to earlier stages of aortic stenosis progression.
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.
