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Ann Thorac Surg 1996;61:1587-1589
© 1996 The Society of Thoracic Surgeons
Division of Cardiovascular Surgery, Toronto General Division, The Toronto Hospital, EN 13-219, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4
To the Editor:
We have read with interest the case report by Matsuda and colleagues [1] describing a modification of the endocardial patch method [2, 3] to repair a ventricular septal defect (VSD) after myocardial infarction. Matsuda and associates employed a conical porcine pericardial sack sewn in an inverted fashion (ie, convex side of the sack toward the left ventricular [LV] base) onto the LV endocardium with the suture line at a level proximal to the infarction, parallel to the mitral annular plane, and then reverted the sack (convex side toward the LV apex). They concluded that the sack technique provides a good operative view and shortens operation time; they also described that the sack technique can be applied for LV free wall rupture after myocardial infarction or mitral valve replacement.
When the VSD is located on the distal (ie, close to the apex) ventricular septum as illustrated in Figure 1A
, the sack may be applied to the LV endocardium via left ventriculotomy (left panel) as easily as with the endocardial patch method (right panel), because there is no structure in the LV lumen near the apex. When the VSD or ischemic area is located more proximally (ie, close to the LV base) as shown in Figure 1B, however, several concerns should be raised as follows. First, the suture line of the sack may interfere with the papillary muscles (left panel). Under this condition, papillary muscle dysfunction or leak through the complex suture line may develop. This concern will be more serious for a VSD on the posterior septum, the majority of which occur in the proximal half of the ventricular septum [4]. Second, the sack covers a large area of healthy endocardium, which may cause diastolic or even systolic dysfunction late postoperatively. This potential problem can be more likely when thickening, calcification, or thrombi formation between the sack and LV endocardium develops in the late phase. As a rule, using the patch, we try to cover just the ischemic area that includes the VSD and marginally ischemic zone, and leave most of the intact endocardium alone (right panel of Fig 1B). Third, Matsuda and associates employed a sack that is larger than the ischemic area; we use an endocardial patch with a size comparable with the ischemic LV area to surgically remodel the LV in both shape and size. We close the infarcted/ischemic LV wall, but the ischemic LV wall per se cannot necessarily maintain the proper shape and size of the LV unless the underlying patch does so. How can a sack with redundant size serve for that remodeling purpose? Fourth, the suture line of the pericardial sack can be very far from the ventriculotomy on the side of the LV free wall, which gives poor operative exposure as compared with the patch repair method.
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), because rupture after mitral valve replacement almost always occurs near the mitral annulus, near the base of the papillary muscles, or somewhere in between [5]. In that case, the sack might interfere with papillary muscle/chordae tendineae mechanics or cause LV outflow obstruction (see Fig 1C, left panel). Moreover, repair of rupture after mitral valve replacement is an emergency, life-saving procedure and, therefore, simple and fast methods such as endocardial patch repair should be more beneficial. Because of the above concerns, we believe that the indication of the pericardial ``sack'' technique should be limited to selected patients who have distal VSD or ischemia of the distal septum. We also believe that the endocardial patch repair technique (1) is a safe, simple procedure once a surgeon becomes accustomed to it; (2) provides reproducible results as well as good intraoperative exposure for not only VSDs (including proximal and distal VSDs, either on the anterior or posterior septum), but also LV rupture after mitral valve replacement [6], LV aneurysm [7], or LV false aneurysm [8] after myocardial infarction; and (3) may help proper remodeling of the diseased part of the LV wall or septum, because it does not distort the LV geometry or compromise the intact LV wall.
References
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