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Ann Thorac Surg 2006;81:2324-2325
© 2006 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima City, Kagoshima, Japan
b Department of Cardiology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima City, Kagoshima, Japan
Accepted for publication March 16, 2005.
* Address correspondence to Dr Ueno, Department of Thoracic and Cardiovascular Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima City, Kagoshima, 890-8520 Japan (Email: tueno{at}m.kufm.kagoshima-u.ac.jp).
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| Introduction |
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| Technique |
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Intraoperative transesophageal echocardiography demonstrated that the tethering on medial posterior leaflet by the laterally displaced posterior papillary muscle (PPM) contributed to mitral regurgitation in addition to the enlargement of the mitral annulus. Under cardioplegic arrest, the infarcted LV wall between the left anterior descending artery and a diagonal branch was incised. The anterior papillary muscle appeared almost intact. The PPM had two heads, a large and a small one separated by a distance of approximately 1 cm. The large head appeared to consist mostly of scar tissue and the small one was a mixture of several grades of infarcted tissue. To correct tethering originating mainly from the PPM, its larger head was anchored to the anterior papillary muscle by placing two pericardium-pledgetted 3-0 Nespolene sutures (Alfresa Pharma, Co, Tokyo, Japan) (papillary realignment) to lift the large head toward the mitral valve. Because the small head of the PPM was located apart from the large head, it was impossible to approximate it together with the large head.
As a new approach to lift the subvalvular apparatus and to shorten the tethering distance toward the mitral annulus, an autologous pericardium-pledgetted 3-0 Nespolene suture was passed to one side of the small PPM base from the LV lumen to the outside, and then from outside to inside toward another side of the PPM base, and then it was tied (Fig 1). Consequently the whole small PPM, which had been laterally deviated, was shifted medially and directed toward the mitral valve. The LV wall outside the base of the small PPM, in which local dimpling was created by the previously mentioned procedure, was reinforced by placing a felt-pledgetted 3-0 Nespolene suture. Consequently the small head of the PPM was relocated and the tethering distance was shortened.
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An echocardiography performed 1 week postoperatively did not detect tethering of the mitral valve and regurgitation. The coaptation of the mitral valve, which had been dislocated toward the apex preoperatively, was reversed to the original level of the mitral annulus. Although follow-up echocardiography 7 weeks later showed dilatation of the LV chamber to approximately its preoperative size (possibly due to progressive LV remodeling), mitral regurgitation due to tethering was not detected.
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To reposition the laterally displaced PPM toward the mitral valve, we performed standard papillary realignment for its large head and regional LV plication (our new approach) for its small head. Although both procedures were supposed to work to terminate tethering of the mitral valve, it was hard to tell which procedure worked to what degree. Our method is technically easy and should be quite useful in cases such as ours in which the displaced PPM was separated into multiple heads with considerable distance and each head contributed to tethering and mitral regurgitation to various degrees. It is noteworthy that despite LV dilatation as a consequence of progressive remodeling, tethering of the mitral valve was still attenuated, and there was physiologic coaptation and no recurrence of regurgitation on follow-up echocardiography.
There are a few limitations to our method. First, our method is better suited to cases requiring simultaneous ventriculoplasty for LV remodeling and dilatation by ischemia. Through a left atrial approach, our method may be technically demanding. Second, the LV wall adjacent to the base of the PPM should be adequately thin to be inverted without excessive wall tension. With the same reason as previously described, our method would not be indicated in the cases without transmural myocardial infarction. Although our surgical method is believed to be physiologic in that it is aimed at geometric correction of the laterally displaced PPM and its consequent mitral regurgitation, further clinical experience with this procedure may be necessary to establish its significance.
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