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Ann Thorac Surg 2006;82:1727-1728
© 2006 The Society of Thoracic Surgeons
University of Florence, Via dei Fossi 12, Firenze, 50123 Italy
(Email: marad{at}tin.it).
The article by Tulner and colleagues [1] is a fine study on a small series of patients that adds to our understanding of surgical ventricular restoration (SVR). They look at 21 patients at baseline and compare echocardiographic and other findings at 6 months after surgery. New and interesting aspects of this study include the evaluation of biventricular function and left ventricular asynchrony after SVR.
Regarding right ventricular function, there are currently no studies that report the effects of SVR on right ventricular (RV) function and the results of the present article are important. However, the number of patients is very small and we cannot derive any evidence that SVR per se' induces right ventricular reverse remodeling. Tricuspid repair may be responsible for RV reverse remodeling and the authors recommend tricuspid repair with SVR if the annulus is dilated or if tricuspid regurgitation is at least moderate and right ventricular function is depressed. At San Donato Hospital, Milan, Italy, we consider dilatation of the right ventricle and depressed RV function a contraindication to SVR, because we have observed a bad outcome in these patients. We have observed a decrease in RV function, as evaluated by tricuspid annulus systolic excursion (TAPSE) after SVR, rather than an improvement. Perhaps TAPSE is not a good indicator of ventricular function, but we very rarely add tricuspid repair to SVR.
The authors also provide a measure of RV function by tissue Doppler imaging (peak systolic velocity of the right free wall). No differences among patients who received mitral or tricuspid (or both) repair and those who had SVR and coronary artery bypass grafting alone were observed, and the reader concludes that the beneficial effect on the right ventricle is due to SVR. Thus, the current article opens a very important issue to discussion, but additional studies and a larger number of patients are needed.
The left ventricular asynchrony is mechanical asynchrony, which is due to a nonuniform distribution of contractile properties and to a nonuniform distribution of the load on each different ventricular segment. We reported that postinfarction cardiomyopathy, in the absence of electrical conduction delay, is highly asynchronous when several different contiguous segments are evaluated [2]. The current study seems to confirm that SVR significantly reduces asynchrony. We agree with the authors that a possible mechanism by which SVR improves mechanical synchrony is a reduction in regional wall stress. The basic concept is that each single contractile unit of ventricular myocardium interacts with units placed in the series. When a segment has depressed contractility it is tethered by normal contractile adjacent segments which in turn show early shortening. Each contractile element, in fact, responds to the relationship of force-velocity and length, which is at the base of the general law of muscles. The effective afterload of each segment reflects the intraparietal transmission of stress and is only indirectly affected by ventricular afterload represented by intraventricular pressure. Thus, in the current article, the abnormal average preoperative septal-lateral contraction delay can be attributed mainly to regional abnormal wall stress remote from the infarcted myocardium and reduction of septal-lateral contraction delay by SVR to make remote regions more synergic.
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