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The Annals of Thoracic Surgery, Vol 57, 407-415, Copyright © 1994 by The Society of Thoracic Surgeons
H Nakajima, H Niinami, TL Hooper, RL Hammond, HO Nakajima, H Lu, R Ruggiero, GA Thomas, FW Mocek and R Fietsam Jr
The mechanism of effectiveness of cardiomyoplasty was evaluated in the
setting of chronic left ventricular dysfunction in terms of the
pressure-volume relationship. The distal branches of the left coronary
artery were ligated in 12 sheep. Seven sheep died and the 5 survivors
underwent cardiomyoplasty using a left latissimus dorsi graft 10 to 12
weeks later. These muscle grafts were then electrically conditioned for 2
months. The systemic pressure and cardiac output were not different between
the postinfarction and postcardiomyoplasty period with the pacemaker off or
on. However, the pressure-volume loops were altered by cardiomyoplasty in
all 5 animals. Emax, which is an index of ventricular contractility,
increased after cardiomyoplasty from 2.66 +/- 0.92 to 4.59 +/- 1.73 mm
Hg/mL (mean +/- the standard deviation; p < 0.05), but did not change
between the pacemaker off and on situations. The pressure-volume area,
which strongly correlates with myocardial oxygen consumption, decreased
after cardiomyoplasty (1,932 +/- 615 mm Hg.mL), compared with before
cardiomyoplasty (3,776 +/- 1,201 mm Hg.mL) (p < 0.05), but did not
change between pacemaker off and on. The probable mechanism responsible for
the effectiveness of cardiomyoplasty is an "active" support or constraint
of the damaged myocardium by the latissimus dorsi and the prevention of
further ventricular dilation. This suggests that left ventricular systolic
function can be augmented by cardiomyoplasty, but that it is a secondary
mechanism of action.
ARTICLES
Cardiomyoplasty: probable mechanism of effectiveness using the pressure- volume relationship
Division of Cardiothoracic Surgery, Wayne State University, Detroit, MI 48201.
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