Ann Thorac Surg 2001;72:1447
© 2001 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, Austin and Repatriation Medical Center, Studley Rd, Heidelberg, Victoria 3084, Australia
To the Editor
It is gratifying to get a response from surgeons on a very new technique that is being studied in a trial format . I do not claim to have all the answers, but I will attempt to clarify the article and answer the questions posed.
First, the early work on this concept of ventricular containment was performed in a large series of sheep with pacing-induced dilated cardiomyopathy. My colleagues and I  presented our proof-of-concept study in 1999. Our early results in humans were obtained as part of a phase I safety study. The aim of the study was to show that the procedure could be done safely as an adjunct to a conventional cardiac operation, in this case, coronary artery bypass grafting along with left ventricular reconstruction. The left ventricular diameter was reduced in 4 patients with a technique that attempts to restore left ventricular geometry . This is quite different from the Batista procedure, which is essentially excision of a large strip of normal muscle along with linear repair .
It is possible that the early reduction in size and the improvement in functional class were due to a combination of coronary artery revascularization and left ventricular reconstruction. We started our arm of a worldwide multicenter randomized trial to answer this question. I emphasize at this stage that the functional evaluations and the exercise test results were assessed by independent observers. The number of patients was small, and one outlying value or incomplete test was enough to render some of the paired data insignificant. Complete revascularization was performed in all patients and as mentioned in the report , all grafts were patent at 6 months on repeat angiography. Chronic ventricular dilatation does not occur with ischemia per se but is usually due to remodeling scars or volume overload .
The tension of the wrap is an interesting point. In our original report , we stressed a snug fit while wrapping the mesh around the heart. It is impossible to measure pressure between the cardiac-support device and the epicardium when a woven mesh is used. However, some experimental animal work done in our laboratory and at the Henry Ford Research Institute, Detroit, MI, suggests that an acute reduction of greater than 10% in volume with the mesh causes diastolic dysfunction (unpublished data).
The left ventricular end-diastolic diameter decreased significantly early postoperatively and then increased slightly thereafter. The value stabilized at about the same level at 12 months and 18 months. Similarly, ejection fraction and functional class showed the same significant improvement (the values being more significant because they showed later) and remained stable at 18 months.
The results of randomized studies involving ventricular containment are at least 12 to 18 months away. This is just one of many new techniques for surgical management of heart failure, although some have been adopted without the benefit of randomized studies.
This article has been cited by other articles:
A. Lembcke, S. Dushe, S. Sonntag, C. Kloeters, C. N. H. Enzweiler, T. H. Wiese, B. Hamm, F.-X. Kleber, and W. F. Konertz
Changes in right ventricular dimensions and performance after passive cardiac containment
Ann. Thorac. Surg., September 1, 2004; 78(3): 900 - 905.
[Abstract] [Full Text] [PDF]
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