Key result
Simulated left ventricular assistance device support reduced left ventricular mean myofiber stress at end diastole from 13.7 kPa to 1.1 kPa (p < 0.001) at 12 k RPM, while increasing leftward septal shift and right ventricular loading.
Why the study?
Does simulated LVAD support alter right ventricular mechanics and septal wall motion in a computational model of dilated chronic heart failure?
Does simulated LVAD support alter right ventricular mechanics and septal wall motion in a computational model of dilated chronic heart failure?
Absolute Event Rate: 1.1% vs 13.7%
p-value: p=<0.001
Patient-specific computational modeling reveals that LVAD support introduces unnatural septal bending and shifts the RV pressure-volume loop, providing a biomechanical mechanism for post-LVAD right heart dysfunction.
Predictive computation models offer the potential to uncover the mechanisms of treatments whose actions cannot be easily determined by experimental or imaging techniques. This is particularly relevant for investigating left ventricular mechanical assistance, a therapy for end-stage heart failure, which is increasingly used as more than just a bridge-to-transplant therapy. The high incidence of right ventricular failure following left ventricular assistance reflects an undesired consequence of treatment, which has been hypothesized to be related to the mechanical interdependence between the two ventricles. To investigate the implication of this interdependence specifically in the setting of LVAD support, we introduce a patient-specific finite-element model of dilated chronic heart failure. The model geometry and material parameters were calibrated using patient-specific clinical data, producing a mechanical surrogate of the failing in vivo heart that models its dynamic strain and stress throughout the cardiac cycle. The model of the heart was coupled to lumped-parameter circulatory systems to simulate realistic ventricular loading conditions. Finally, the impact of ventricular assistance was investigated by incorporating a pump with pressure-flow characteristics of an LVAD (HeartMate II™ operating between 8k–12k RPM) in parallel to the left ventricle. This allowed us to investigate the mechanical impact of acute left ventricular assistance at multiple operating-speeds on right ventricular mechanics and septal wall motion. Our findings show that left ventricular assistance reduces myofiber stress in the left ventricle and, to a lesser extent, right ventricle free wall, while increasing leftward septal-shift with increased operating-speeds. These effects were achieved with secondary, potentially negative effects on the interventricular septum which showed that support from left ventricular assistance devices introduces unnatural bending of the septum and with it, increased localized stress regions. Left ventricular assistance unloads the left ventricle significantly and shifts the right ventricular pressure-volume-loop toward larger volumes and higher pressures; a consequence of left-to-right ventricular interactions and a leftward septal shift. The methods and results described in the present study are a meaningful advancement of computational efforts to investigate heart-failure therapies in silico and illustrate the potential of computational models to aid understanding of complex mechanical and hemodynamic effects of new therapies.
No takes yet. Share an insight, caveat, or question.
Sack et al. (2018) studied Dilated chronic heart failure (n=1). Left ventricular assistance device (LVAD) support vs. No intervention (unsupported chronic heart failure) was evaluated on Left ventricular mean myofiber stress at end diastole (kPa) (p=<0.001). Simulated left ventricular assistance device support reduced left ventricular mean myofiber stress at end diastole from 13.7 kPa to 1.1 kPa (p < 0.001) at 12 k RPM, while increasing leftward septal shift and right ventricular loading.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: