Biomechanical factors in the biology of aortic wall and aortic valve diseases

Cardiovasc Res. 2013 Jul 15;99(2):232-41. doi: 10.1093/cvr/cvt040. Epub 2013 Mar 3.

Abstract

The biomechanical factors that result from the haemodynamic load on the cardiovascular system are a common denominator of several vascular pathologies. Thickening and calcification of the aortic valve will lead to reduced opening and the development of left ventricular outflow obstruction, referred to as aortic valve stenosis. The most common pathology of the aorta is the formation of an aneurysm, morphologically defined as a progressive dilatation of a vessel segment by more than 50% of its normal diameter. The aortic valve is exposed to both haemodynamic forces and structural leaflet deformation as it opens and closes with each heartbeat to assure unidirectional flow from the left ventricle to the aorta. The arterial pressure is translated into tension-dominated mechanical wall stress in the aorta. In addition, stress and strain are related through the aortic stiffness. Furthermore, blood flow over the valvular and vascular endothelial layer induces wall shear stress. Several pathophysiological processes of aortic valve stenosis and aortic aneurysms, such as macromolecule transport, gene expression alterations, cell death pathways, calcification, inflammation, and neoangiogenesis directly depend on biomechanical factors.

Keywords: Abdominal aortic aneurysm; Aortic stenosis; Inflammation; Thoracic aortic aneurysm.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Aorta / metabolism
  • Aorta / pathology
  • Aorta / physiopathology*
  • Aortic Diseases / metabolism
  • Aortic Diseases / pathology
  • Aortic Diseases / physiopathology*
  • Aortic Valve / metabolism
  • Aortic Valve / pathology
  • Aortic Valve / physiopathology*
  • Biomechanical Phenomena
  • Heart Valve Diseases / metabolism
  • Heart Valve Diseases / pathology
  • Heart Valve Diseases / physiopathology*
  • Hemodynamics*
  • Humans
  • Mechanotransduction, Cellular*
  • Models, Cardiovascular
  • Regional Blood Flow
  • Stress, Mechanical