| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||
Ann Thorac Surg 1995;60:998
© 1995 The Society of Thoracic Surgeons
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 the border zone region over time. They demonstrated that systolic fractional shortening, a measure of strain, decreased up to 6 weeks out from transmural infarction. Subsequently, strain increased a by a small amount up to 8 weeks from infarction.
Our study was not longitudinal. We quantitated strains at only one time point: 8 to 12 weeks after transmural infarction when the aneurysms were mature. Our interest was in examining in detail the function of the border zone region over the cardiac cycle to see if there were a particular phase of the cardiac cycle to which the dysfunction was limited. Our results demonstrated that it was during the relatively short isovolumic interval that the dysfunction, that is the positive circumferential strains, occurred.
Regarding your second question, as to what may be causing the dysfunction in the border zone region, it has been suggested in other studies that increased border zone stress may contribute to the dysfunction. Because the ventricular pressure is highest at the end of isovolumic systole and the wall has not yet undergone systolic thickening, the wall stress is highest at this point in the cardiac cycle. Possibly, the border zone regions are already damaged with some loss of muscle fibers and an increase in collagen. Perhaps there is some persistent ischemic injury or stunning that prevents the border zone regions from developing and maintaining isometric tension against a high afterload in isovolumic systole. Further studies are required to clarify the factors that cause the isovolumic dysfunction.
DR GORDON N. OLINGER (Milwaukee, WI): Doctor Moulton, alluding to the concept of remodeling, does this model allow you to look at the same border zone segments over a period of time? In other words, can you restudy these animals and know that you are looking at the same areas, so that in fact you could look longitudinally at the concept of remodeling, which, from a pathogenic standpoint, appears to be well explained in part by your study.
DR MOULTON: Doctor Olinger, as you know, the magnetic resonance imaging tag lines persist for only a short period of time-usually only 700 to 800 milliseconds. Therefore, to follow the same section of myocardium over multiple image sessions requires a more permanent implantable marker. We have used tantalum markers sutured to the epicardium to mark a piece of myocardium over time. They are nonferromagnetic and show up nicely on the magnetic resonance images.
DR NORMAN A. SILVERMAN (Detroit, MI): There was some initial work showing a transmural distribution in the stress/strain deformation, at least with acute ischemia. One of the proposals you had was that there may be ongoing stunning in the myocardium. Was there a transmural difference in the deformation with the subendocardium showing the most strain deformation, suggesting persistent ischemia?
DR MOULTON: Thank you for your question Dr Silverman. Currently, magnetic resonance tagging techniques allow us to place tag lines of 5 mm at the finest across the wall of the in vivo beating heart because finer tag lines fade too rapidly. Consequently, if the tag lines are placed at end diastole when the wall is very thin, we can place only one tag box transmurally across the ventricular wall. This does not allow us to compute transmural distributions of strain. In an isolated heart preparation, we can place tag lines as close together as 1.5 mm, allowing us to compute transmural strains.
DR SILVERMAN: Having gone to a Coding Committee, I am now one of the ``dumb surgeons,'' so could you just explain how a different repair with the stunned area attached to a fixed piece of Dacron that cannot shorten is going to improve systolic function?
DR MOULTON: The idea is, and this is only a theory because our study did not specifically address this issue, that the suture line of a linear repair will act as a boundary condition or constraint on the border zone region creating a high local afterload against which the border zone must contract. However, if the weakened border zones were sutured over a stiff Dacron patch, then the wall stress or afterload acting on those regions might not be concentrated on the border zones, but instead on more normal regions of myocardium. Thus, the weakened border zones might be able to contract over the Dacron patch. Again, this is only a theory, further studies are required to confirm this hypothesis.
DR WILLIAM A. BAUMGARTNER (Baltimore, MD): Doctor Moulton, I have a question. Because strain does not define functional evaluation or potential of the tissues, I am intrigued by the method. Do you have any histologic examination of the border zone or any perfusion mapping to know what the quality of the tissue is in that border zone?
DR MOULTON: Doctor Baumgartner, the histologic sections that I demonstrated, which were performed by Dr Erol Williams in Dr Jeffrey Rottman's laboratory at Jewish Hospital in St. Louis, demonstrated a slight increase in the collagen content of the border zone regions when compared with more normal remote regions. This may indicate some replacement of border zone myocytes with collagen. With respect to measuring perfusion in these regions, as far as I know, no one has examined perfusion in the border zone region of left ventricular aneurysm. There have been, of course, many studies looking at perfusion in the so-called functional border zone adjacent to acutely ischemic myocardium.
Related Article
Ann. Thorac. Surg. 1995 60: 986-997.
| ||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
