HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content

J Thorac Cardiovasc Surg 2008;135:291
© 2008 The American Association for Thoracic Surgery

Invited Commentary

Discussion

Dr Frank W. Sellke (Boston, Mass). TMR was found several years ago to improve perfusion and function in animals, yet most clinical trials have had negative or barely positive results. Do you think you are comparing TMR with no TMR in a clinically relevant model? We don't do TMR on patients that don't have coronary disease or hypercholesterolemia or other risk factors for vascular disease. Would you have seen the same changes had you used a model with endothelial dysfunction and vascular disease?

Dr Atluri. I believe we would have. The goal in this study is that we were trying to create a region of myocardial ischemia, a true region of myocardial hypocontractility. I think the key is that we are looking at regional dysfunction within our area of interest. Yes, therapy did create a difference in this model. What we were basically trying to replicate is not necessarily the global dysfunction but the regional contractile dysfunction and malperfusion that we are trying to treat. In human beings, . . . [Full Text of this Article]