Computed Tomography-based Patient-specific Biomechanical and Fluid Dynamic Study of Anomalous Coronary Arteries with

Gianluca Rigatelli1, Marco Zuin1,2

  • 1Cardiovascular Diagnosis and Endoluminal Interventions Unit, Rovigo General Hospital, Rovigo, Italy.

Heart International
|October 24, 2022
PubMed

Insights

Anomalous coronary arteries with intramural course (ACAOS-IM) cause vessel compression and pressure drop. Stenting normalizes flow, corrects deformation, and reverses pressure loss in these coronary anomalies.

Area of Science:

  • Cardiovascular Medicine
  • Biomedical Engineering
  • Medical Imaging

Background:

  • Anomalous coronary arteries originating from the opposite sinus of Valsalva (ACAOS) are clinically significant coronary artery anomalies.
  • The pathophysiology and stenting impact of the intramural (IM) course segment in ACAOS-IM remain unclear.

Purpose of the Study:

  • To elucidate the pathophysiology of ACAOS-IM using patient-specific models.
  • To evaluate the biomechanical impact of stenting the intramural segment in ACAOS-IM.

Main Methods:

  • Utilized computed tomography (CT) for patient-specific coronary vessel reconstruction.
  • Applied computational fluid dynamics (CFD) and biomechanical analysis to simulate exercise conditions before and after virtual stenting.
  • Analyzed blood pressure gradients, flow, vorticity, wall shear stress (WSS), and IM segment deformation.

Main Results:

  • Higher basal WSS values were observed in the IM course of both L- and R-ACAOS compared to other segments.
  • Stenting significantly decreased WSS and vorticity magnitude.
  • Biomechanical analysis revealed IM segment compression and twisting, causing a significant distal pressure drop (32-35%) that was corrected by stenting.

Conclusions:

  • The IM segment in ACAOS-IM experiences phasic compression, deformation, and twisting, leading to reduced distal pressure.
  • Stenting the IM segment normalizes the coronary flow profile, corrects segment deformation, and restores distal pressure in both L- and R-ACAOS subtypes.
Abstract

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