Perspective
A new “twist” on right heart failure with left ventricular assist systems

https://doi.org/10.1016/j.healun.2017.03.014Get rights and content

Despite significant efforts to predict and prevent right heart failure, it remains a leading cause of morbidity and mortality after implantation of left ventricular assist systems (LVAS). In this Perspective, we review the underappreciated anatomic and physiologic principles that govern the relationship between left and right heart function and contribute to this phenomenon. This includes the importance of considering the right ventricle (RV) and pulmonary arterial circuit as a coupled system; the contribution of the left ventricle (LV) to RV contractile function and the potential negative impact of acutely unloading the LV; the influence of the pericardium and ventricular twist on septal function; the role of RV deformation in reduced mechanical efficiency after device placement; and the potential of ongoing stressors of an elevated right-sided preload. We believe an appreciation of these complex issues is required to fully understand the expression of the unique phenotypes of right heart failure after LVAS implantation and for developing better prognostic and therapeutic strategies.

Section snippets

Determinants of RH function

In the context of the RH, we focus specifically on the right ventricle (RV) in an effort to appreciate its failure with LVAS.4 Further, for purposes of this study, we define RV failure as the inability of the RV to support optimal cardiac blood flow in the presence of adequate preload. The 3 principal determinants of ventricular function, preload, contractility and afterload, uniquely assimilate to contribute to the manifestation of a diseased right-sided system. Changes in preload can directly

RV contractility impaired before LVAS implantation

Many investigations have focused on the development of pre-implant predictive models of RV failure.15 Valid predictive performance of a pre-operative risk model depends on: (a) the degree to which impaired RV function is present in those who develop post-operative RV failure; (b) the ability of our current tools to detect impaired RV contractility before LVAS implant; and (c) the unknown variable of the stresses encountered peri-operatively by the RV, a variable difficult to assess

RV contractility compromise during LVAS implantation

The unique embryology and resultant anatomy of the RV contributes to its contractile function. The RV and LV are integrated rather than distinct structures, sharing the interventricular septum. However, their embryologic origin is distinct. During development, mesodermal cells, designated as the primary and secondary (or anterior) heart fields, form in the anterior embryo. Although the left and right atria and the LV are formed by the primary heart field, the RV is formed by the secondary heart

RV contractility decline after LVAS implantation

The RV is dependent on the LV for a significant portion of its contractile function. In a canine model, Damiano and colleagues electrically isolated the RV and LV and, using pacing experiments, estimated that the LV contributes as much as 50% to RV pressure generation, presumably due to the shared fibers (Figure 2A).49 Further support for this finding comes from studies in which the main pulmonary artery and aorta of rabbits were banded to increase afterload. As one would expect,

Disclosure statement

K.B.S. is a consultant for Medtronic and Abbott. M.R.M. has consulting relationships with Abbott, Medtronic, Johnson and Johnson (Janssen), Mesoblast and Stealth Biotherapeutics; he is also Editor of JHLT and his views should not be considered representative of the journal or the ISHLT, but instead constitute his personal perspectives. R.J.T. is a consultant for Abbott and Abiomed and has received research support from Boston Scientific and Actelion.

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