Ann Thorac Surg 1995;60:998
© 1995 The Society of Thoracic Surgeons
Discussion
Discussion
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See also page 986.
DR MARK B. RATCLIFFE (San Francisco, CA): This is a very nice study. As I am sure you are aware, the cardiology and magnetic resonance imaging groups at the University of Pennsylvania, with Chris Kramer as the lead researcher and Leon Axel as the senior investigator did a similar experiment and presented it in Circulation last year. They focused on somewhat different things, specifically on the percent shortening of the adjacent, noninfarcted myocardium, and showed that the percent shortening was originally approximately 25%, decreased to about 5%, and then rose at 8 weeks up to 15%. However, they were not just focusing on isovolumic systole, but on all of systole.
I have several questions: First of all, did you look at percent systolic shortening and if so were your findings similar to these of Dr Kramer. Second, the negative strains that you see in isovolumic systole must increase the preload on this noninfarcted myocardium. If the adjacent myocardium could shorten freely, an increase in preload should increase stroke work and percent shortening. Do you think, therefore, that your findings provide indirect evidence for tethering and increased afterload in this important region?
DR MOULTON: Thank you for your comments Dr Ratcliffe. The study by Kramer and Axel from Circulation last year was a longitudinal study examining fractional shortening in . . . [Full Text of this Article]
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Ann. Thorac. Surg. 1995 60: 986-997.
[Abstract]
[Full Text]
Copyright © 1995 by The Society of Thoracic Surgeons.
