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Ann Thorac Surg 2000;70:1290
© 2000 The Society of Thoracic Surgeons
Discussion
DR CHARLES B. HUDDLESTON (St. Louis, MO): I wonder if you could comment on the general direction of skeletal cardiomyoplasty research. The postgraduate course discussants gave a somewhat pessimistic view of the future of, I guess, a more standard skeletal cardiomyoplasty procedure, and I wonder if it looks like it is headed more in this direction or what your opinion is?
DR THOMAS: Well, I think in regards to the future, the phase 3 clinical trial with cardiomyoplasty has not borne out that it is procedure that is going to gain a lot of popularity. In fact, as far as my knowledge, I do not think it has really generated any evidence of a survival benefit, which is one of the things the trial was designed to do; and therefore, the interest in cardiomyoplasty as a procedure has really waned.
Skeletal muscle represents one of many different ways to provide treatment for the problem of congestive heart failure. Because of the limitation of donor supply, cardiac transplantation, which remains the gold standard, is limited by the number that can be done on a yearly basis. Skeletal muscle holds promise, but it is also in competition with mechanical devices. As time has gone on, mechanical devices have addressed some of the initial problems that occurred with infection and thrombosis. However, I think that there is still a possibility that skeletal muscle powered assist, perhaps in this configuration or in another, might be applicable to patients. Its primary benefit is power supply. However, as things keep getting miniaturized, this may become less important, but, skeletal muscle powered assist still uses autologous tissue, which provides protection from infection and may, in the long run, turn out to be simpler than mechanical devices.
DR JOHN D. MANNON (Philadelphia, PA): First of all, I would like to compliment the authors on the presentation and also on the fact that these are very difficult, long-term experiments. They represent a tremendous effort and I think that you are to be congratulated for that.
I would also like to point out that the histologic slides that you showed, in my opinion, are absolutely spectacular. The muscle is extremely well preserved, with very little degeneration. Have you made any effort to quantitatively map out the quality of the muscle? Is the inner wrap as good as the outer wrap?
And finally, I know years ago there was some speculation that if you stimulated muscles for very long periods of time, they would become too slow and not be able to generate sufficient force. Would you perhaps comment on that?
I enjoyed your presentation and it is very interesting work.
DR THOMAS: Thank you, Dr Mannion. In regards to your first question concerning looking in a more formal fashion, we did in this study, and it will be in the manuscript. We looked at numerous points on the skeletal muscle ventricles. They were basically divided up into sections at the base, at the mid-portion and at the apex. Cardinal points completely around the SMV were sampled in each area. This long-term dog, the one that lasted 4 years, is the one that was evaluated the most extensively histologically. We did not find that the fibrofatty deposition was relegated to just one area. There were some areas of the skeletal muscle, sometimes near the connection between the SMV and the chest wall, where we had a little bit more fibrous and fatty tissue, as compared with other areas that had much better preserved muscle such as we showed. But because we did not section 100% of the SMV, it is hard to give you an exact number as to what percentage had fibrofatty infiltration.
However, we have looked earlier at that exact question in a previous study in which we looked at a series of 44 SMVs that had been in circulation [14]. We found generally that about 60% to 80% of the muscle is well preserved. That seems to also be borne out in these few animals that have survived long term.
The other finding we noted in that previous study is that most of the damage tends to occur early, in the first few weeks, and that SMVs that are in circulation longer tend to stay the same. If we do not have ongoing muscle damage or regeneration or continued fibrosis occurring late, so that most of the damage occurs early, the etiology of the muscle damage is probably related to the process of harvesting the muscle and making the skeletal muscle ventricle. In the future, use of techniques to minimize the trauma to the muscle during harvesting may allow us to preserve more muscle.
DR WOLF SAPIRSTEIN (Washington, DC): Doctor Thomas, this is a very interesting study and device. I wonder if you have any more objective evidence of cardiac support than the rather limited diastolic augmentation that you demonstrated, which is much less than the systolic pressure. And the reduction in afterload, could it not have just been developed from substituting a low resistance bypass of the aorta?
DR THOMAS: I think I got part of it. I may not have gotten the whole question. The first part of what you were asking was about the chronic assist, whether we had looked at other methods of trying to assess it rather than just arterial pressure. The second one I did not catch.
DR SAPIRSTEIN: I was wondering if there is some objective evidence of cardiac support that your device exhibited. The diastolic augmentation was very minimal compared with systolic pressure that was maintained and the afterload reduction could have been just provided by the bypass circuit of the Y graft.
DR THOMAS: I guess what I can do to best answer your questions is to show some slides from other studies that we’ve done here. We have looked specifically at left ventricular function. With the contraction of the skeletal muscle ventricle, you can see that there is a marked reduction of left ventricular stroke work which would, I think, address your question about whether we looked at specifically what it was doing to the heart. In this long-term series, because of repeated access to the peripheral arteries, it was not possible to continually access the left ventricle and end up with a surviving animal long term.
Just one thing further along this line, we used propranolol in these earlier studies and did see significant increases in diastolic augmentation under failure conditions.
Finally, in regards to left ventricular mechanics, we have previously published this study dealing with changes in preload recruitable stroke work and maximal elastance and saw that with augmentation both of those parameters increased significantly.
Related Article
Ann. Thorac. Surg. 2000 70: 1281-1289.
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