Influence of prolonged ventricular assistance on myocardial histopathology in intact heart.
BACKGROUND
The unloading effect of ventricular assistance on the injured myocardium may adversely affect the compensatory hypertrophy of the residual intact myocardium because myocardial protein synthesis is partly controlled by cardiac work. The influence of prolonged ventricular assistance on normal myocardium was evaluated from a pathologic point of view.


METHODS
A ventricular assist device was chronically implanted in 5 goats using left atrium-aorta bypass. The pumping ratio was fixed at 70 beats/min. Left ventricular biopsy samples were taken before and 1 month after assistance.


RESULTS
Although the volume densities of myocytes and interstitial tissue in the myocardium showed no significant changes after 1 month of support, the myocyte volume density to nuclear volume density ratio and the interstitial tissue volume density to nuclear volume density ratio decreased significantly (p < 0.01 and p < 0.05, respectively). A cross-sectional area of myocyte showed decreases of 20.9% to 49.5%, whereas the nuclear cross-sectional area showed no significant changes. In addition, myofibrillar volume density in the cytoplasm decreased from 54.9 +/- 2.3% to 49.1 +/- 4.4%.


CONCLUSIONS
The results indicate that long-term ventricular assistance in the intact heart leads to myocardial atrophy. This suggests that in the damaged heart subjected to prolonged unloading by ventricular assistance, there is the possibility of limiting compensatory hypertrophic changes in the residual intact myocardium.
Kinoshita
M
M
Department of Artificial Organs, Research Institute, Osaka, Japan.
Takano
H
H
Takaichi
S
S
Taenaka
Y
Y
Nakatani
T
T
D000818:Animals; D001284:Atrophy / Q000209:etiology; D002467:Cell Nucleus / Q000648:ultrastructure; D003593:Cytoplasm / Q000648:ultrastructure; D006041:Goats; D006353:Heart-Assist Devices / Q000009:adverse effects*; D008854:Microscopy, Electron; D008928:Mitochondria / Q000648:ultrastructure; D009206:Myocardium / Q000473:pathology*; D009210:Myofibrils / Q000648:ultrastructure