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Published on: October 16, 2021
Lipoprotein(a) is associated with mitral annular calcification but not mitral regurgitation: A propensity-matched
Daoud Eldawud1, Md Fahim1, Keston Rattan1
1Department of Medicine, SUNY Downstate Health Sciences University, 450 Clarkson Avenue, Brooklyn, NY 11203, USA (Eldawud, Fahim, and Rattan).
Insights
Elevated Lipoprotein(a) [Lp(a)] is linked to mitral annular calcification (MAC) but not other mitral valve diseases. This study suggests Lp(a) may play a role in MAC development.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Epidemiology
Background:
- Lipoprotein(a) [Lp(a)] is a genetically determined cardiovascular risk factor.
- Lp(a) is increasingly linked to calcific valvular disease, with a well-established role in aortic stenosis.
- The association between Lp(a) and mitral valve pathology, including mitral annular calcification (MAC), mitral stenosis (MS), and mitral regurgitation (MR), is uncertain.
Purpose of the Study:
- To evaluate the association between elevated Lp(a) levels and mitral valve disease.
- To investigate the role of Lp(a) in MAC, MS, MR, and mitral valve prolapse (MVP) in a large, real-world cohort.
Main Methods:
- Retrospective observational analysis of over 130,000 adults with Lp(a) measurements from the TriNetX research network.
- Propensity score matching (1:1) of patients with Lp(a) >50 mg/dL to those with Lp(a) <50 mg/dL across 54 variables.
- Kaplan-Meier survival estimates and log-rank tests were used to assess outcomes, with MAC as the primary outcome and MR, MS, MVP as secondary outcomes. Aortic stenosis (AS) served as a positive control.
Main Results:
- Elevated Lp(a) was significantly associated with MAC (HR 1.330, P < .001) and AS (HR 1.313, P < .001).
- No significant associations were found between elevated Lp(a) and MR (HR 1.006, P = .856), MS (HR 1.178, P = .280), or MVP (HR 1.035, P = .710).
- The matched cohorts each comprised 66,292 patients.
Conclusions:
- Elevated Lp(a) is independently associated with MAC in a large, multicenter, propensity-matched cohort.
- Lp(a) was not significantly associated with MS, MR, or MVP.
- Findings suggest a potential role for Lp(a) in MAC pathogenesis, warranting further prospective studies to confirm causality and clinical implications.
Background:
Lipoprotein(a) [Lp(a)] is a genetically determined cardiovascular risk factor increasingly linked to calcific valvular disease. Although its role in aortic stenosis is well established, the association between Lp(a) and mitral valve pathology, particularly mitral annular calcification (MAC), mitral stenosis (MS), and mitral regurgitation (MR), remains uncertain.
Objective:
To evaluate the association between elevated Lp(a) levels and mitral valve disease in a large, real-world cohort.
Methods:
We conducted a retrospective observational analysis using the TriNetX research network, including over 130,000 adults with available Lp(a) measurements. Patients with Lp(a) >50 mg/dL were propensity score matched 1:1 to those with Lp(a) <50 mg/dL across 54 demographic, clinical, and treatment variables. Valvular outcomes were defined using administrative codes. Kaplan-Meier survival estimates and log-rank tests were calculated in the matched cohorts. The primary outcome was MAC, with MR, MS, and mitral valve prolapse (MVP) as secondary outcomes. AS served as a positive control.
Results:
Each matched cohort included 66,292 patients. Elevated Lp(a) was significantly associated with the primary outcome of MAC (hazard ratio [HR] 1.330, 95% CI 1.172-1.509, P < .001). The positive control outcome of AS(Aortic stenosis) was also significant (HR 1.313, 95% CI 1.175-1.466, P < .001). No significant associations were observed for the secondary outcomes of MR (HR 1.006, 95% CI 0.940-1.077, P = .856), MS (HR 1.178, 95% CI 0.875-1.587, P = .280), or MVP (HR 1.035, 95% CI 0.863-1.241, P = .710).
Conclusion:
In this large multicenter propensity-matched cohort, elevated Lp(a) was independently associated with MAC but not with MS, MR, or mitral valve prolapse. These findings support a potential role of Lp(a) in mitral annular calcification and highlight the need for prospective studies to clarify causality and clinical implications.
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