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Increased Aortic Valve Calcification in Familial Hypercholesterolemia: Prevalence, Extent, and Associated Risk

Gert-Jan R Ten Kate1, Sven Bos2, Admir Dedic1

  • 1Department of Radiology, Erasmus Medical Centre, Rotterdam, the Netherlands; Interuniversitair Cardiologisch Instituut Nederland, Utrecht, the Netherlands; Department of Cardiology, Thorax Centre Rotterdam, Rotterdam, the Netherlands.

Journal of the American College of Cardiology
|December 25, 2015
PubMed

Insights

Heterozygous familial hypercholesterolemia (he-FH) is linked to increased aortic valve calcification (AoVC). LDLR-negative mutations are the strongest predictor of AoVC extent, emphasizing LDL-C metabolism

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Radiology

Background:

  • Familial hypercholesterolemia (FH) is characterized by elevated LDL cholesterol (LDL-C) due to LDL receptor (LDLR) mutations.
  • Homozygous FH exhibits 100% prevalence of symptomatic aortic valve calcification (AoVC).
  • The prevalence and risk factors for AoVC in heterozygous FH (he-FH) are not well understood.

Purpose of the Study:

  • To determine the prevalence and extent of subclinical AoVC in asymptomatic he-FH patients.
  • To identify risk modifiers associated with AoVC in he-FH.
  • To compare AoVC in he-FH patients versus non-FH controls.

Main Methods:

  • 145 asymptomatic he-FH patients and 131 controls underwent CT calcium scoring.
  • AoVC was defined by calcium in aortic valve leaflets; extent was measured by AoVC-score (Agatston units).
  • Risk modifiers investigated included LDLR mutation status (LDLR-negative), maximum untreated LDL-C (maxLDL), LDL-C, blood pressure, and coronary artery calcification (CAC).

Main Results:

  • AoVC prevalence (41% vs 21%) and AoVC-score (51 vs 21) were significantly higher in he-FH patients compared to controls (p < 0.001 and p = 0.007, respectively).
  • Independent predictors of AoVC included age, untreated maxLDL, CAC, and diastolic blood pressure.
  • LDLR-negative mutations were the strongest predictor of AoVC-score (OR: 4.81; p < 0.001).

Conclusions:

  • Asymptomatic he-FH is associated with a high prevalence and significant extent of subclinical AoVC.
  • LDLR-negative mutations represent a critical risk factor for AoVC in he-FH.
  • These findings underscore the crucial role of LDL-C metabolism in the etiology of AoVC.
Abstract

Keywords:
LDLR-negative mutationaortic valve calcificationcalcific aortic stenosiscoronary artery calcificationfamilial hypercholesterolemialow-density lipoprotein receptor

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