Related Experiment Video

Updated: May 13, 2025

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
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Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro

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High-Intensity Statins Promote PCSK9 Secretion and aortic valve calcification in patients with severe aortic

Veronika A Myasoedova1, Matteo Franchi2, Donato De Giorgi1

  • 1Centro Cardiologico Monzino IRCCS, Milan 20138, Italy.

Pharmacological Research
|April 16, 2025
PubMed

Insights

High-intensity statin therapy may accelerate aortic valve calcification and increase hospitalization for aortic stenosis. Further research is needed to determine optimal lipid-lowering strategies for patients with or at risk of aortic stenosis.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Pharmacology

Background:

  • Aortic stenosis (AS) is a prevalent valvular disease causing significant morbidity and mortality.
  • Statins are known to affect proprotein convertase subtilisin/kexin type 9 (PCSK9) production, a factor implicated in calcification.
  • The precise impact of statin therapy on aortic valve calcification remains an area of active investigation.

Purpose of the Study:

  • To investigate the effect of statins on aortic valve interstitial cell (VIC) calcification in vitro.
  • To evaluate the association between statin intensity and aortic valve calcium (AVC) accumulation in patients with AS.
  • To assess the real-world impact of high-intensity statin therapy on hospitalization rates for non-rheumatic aortic valve disease.

Main Methods:

  • In vitro experiments using VICs to assess PCSK9 secretion and calcification in response to statins.
  • Analysis of contrast-enhanced computed tomography scans to quantify AVC content in AS patients stratified by statin use (high-intensity, low-intensity, non-users).
  • Retrospective analysis of real-world data to determine hospitalization rates for non-rheumatic aortic valve disease.

Main Results:

  • Statins significantly increased PCSK9 secretion and VIC calcification in a dose-dependent manner in vitro, effects mitigated by PCSK9 inhibition.
  • AS patients on high-intensity statins showed higher AVC content compared to low-intensity or non-users.
  • High-intensity statin users exhibited accelerated annual AVC accumulation and a 30% increased hospitalization rate for non-rheumatic aortic valve disease.

Conclusions:

  • Statin therapy, particularly high-intensity, may promote aortic valve calcification and adverse clinical outcomes.
  • PCSK9 plays a role in statin-mediated VIC calcification.
  • Further research is crucial to optimize lipid-lowering strategies for AS management and to clarify the relationship between statins and aortic valve health.

Keywords:
Aortic valve calcificationAortic valve disease hospitalizationPCSK9Statin intensity

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