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The Stiffness of the Ascending Aorta Has a Direct Impact on Left Ventricular Function: An In Silico Model.
Goetz, Wolfgang Anton; Yao, Jiang; Brener, Michael; Puri, Rishi; Swaans, Martin; Schopka, Simon; Wiesner, Sigrid; Creutzenberg, Marcus; Sievert, Horst; Kassab, Ghassan S.
Afiliación
  • Goetz WA; Cardiothoracic Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
  • Yao J; Dassault Systèmes, Johnston, RI 02919, USA.
  • Brener M; Division of Cardiology, Columbia University Irving Medical Center, New York, NY 10027, USA.
  • Puri R; Cleveland Clinic, Cleveland, OH 44195, USA.
  • Swaans M; St. Antonius Ziekenhuis, 3435 Nieuwegein, The Netherlands.
  • Schopka S; Cardiothoracic Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
  • Wiesner S; Cardiothoracic Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
  • Creutzenberg M; Cardiothoracic Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
  • Sievert H; CardioVascular Center, 60389 Frankfurt, Germany.
  • Kassab GS; California Medical Innovations Institute, San Diego, CA 92121, USA.
Bioengineering (Basel) ; 11(6)2024 Jun 12.
Article en En | MEDLINE | ID: mdl-38927839
ABSTRACT
During systole, longitudinal shortening of the left ventricle (LV) displaces the aortic root toward the apex of the heart and stretches the ascending aorta (AA). An in silico study (Living Left Heart Human Model, Dassault Systèmes Simulia Corporation) demonstrated that stiffening of the AA affects myocardial stress and LV strain patterns. With AA stiffening, myofiber stress increased overall in the LV, with particularly high-stress areas at the septum. The most pronounced reduction in strain was noted along the septal longitudinal region. The pressure-volume loops showed that AA stiffening caused a deterioration in LV function, with increased end-systolic volume, reduced systolic LV pressure, decreased stroke volume and effective stroke work, but elevated end-diastolic pressure. An increase in myofiber contractility indicated that stroke volume and effective stroke work could be recovered, with an increase in LV end-systolic pressure and a decrease in end-diastolic pressure. Longitudinal and radial strains remained reduced, but circumferential strains increased over baseline, compensating for lost longitudinal LV function. Myofiber stress increased overall, with the most dramatic increase in the septal region and the LV apex. We demonstrate a direct mechanical pathophysiologic link between stiff AA and reduced longitudinal left ventricular strain which are common in patients with HFpEF.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Bioengineering (Basel) Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Bioengineering (Basel) Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Suiza