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Ann Thorac Surg 1994;57:407-415
© 1994 The Society of Thoracic Surgeons

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Articles

Cardiomyoplasty: Probable mechanism of effectiveness using the pressure-volume relationship

^a Division of Cardiothoracic Surgery, Wayne State University, Detroit, Michigan, USA
^b Second Department of Physiology, Okayama University Medical School, Okayama, Japan

Accepted for publication April 7, 1993.

^_* Address reprint requests to Dr Baciewicz, Division of Cardiothoracic Surgery, Wayne State University, Harper Professional Bldg, Suite 228, 4160 John R, Detroit, MI 48201.

	Abstract

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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.

	Footnotes

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This work was supported by NIH Reasearch Grant HL 34778.

	References

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