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Ann Thorac Surg 1998;65:1544
© 1998 The Society of Thoracic Surgeons


Original articles: cardiovascular


    Discussion
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 Discussion
 
DR TODD K. ROSENGART (New York, NY): Doctor Sellke, I congratulate you on your pioneering work, including institution of this clinical trial.

We have now administered vascular endothelial growth factor to 3 patients, using an adenovirus as the transfection vector. All 3 have done well. Our study was designed very similar to yours. Our question now as we begin to analyze results, and as you have alluded to, is the importance of a watershed effect based on collaterals from bypass vessels. My first question is, do you have any data regarding the baseline occurrence of collateralization in standard coronary bypass patients, and are you going to be looking at that in any way? Second, would not angiography be useful in terms of defining the collaterals, and do you have any intentions of including angiography in your studies?

DR SELLKE: To answer your first question, everyone with coronary disease has a degree of collateralization. Some patients have an occluded left anterior descending artery and have very little functional detriment. However, we tend to operate on patients with anginal symptoms. Therefore, in most cases, collateralization is not complete. The way to answer your question is to add a control arm in which the heparin alginate slow-release devices are administered without concurrent administration of basic fibroblast growth factor. We have now initiated a phase II clinical trial with the addition of this control arm, so hopefully we will know the answer to your question soon.

Angiography will pick up collateral vessels of a certain size, those greater than several hundred micrometers in diameter. However, many of these collaterals are similar to what you see in the porcine model. They are of small caliber and do not show up very well on angiography. However, they do have physiologic importance. Angiography therefore may have some utility in detecting new collateral vessel formation; however, magnetic resonance imaging and perhaps other perfusion studies may be a better gold standard.

DR BRUCE W. LYTLE (Cleveland, OH): I have one question. In your abstract you state that all patients examined demonstrated enhanced perfusion to the unrevascularized myocardium and improved or similar myocardial contractile function by magnetic resonance imaging and a near-normal stress test. Let me make certain that I understand this. When you showed your thallium scans you said that 3 patients got better and the rest of them did not.

DR SELLKE: Right.

DR LYTLE: Now, are you saying, then, that by magnetic resonance imaging all of them looked good in terms of increased perfusion?

DR SELLKE: When we initially looked at the scans, it appeared like there was clear enhancement. But, again, you have to compare the ungrafted area with the normally perfused or grafted territory. So it is difficult to know the absolute change just on a thallium or a sestamibi scan. What I am presenting here is the more conservative estimate, whereas in the initial review, it appeared as if there was significant enhancement in all patients.

DR LYTLE: The reason for the discrepancy is that you went back over your scans and you changed your mind, is that right?

DR SELLKE: Exactly. What we present now is very conservative. There is probably efficacy, but I did not want to say that without knowing for sure.





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