The consequence of ventricular assist on acute profound biventricular failure with induced severe myocardial injury.
The effect of ventricular assist on acute profound biventricular failure (BVF) was examined in chronic animal experiments using 10 adult goats. Induction of BVF was achieved by normothermic anoxic arrest for 30-60 min during the use of a left ventricular assist system (LVAS, eight goats), or biventricular assist system (BVAS, two goats). The LVAS could maintain near normal circulation with volume loading in six goats, and three of eight goats were weaned from LVAS after 13-18 days. In the early stages, left atrial pressure was significantly higher, and right atrial pressure was significantly lower, compared with measurements in nonweaned goats. During BVAS, circulation was well maintained without volume loading, but neither of the two goats could be weaned from VAS. Myocardial fibrosis in goats without myocardial recovery was significantly more severe. Left ventricular wall thickness was thinner in nonweaned goats and there was a significant inverse correlation between the thickness of the left ventricular free wall and the assist duration in nonweaned goats. Based on these data, it was concluded that myocardial damage was severe in nonweaned cases, and the potential for healing is affected by the severity of myocardial damage before VAS application. Prolonged unloading with VAS of these severely damaged hearts caused loss of left ventricular wall thickness.
Nakatani
T
T
Department of Biomedical Engineering, National Cardiovascular Center Research Institute, Osaka, Japan.
Takano
H
H
Noda
H
H
Taenaka
Y
Y
Kinoshita
M
M
D000818:Animals; D005355:Fibrosis; D006041:Goats; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology*; D006353:Heart-Assist Devices; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D012770:Shock, Cardiogenic / Q000473:pathology / Q000503:physiopathology