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Ann Thorac Surg 1994;57:1540-1544
© 1994 The Society of Thoracic Surgeons


Articles

Autogenous cardiac assist with chronic descending thoracic aortomyoplasty

Robert R. Lazzara, MDa, Dennis R. Trumble, MSb, James A. Magovern, MDc,*

a Cardiothoracic Surgical Research, Allegheny-Singer Research Institute USA
b Department of Surgery, Allegheny General Hospital USA
c Allegheny Campus, The Medical College of Pennsylvania, Pittsburgh, Pennsylvania, USA

Accepted for publication October 12, 1993.

* Address reprint request to Dr Magovern, Department of Surgery, Allegheny General Hospital, 320 E North Ave, Pittsburge, PA 15212.

Alternative surgical treatments to orthotopic cardiac transplantation are needed for patients with heart failure. We hypothesized that descending thoracic aortomyoplasty with conditioned (fatigue-resistant) latissimus dorsi muscle could provide diastolic augmentation that would improve left ventricular function. Six mongrel dogs were studied. The left latissimus dorsi muscle was wrapped clockwise around the descending thoracic aorta. Left ventricular volume was measured with a conductance catheter. Aortic and left ventricular pressures were measured with a micromanometer The following were measured after descending thoracic aortomyoplasty at baseline and with the descending thoracic aortomyoptasty stimulated 1:1 with the heart rate: stroke work, stroke volume, left ventricular peak pressure, maximum rate of increase of left ventricular pressure, diastolic relaxation time constant, peak rate of pressure decay, left ventricular end-diastolic pressure, endocardial viability ratio, mean diastolic aortic pressure, peak diastolic aortic pressure, and time-averaged aortic diastolic velocity. Before data collection, the latissimus dorsi was stimulated (5 pulses delivered at 33 Hz at a rate of 28 per minute for 4 weeks) with burst stimulation to induce fatigue resistance. Results (expressed as the mean ± the standard error of the mean) showed significant improvement in the indices of ventricular contractility (maximum rate of increase of left ventricular pressure, 1,217 ± 83 to 1,414 ± 91 mm Hg/s) and diastolc relaxation mechanics (peak rate of pressure decay, 1,152 ± 92 to 1,282 ± 79 mm Hg/s; diastolic relaxation time constant 43 ± 2 to 38 ± 2 ms). Significant differences were noted with stimulation at 1:1 in the endocardial viability ratio (0.90 ± 0.05 to 1.14 ± 0.04), an index of myocaidial oxygen supply. Systemic diastolic pressures (peak diastolic aortic pressure, 95 ± 6 to 107 ± 5 mm Hg; mean diastolic aortic pressure, 92 ± 6 to 102 ± 6 mm Hg) and the tune-averaged aortic diastolic velocity (1.5 ± 0.6 to 3.3 ± 1.0 m/s) increased significantly. We conclude that descending thoracic aortomyoplasty stimulation with conditioned latissimus dorsi muscle can improve indkes of ventricular contractility, diastolic relaxation mechanics, diastolic pressures, and diastolic aortic velocity in the nonfailed canine heart. Farther studies with the chronic failed heart model are required.




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