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Impact of Lipoprotein(a) on Valvular and Cardiovascular Outcomes in Patients With Calcific Aortic Valve Stenosis
Arnaud S Girard1, Audrey Paulin1, Hasanga D Manikpurage1
1Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec-Université Laval Québec QC Canada.
Insights
High lipoprotein(a) levels increase the risk of cardiovascular events in patients with calcific aortic valve stenosis (CAVS). Further research into lipoprotein(a)-lowering therapies is recommended for managing CAVS outcomes.
Area of Science:
- Cardiology
- Biochemistry
- Genetics
Background:
- Lipoprotein(a) (Lp(a)) is a known independent risk factor for calcific aortic valve stenosis (CAVS).
- The association between elevated Lp(a) levels and adverse cardiovascular or valvular outcomes in CAVS patients remains unclear.
Purpose of the Study:
- To investigate the relationship between Lp(a) levels and the risk of valvular and cardiovascular events in patients diagnosed with CAVS.
Main Methods:
- A cohort of 1962 UK Biobank participants with CAVS and no prior aortic valve replacement was analyzed.
- Cox proportional hazard regression models were employed to assess the impact of Lp(a) on outcomes over a 5-year follow-up period.
Main Results:
- Patients with Lp(a) levels ≥125 nmol/L had a significantly higher risk of aortic valve replacement (HR, 1.58), AVR or cardiac death (HR, 1.43), and overall cardiovascular/valvular events (HR, 1.36).
- These associations remained consistent across different demographic and clinical subgroups.
Conclusions:
- Elevated Lp(a) levels are a significant predictor of adverse valvular and cardiovascular outcomes in patients with CAVS.
- Long-term randomized clinical trials are warranted to evaluate the efficacy of Lp(a)-lowering therapies in improving cardiovascular health for CAVS patients.
Background:
Lp(a) (lipoprotein(a)) is an independent risk factor for calcific aortic valve stenosis (CAVS). Whether patients with CAVS and high Lp(a) levels are at higher risk of valvular or cardiovascular events is unknown. The aim of this study is to determine whether higher Lp(a) levels are associated with valvular and cardiovascular outcomes in patients with CAVS.
Methods And Results:
We identified 1962 patients from the UK Biobank with an electronic health record or self-reported CAVS diagnosis but who did not previously undergo aortic valve replacement (AVR) and had a minimal follow-up time of 2.5 years. Cox proportional hazard regression was used to evaluate the effect of Lp(a) on AVR, AVR or cardiac death, and valvular or cardiovascular events (AVR, cardiac death, myocardial infarction, stroke, heart failure, or coronary artery bypass grafting). The maximal follow-up time was set to 5 years. During the follow-up, 198 patients underwent AVR, 260 had AVR or cardiac death, and 435 had at least 1 valvular or cardiovascular event. Patients with Lp(a) levels ≥125 versus <125 nmol/L were at higher risk of AVR (hazard ratio [HR], 1.58 [95% CI, 1.17-2.12]), AVR or cardiac death (HR, 1.43 [95% CI, 1.10-1.86]), and cardiovascular or valvular events (HR, 1.36 [95% CI, 1.11-1.68]). Point estimates were comparable in men versus women, younger versus older patients, and in patients with higher versus lower plasma C-reactive protein levels.
Conclusions:
In patients with CAVS, Lp(a) levels predicted a higher risk of valvular and cardiovascular outcomes. The impact of Lp(a)-lowering therapies on valvular and cardiovascular health should be assessed in a long-term randomized clinical trial.
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