TY - JOUR
T1 - A novel intra-ventricular assist device enhances cardiac performance in normal and acutely failing isolated porcine hearts
AU - van Dort, Daniel I. M.
AU - Thannhauser, Jos
AU - Morshuis, Wim J.
AU - Geuzebroek, Guillaume S. C.
AU - Duncker, Dirk J.
N1 - Publisher Copyright:
© The Author(s) 2021.
PY - 2022/4
Y1 - 2022/4
N2 - Background:We recently demonstrated that a novel intra-ventricular membrane pump (IVMP) was able to increase the pump function of isolated beating porcine hearts. In follow-up, we now investigated the impact of the IVMP on myocardial oxygen consumption and total mechanical efficiency (TME) and assessed the effect of IVMP-support in acutely failing hearts.Methods:In 10 ex vivo beating porcine hearts, we studied hemodynamic parameters, as well as arterial and coronary venous oxygen content. We assessed cardiac power (CP), myocardial oxygen consumption (MVO2), and TME (CP divided by MVO2) under baseline conditions and during IVMP-support. Additionally, five isolated hearts were subjected to global hypoxia to investigate the effects of IVMP-support on CP under conditions of acute heart failure.Results:Under physiological conditions, baseline CP was 0.36 +/- 0.10 W, which increased to 0.65 +/- 0.16 W during IVMP-support. This was accompanied by an increase in MVO2 from 18.6 +/- 6.2 ml/min at baseline, to 22.3 +/- 5.0 ml/min during IVMP-support. As a result, TME (%) increased from 5.9 +/- 1.2 to 8.8 +/- 1.8. Acute hypoxia-induced cardiac pump failure reduced CP by 35 +/- 6%, which was fully restored to baseline levels during IVMP-support in all hearts.Conclusion:IVMP-support improved mechanical efficiency under physiological conditions, as the marked increase in cardiac performance only resulted in a modest increase in oxygen consumption. Moreover, the IVMP rapidly restored cardiac performance under conditions of acute pump failure. These observations warrant further study, to evaluate the effects of IVMP-support in in vivo animal models of acute cardiac pump failure.
AB - Background:We recently demonstrated that a novel intra-ventricular membrane pump (IVMP) was able to increase the pump function of isolated beating porcine hearts. In follow-up, we now investigated the impact of the IVMP on myocardial oxygen consumption and total mechanical efficiency (TME) and assessed the effect of IVMP-support in acutely failing hearts.Methods:In 10 ex vivo beating porcine hearts, we studied hemodynamic parameters, as well as arterial and coronary venous oxygen content. We assessed cardiac power (CP), myocardial oxygen consumption (MVO2), and TME (CP divided by MVO2) under baseline conditions and during IVMP-support. Additionally, five isolated hearts were subjected to global hypoxia to investigate the effects of IVMP-support on CP under conditions of acute heart failure.Results:Under physiological conditions, baseline CP was 0.36 +/- 0.10 W, which increased to 0.65 +/- 0.16 W during IVMP-support. This was accompanied by an increase in MVO2 from 18.6 +/- 6.2 ml/min at baseline, to 22.3 +/- 5.0 ml/min during IVMP-support. As a result, TME (%) increased from 5.9 +/- 1.2 to 8.8 +/- 1.8. Acute hypoxia-induced cardiac pump failure reduced CP by 35 +/- 6%, which was fully restored to baseline levels during IVMP-support in all hearts.Conclusion:IVMP-support improved mechanical efficiency under physiological conditions, as the marked increase in cardiac performance only resulted in a modest increase in oxygen consumption. Moreover, the IVMP rapidly restored cardiac performance under conditions of acute pump failure. These observations warrant further study, to evaluate the effects of IVMP-support in in vivo animal models of acute cardiac pump failure.
UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=eur_pure&SrcAuth=WosAPI&KeyUT=WOS:000657067800001&DestLinkType=FullRecord&DestApp=WOS
U2 - 10.1177/03913988211003912
DO - 10.1177/03913988211003912
M3 - Article
C2 - 33818165
VL - 45
SP - 388
EP - 396
JO - International Journal of Artificial Organs
JF - International Journal of Artificial Organs
SN - 0391-3988
IS - 4
ER -