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Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
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Association between blood pressure traits, hypertension, antihypertensive drugs and calcific aortic valve stenosis: a

Wen-Hua Lei1,2, Jia-Liang Zhang1,2, Yan-Biao Liao1,2

  • 1Department of Cardiology, West China Hospital, Sichuan University, No.37 Guoxue Street, Chengdu 610041, China.

Journal of Geriatric Cardiology : JGC
|May 12, 2025
PubMed

Insights

Hypertension causally increases the risk of calcific aortic valve stenosis (CAVS). Certain blood pressure medications, like calcium channel blockers, may help prevent CAVS by lowering systolic blood pressure.

Area of Science:

  • Cardiovascular Genetics
  • Pharmacogenomics
  • Epidemiology

Background:

  • Hypertension is a known risk factor for calcific aortic valve stenosis (CAVS).
  • The causal relationship between blood pressure and CAVS, and the efficacy of antihypertensive drugs, remain unclear.

Purpose of the Study:

  • To investigate the causal effect of blood pressure traits on CAVS using Mendelian randomization.
  • To evaluate the direct impact of hypertension on CAVS.
  • To assess the potential protective effects of 12 classes of antihypertensive drugs and their targets on CAVS risk.

Main Methods:

  • Bidirectional two-sample univariable Mendelian randomization (UVMR) analyzed GWAS summary statistics for systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP) against CAVS.
  • Multivariable Mendelian randomization (MVMR) assessed the direct effect of hypertension on CAVS, adjusting for confounders.
  • Drug-target Mendelian randomization (MR) and summary-level MR (SMR) examined the association of antihypertensive drug classes and their target genes with CAVS.

Main Results:

  • UVMR confirmed causal effects of SBP, DBP, and PP on CAVS, with no evidence of reverse causality.
  • MVMR reinforced the causal link between hypertension and CAVS.
  • Drug-target MR indicated that calcium channel blockers (CCBs), loop diuretics, and thiazide diuretics may protect against CAVS by lowering SBP.
  • SMR identified specific gene associations: CACNA2D2 (CCBs) and AGTR1 (ARBs) linked to increased CAVS risk, while SLC12A5 and SLC12A1 (diuretics) were associated with reduced risk.

Conclusions:

  • Hypertension is causally associated with CAVS.
  • Managing SBP with CCBs may offer a preventative strategy for CAVS in hypertensive individuals.
  • Angiotensin receptor blockers (ARBs) might provide CAVS protection independent of blood pressure.
  • Diuretics exhibit a complex relationship with CAVS, with varied effects possibly mediated by different mechanisms.
Abstract

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