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.
Abstract

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