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Discrete Subaortic Stenosis: Perspective Roadmap to a Complex Disease.

Danielle D Massé1, Jason A Shar1, Kathleen N Brown2

  • 1Department of Mechanical and Materials Engineering, Wright State University, Dayton, OH, United States.

Frontiers in Cardiovascular Medicine
|October 16, 2018
PubMed
Summary

Discrete subaortic stenosis (DSS) involves a fibrotic tissue causing left ventricular outflow tract obstruction. Research suggests a hemodynamic cause, not genetic, highlighting the need to understand mechanobiology for better treatment.

Keywords:
aortoseptal anglecongenital heart diseasediscrete subaortic stenosisetiologyhemodynamicsleft ventricular outflow tractwall shear stress

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Area of Science:

  • Cardiovascular Medicine
  • Biomedical Engineering
  • Developmental Biology

Background:

  • Discrete subaortic stenosis (DSS) is a congenital heart defect characterized by fibro-membranous tissue in the left ventricular outflow tract (LVOT).
  • Surgical resection is the current treatment but carries risks and high recurrence rates.
  • A hemodynamic etiology, involving abnormal shear forces on the septal wall due to LVOT geometry, is increasingly supported over a genetic cause.

Purpose of the Study:

  • To review the current understanding of DSS pathogenesis.
  • To identify knowledge gaps regarding the mechanobiological processes underlying DSS.
  • To propose research strategies for elucidating the role of altered shear forces in DSS development.

Main Methods:

  • This paper is a perspective review, synthesizing existing knowledge on DSS.
  • It discusses the potential role of hemodynamic forces in triggering fibrotic responses.
  • It outlines a research roadmap to investigate mechanobiological mechanisms.

Main Results:

  • Current understanding suggests DSS may arise from abnormal shear stress in the LVOT, leading to fibrosis.
  • Significant knowledge gaps exist in validating this hemodynamic hypothesis and understanding the specific mechanobiological pathways.
  • The proposed research strategies aim to address these gaps.

Conclusions:

  • Further research into the mechanobiology of DSS is crucial for understanding its pathogenesis.
  • Elucidating the role of shear forces could lead to novel therapeutic targets for preventing fibrotic lesions.
  • Findings may also inform the management of other fibrotic cardiovascular diseases.