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Ann Thorac Surg 2001;71:2079-2080
© 2001 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA
Address reprint requests to Dr Magovern, Department of Cardiothoracic Surgery, Allegheny General Hospital, 320 East North Ave, Pittsburgh PA 15212
e-mail: jmagover{at}wpahs.org
Abstract
As Originally Published in 1994: Dynamic Descending Thoracic Aortomyoplasty: Comparison With Intraaortic Balloon Pump in a Model of Heart Failure by Robert R. Lazzara, MD, Dennis R. Trumble, MS, and James A. Magovern, MD. Cardiothoracic Surgical Research, Allegheny-Singer Research Institute, Department of Surgery, Allegheny General Hospital, and Allegheny Campus, The Medical College of Pennsylvania, Pittsburgh, Pennsylvania
Descending thoracic aortomyoplasty (DTA) uses the latissimus dorsi muscle to compress the proximal descending thoracic aorta as an autogenous diastolic counterpulsator. We studied the hypothesis that DTA could confer hemodynamic benefits equivalent to those yielded by an intraaortic balloon pump (IABP) in dogs (n = 7) with heart failure. The left latissimus dorsi muscle was wrapped around the proximal thoracic aorta and subsequently electrically conditioned to induce fatigue resistance. Heart failure was produced by rapid ventricular pacing after muscle conditioning. Data were collected under three conditions: (1) after the induction of heart failure; (2) with the 20-mL IABP at 1:1; and (3) with the DTA stimulated at 1:1. Effective diastolic counterpulsation was achieved with both the IABP and the DTA. The mean diastolic aortic pressure increased from 66 ± 5 mm Hg at baseline to 90 ± 4 mm Hg with the IABP and to 75 ± 4 mm Hg with the DTA. The left ventricular peak and end-diastolic pressures decreased with IABP (95 ± 5 mm Hg versus 88 ± 4 mm Hg and 16 ± 4 mm Hg versus 12 ± 4 mm Hg, respectively; p < 0.05) and with DTA (95 ± 5 mm Hg versus 87 ± 4 mm Hg and 16 ± 4 mm Hg versus 12 ± 4 mm Hg, respectively; p < 0.05). Counter-pulsation with the IABP did not change the end-systolic pressure–volume relationship or the time constant for diastolic relaxation, whereas the DTA increased the end-systolic pressure-volume relationship (3.2 ± 0.6 mm Hg/mL versus 4.0 ± 0.7 mm Hg/mL; p < 0.05) and decreased the time constant for diastolic relaxation (49 ± 5 msec versus 45 ± 6 msec; p < 0.05). These data show that DTA using conditioned skeletal muscle can provide diastolic counterpulsation in animals with compromised cardiac function. In addition, the procedure appears to have an effect on left ventricular contractility that is independent of its effects on cardiac preload and afterload.
We and others have continued to work in the area of diastolic counterpulsation using stimulated skeletal muscle. We have recently presented work on the effects of long-term aortomyoplasty on left ventricular remodeling after myocardial infarction. Magnetic resonance imaging was used to evaluate left ventricular size, mass, and geometry after anterior infarction in sheep. Control animals developed a left ventricular aneurysm with an associated increase in left ventricular size and mass. Animals treated with aortomyoplasty had no change in infarct size, but had less increase in left ventricular size and mass [1].
We believe that the conclusions presented in the original paper are still valid. Chronic diastolic counterpulsation has the potential to be an effective therapy for heart failure, but there are some limitations to this approach. Diastolic blood pressure can be increased 5 to 10 mm Hg, but afterload reduction is not reliably obtained, especially in the chronic setting. Thus, the primary application of this technique would be for patients with ischemic cardiomyopathy, where the increases in diastolic blood pressure might improve perfusion of the ischemic tissue. New approaches, such as myoblast cell implantation and growth factor injection into ischemic myocardium, have also targeted this group of patients for treatment. Taylor and associates have successfully repopulated a left ventricular cryoinfarct in rabbits by injection of autologous skeletal myoblasts into the infarct, demonstrating incorporation of the cells into the tissue and improvements in cardiac function [2]. Many other laboratories are working in this area, using various types of cells for implantation, including bone marrow stromal cells, allogenic fetal cardiomyocytes, or autologous adult cardiomyocytes, in addition to skeletal myoblasts. Rosengart has demonstrated myocardial angiogenesis in a phase I trial in humans with coronary artery disease by direct injection of an adenovirus vector containing the gene for endothelial growth factor (VEGF) [3]. Encouraging clinical results have also been reported in patients with coronary artery disease after direct injection of naked plasmid DNA encoding the gene for VEGF [4]. Currently, these areas are receiving more interest than aortomyoplasty. Other problems with clinical application of direct aortomyoplasty include the potential for aortic trauma and fibrosis of the latissimus dorsi muscle.
We continue to pursue skeletal muscle-based circulatory support, but presently, we are not studying aortomyoplasty. Rather, we are focused on developing a mechanical muscle-energy converter that will translate linear muscle contraction into hydraulic power [5]. This power will then be used to provide circulatory support. Possible methods to utilize this power include mechanical diastolic counterpulsation, cardiac compression, and powering of a left ventricular assist device. This work is funded and will be reported as it develops.
References
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