|
|
||||||||
J Thorac Cardiovasc Surg 2003;126:2110-2111
© 2003 The American Association for Thoracic Surgery
Letter to the editor |
Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan
Savage and colleagues' study1 demonstrated that volume reduction surgery (VRS) in a model of left ventricular (LV) aneurysm without global LV dysfunction plicated only LV apex. On the other hand, apex-sacrificing VRS in our series reduced the diameter of not only LV apex but also LV mid-portion in a model of global LV dysfunction. The effects of volume reduction in akinetic or dyskinetic area are different from hypokinetic area.2 Drs Lunkenheimer and Anderson support reduction of the radius of the ventricle in its upper two thirds (ie, basal). We agree with them on that point, and reduction of the upper two thirds of left ventricle is the same as our apex-sparing VRS. In clinical series, however, no one has described or advocated reduction of the radius of the ventricle in its upper two thirds. The letter by Drs Lunkenheimer and Anderson focused on the issue in LV aneurysm or ischemic cardiomyopathy (raised by Savage and colleagues1), but the disease that we studied via this animal model was dilated cardiomyopathy (ie, nonischemic). From this viewpoint, their criticism is interesting and important but misdirected.
Konertz and coworkers3 reported excellent results of VRS but they also did not described reduction of the upper two thirds of left ventricle, and a majority of their cases are ischemic cardiomyopathy. Again, our study was focused on the dilated cardiomyopathy (nonischemic cardiomyopathy, a different disease). It is difficult to adopt their results to our study.
Theoretically the therapeutic effect of reducing ventricular radius is at least in part dependent on the degree of preexisting ventricular dilation. In the clinical setting, however, operative mortality is high and LV redilatation and dysfunction are not rare after VRS.4-10 This suggests that the theoretical concept is not necessarily reproducible in the clinical situation and that the way to excise and repair the LV is also important. Although there are some limitations due to the model of acute heart failure induced by ß-blocker, the heart rate before and after VRS was statistically no different between the 2 groups. LV contractility in apex-sparing VRS was shown to be superior to apex-sacrificing VRS, and LV end-diastolic pressure was lower in apex-sparing VRS. Those differences between the 2 groups were significant.
Batista's group described an incision made at the apex of the left ventricle. In our article,2 we never stated that Batista and colleagues advocated the apex resection, but they did not try to preserve the apex as much as possible. In fact, Lunkenheimer and colleagues11 use the term "oyster-shaped excision" in their case report, following the scheme of Batista's operation by widely resecting the LV apex. Throughout our article we tried to show the potential pitfall of the great operation described by Batista and colleagues and to improve it. There would be some ischemic damage extending beyond the plicated segment in VRS, and we have described plication effects in the adjacent area in our study limitation. It is unknown, however, whether the ischemic damage follows according to the position of resection or plication area. However, this potential concern of compromising the marginal arteries is equally applicable to conventional Batista procedure. Further investigation would be warranted.
We have already demonstrated these 2 types of VRS in a model of chronic dilated cardiomyopathy.12 Elevation of LV end-diastolic pressure and LV redilatation were remarkable from 1 week after apex-sacrificing VRS but not in apex-sparing VRS. Drs Lunkenheimer and Anderson described in their letter that resection of any part of LV wall, including the septum, is tolerated without impairing LV function when the left ventricle is dilated. However, septal anterior ventricular exclusion or pacopexy reduces the septal and anterior wall without amputating the LV apex and yields good clinical results.13,14 We think those results are compatible with our study.
In addition, results of some clinical cases that underwent the apex-sparing VRS in our unit have been excellent so far. Thus we believe that it is important to reduce the LV volume in dilated left ventricle with severe LV dysfunction. Apex-sparing VRS may improve the clinical results.
Although the hypothesis by Dr Torrent-Guasp and colleagues is very interesting,15 there is no scientific proof so far. Therefore the relationship between cause and result in the improved LV function after the apex-sparing VRS and preservation of single muscle band is still unknown, and further study will be required.
| References |
|---|
|
|
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |