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Ann Thorac Surg 1993;55:72-77
© 1993 The Society of Thoracic Surgeons
a Department of Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania USA
b Surgical Research, Allegheny-Singer Research Institute, Pittsburgh, Pennsylvania USA
c Medical College of Pennsylvania, Pittsburgh, Pennsylvania USA
Accepted for publication April 10, 1992.
* Address reprint requests to Dr James A. Magovern, Department of Surgery, Allegheny General Hospital, 320 East North Ave, Pittsburgh, PA 15212.
This experiment was designed to analyze the mechanism of ventricular augmentation generated with bilateral anterior cardiomyoplasty by comparing it in an acute setting with its components, the left anterior cardiomyoplasty and the right anterior cardiomyoplasty. Hemodynamic variables were measured in 8 dogs before and after each flap was positioned around the heart. Stimulation was achieved by R-wave synchronous latissimus burst pacing at a ratio of 1:4, an amplitude of 5 V, a frequency of 33 Hz, and a duration of 30% of the R-R interval. Hemodynamic changes were again recorded during latissimus stimulation. Construction of the bilateral anterior wrap (static cardiomyoplasty) caused some depression of baseline hemodynamic function, which was greater than that caused by either the static right or left anterior cardiomyoplasty. With stimulation of the muscles (dynamic cardiomyoplasty), the bilateral wrap caused significant biventricular augmentation. Evaluation of the components of the bilateral wrap demonstrated that dynamic right anterior cardiomyoplasty also provided significant biventricular augmentation, but the dynamic left anterior cardiomyoplasty augmented only right-sided variables. The mechanism of biventricular compression by the bilateral procedure is due mostly to the right wrap. The right anterior cardiomyoplasty may provide significant biventricular compression for treatment of heart failure, without the complexity associated with bilateral anterior cardiomyoplasty.
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