Modeling the impact of concomitant aortic stenosis and coarctation of the aorta on left ventricular workload

J Biomech. 2011 Nov 10;44(16):2817-25. doi: 10.1016/j.jbiomech.2011.08.001. Epub 2011 Sep 28.


Coarctation of the aorta (COA) is an obstruction of the aorta and is usually associated with bicuspid and tricuspid aortic valve stenosis (AS). When COA coexists with AS, the left ventricle (LV) is facing a double hemodynamic load: a valvular load plus a vascular load. The objective of this study was to develop a lumped parameter model, solely based on non-invasive data, allowing the description of the interaction between LV, COA, AS and the arterial system. First, a formulation describing the instantaneous net pressure gradient through the COA was introduced and the predictions were compared to in vitro results. The model was then used to determine LV work induced by coexisting AS and COA with different severities. The results show that LV stroke work varies from 0.98J (no-AS; no-COA) up to 2.15J (AS: 0.61cm(2)+COA: 90%). Our results also show that the proportion of the total flow rate that will cross the COA is significantly reduced with the increasing COA severity (from 85% to 40%, for a variation of COA severity from 0% to 90%, respectively). Finally, we introduced simple formulations capable of, non-invasively, estimating both LV peak systolic pressure and workload. As a conclusion, this study allowed the development of a lumped parameter model, based on non-invasive measurements, capable of accurately investigating the impact of coexisting AS and COA on LV workload. This model can be used to optimize the management of patients with COA and AS in terms of the sequence of lesion repair.

MeSH terms

  • Animals
  • Aortic Coarctation / complications
  • Aortic Coarctation / physiopathology*
  • Aortic Coarctation / therapy
  • Aortic Valve Stenosis / complications
  • Aortic Valve Stenosis / physiopathology*
  • Aortic Valve Stenosis / therapy
  • Blood Flow Velocity
  • Blood Pressure*
  • Heart Ventricles / physiopathology*
  • Humans
  • Models, Cardiovascular*