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Purpose <p>Aortic stenosis (AS) commonly coexists with coronary artery disease (CAD), yet the direct hemodynamic link between valve function, coronary flow waveforms, and spatial wall shear stress (WSS) remains poorly defined. This study isolates and quantifies how AS-induced flow alterations generate atheroprone coronary environments.</p> Methods <p>An in vitro mock circulation loop modeled severe AS (effective orifice area 0.7&#xa0;cm<sup>2</sup>) and post-transcatheter aortic valve replacement (TAVR, Evolut R™) under 54 physiological states (heart rate 80–150&#xa0;bpm; stroke volume 40–65&#xa0;ml). Time-resolved coronary blood flow (CBF) measurements served as inlet boundary conditions for patient-specific computational fluid dynamics (CFD) simulations of coronary hemodynamics. Atherosclerotic risk was assessed using surface areas exposed to shear thresholds associated with plaque initiation or vulnerability: oscillatory shear index (OSI &gt; 0.2), relative residence time (RRT &gt; 4&#xa0;Pa⁻<sup>1</sup>), endothelial cell activation potential (ECAP &gt; 0.5&#xa0;Pa⁻<sup>1</sup>), and time-averaged WSS (TAWSS &lt; 0.45&#xa0;Pa or &gt; 4&#xa0;Pa).</p> Results <p>Compared to TAVR, severe AS produced higher systolic transvalvular pressure gradients (45–70&#xa0;mmHg vs. 10–25&#xa0;mmHg) and lower aortic–sinus gradients, particularly at elevated heart rates (HR). Diastolic CBF was elevated at normal HR but declined with increasing HR, resulting in increased pulsatility and reduced coronary flow reserve. CFD revealed larger regions of atheroprone WSS in AS, predominantly on convex arterial curvatures, while elevated WSS localized to concave regions. TAVR reduced adverse WSS exposure by 30–50%.</p> Conclusion <p>AS induces hemodynamic disturbances associated with atheroprone environments through altered coronary flow and adverse WSS patterns. TAVR mitigates these effects, highlighting opportunities for valve design optimization to improve the local coronary fluid-dynamic environment.</p> Graphical Abstract <p></p>

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Hemodynamic Effects of Aortic Stenosis on Coronary Flow Dynamics

  • 期刊论文

  • 发表日期：

    2026年8月5日

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  • Roy Banay,
  • Shiri Polak,
  • Matan Danon,
  • Oren Salimi,
  • Ed David Hausmann,
  • Ron Waksman,
  • Yonathan Hasin,
  • Idit Avrahami

摘要

Purpose

Aortic stenosis (AS) commonly coexists with coronary artery disease (CAD), yet the direct hemodynamic link between valve function, coronary flow waveforms, and spatial wall shear stress (WSS) remains poorly defined. This study isolates and quantifies how AS-induced flow alterations generate atheroprone coronary environments.

Methods

An in vitro mock circulation loop modeled severe AS (effective orifice area 0.7 cm2) and post-transcatheter aortic valve replacement (TAVR, Evolut R™) under 54 physiological states (heart rate 80–150 bpm; stroke volume 40–65 ml). Time-resolved coronary blood flow (CBF) measurements served as inlet boundary conditions for patient-specific computational fluid dynamics (CFD) simulations of coronary hemodynamics. Atherosclerotic risk was assessed using surface areas exposed to shear thresholds associated with plaque initiation or vulnerability: oscillatory shear index (OSI > 0.2), relative residence time (RRT > 4 Pa⁻1), endothelial cell activation potential (ECAP > 0.5 Pa⁻1), and time-averaged WSS (TAWSS < 0.45 Pa or > 4 Pa).

Results

Compared to TAVR, severe AS produced higher systolic transvalvular pressure gradients (45–70 mmHg vs. 10–25 mmHg) and lower aortic–sinus gradients, particularly at elevated heart rates (HR). Diastolic CBF was elevated at normal HR but declined with increasing HR, resulting in increased pulsatility and reduced coronary flow reserve. CFD revealed larger regions of atheroprone WSS in AS, predominantly on convex arterial curvatures, while elevated WSS localized to concave regions. TAVR reduced adverse WSS exposure by 30–50%.

Conclusion

AS induces hemodynamic disturbances associated with atheroprone environments through altered coronary flow and adverse WSS patterns. TAVR mitigates these effects, highlighting opportunities for valve design optimization to improve the local coronary fluid-dynamic environment.

Graphical Abstract