Patients undergoing mitral valve reconstruction often require additional procedures to address the following associated disorders: left atrial thrombus formation, atrial calcification, giant left atrium, and atrial fibrillation.
LEFT ATRIAL THROMBUS FORMATION
Thrombus formation in the left atrium ( Fig. 16-1 ) is frequently observed in long-lasting rheumatic valvular disease, triggered enlarged left atrium, atrial fibrillation, endocardial lesions, and low cardiac output. In degenerative valvular disease, atrial thrombus formation can be observed in elderly patients or in those with low cardiac output or hematological disorders. Atrial fibrillation is the major contributing factor for atrial thrombus formation in these conditions. Different types of thrombus can be observed :
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Left atrial appendage thrombus is the most common location (a) . The thrombus is usually organized and adherent to the endothelium. It should be completely removed before closing the orifice of the atrial appendage. The absence of an intraoperative visible thrombus does not preclude the existence of thrombus formation during the course of the disease, in particular in the presence of a large appendage, an irregular endocardial surface, or a history of stroke. In these circumstances, the left atrial appendage should also be closed. The closure of the left atrial appendage is performed in most instances by endoatrial direct suturing. This technique is preferred to external ligation, which may not completely occlude the base of the appendage, a cause of recurrent thrombus formation. Whenever the orifice of the atrial appendage is calcified, the closure is carried out using a pericardial patch.
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Extended thrombus covering a large surface of the left atrium can be approached using different techniques. Whenever the thrombus can be separated easily from the left atrial wall, it should be removed, excising occasional endothelial bands. Whenever the thrombus cannot be separated easily, it can be left in place provided that its surface is regular. Whenever an irregular surface with or without ulcerations or spots of calcification is present, the thrombus should be removed en bloc . This thromboendocardiectomy may leave areas of thin atrial tissue or a block of calcification, which should be covered by a large pericardial patch ( Fig. 16-2 ).
FIGURE 16-2
ATRIAL CALCIFICATION
Atrial calcification may or may not be associated with thrombus formation. Extensive calcification may involve the entire atrium with the orifices of the mitral valve and pulmonary veins usually intact ( Fig. 16-3 ). If the surface is regular and free from thrombus, the calcium formation should be left in place. If the surface is irregular with adherent thrombus, the calcium formation is preferably dissected from the atrial wall. The dissecting knife should be oriented so as to remain in contact with the calcium at all times. Usually, calcification is minimal at the mitral valve orifice and the pulmonary valve ostia. At these levels, the endocardium is simply cut to remove the calcium en bloc . Following this procedure, it is advisable to reduce the left atrium size to improve atrial flow.
GIANT LEFT ATRIUM
The volume of a severely enlarged left atrium should be reduced as much as possible to improve atrial flow and to minimize the risk of thrombus formation ( Fig. 16-4 ). A variety of techniques have been described. The preferred one is a helicoidal plication of the atrium using 4-0 monofilament continuous sutures starting at the appendage, progressing between the left pulmonary vein ostia and the posterior mitral annulus, and then plicating the diaphragmatic part of the left atrium ( a ). Another more complex alternative is “H plication” of the left atrium ( b ). In this technique, one horizontal branch of plication involves the atrial tissue between the left pulmonary veins and the mitral valve. Care should be taken not to injure the circumflex vessels. The other horizontal branch is the extended atriotomy. The transverse branch joins the two horizontal branches between the superior and the inferior right pulmonary veins. The left atriotomy is then closed with large sutures reinforced with Teflon strips.
ATRIAL FIBRILLATION
Recent advances in the understanding of the pathogenesis of atrial fibrillation have been critical for the development of the surgical treatment of this disorder.
Atrial fibrillation is believed to arise from enhanced automaticity at one or more rapidly depolarizing foci or re-entry involving one or more circuits. Haissaguerre and colleagues have recently shown that these foci originate predominantly at the origin of the pulmonary veins, particularly in patients with paroxysmal atrial fibrillation. Infrequently, foci may also occur in the right atrium, the superior vena cava, or the coronary sinus.
Patients with atrial fibrillation are at a sixfold increased risk of stroke and a twofold increased risk of late mortality. Therefore every effort should be made at the time of valve reconstruction to restore sinus rhythm . The classic Cox Maze III cut and sew technique is efficacious but associated with increased postoperative morbidity, particularly bleeding. Today, the Cox Maze procedure has benefited from improved techniques ( Fig. 16-5 ) using a variety of energy sources and lesion sets. The lesion set we prefer isolates the pulmonary veins (a) with a connecting lesion between the inferior left pulmonary vein and the P3 region of the mitral annulus (b) . A connecting lesion to the left atrial appendage may be associated (c) . Right-sided lesions are added in cases of chronic atrial fibrillation or for the treatment of atrial flutter. One lesion extends from the superior to the inferior vena cava (d) , another lesion extends from the right atrial appendage to the anterior segment of the tricuspid annulus (e) , a third lesion extends from the anteroposterior commissure of the tricuspid valve superiorly to the atriotomy (f) , and the final lesion extends from the interatrial septum up to the caudal aspect of the coronary sinus (g) . Following this strategy, we have documented an 80% rate of normal sinus rhythm at 1-year follow-up.
