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Successful management of patients with mitral regurgitation and CAD remains one of the greater challenges in adult cardiac surgery. This group of patients tends to be sicker, and their surgical care is accomplished at higher risk.1,26–30 This is almost certainly because of the complex interaction between the function of the left ventricle and that of the mitral valve. Normal valve function depends on normal function of the entire mitral apparatus, which includes the ventricular wall and the papillary muscles. Similarly, normal ventricular function depends on competence of the mitral valve. Therefore, there is unique potential for CAD and mitral valve disease to interact, making the patient sicker, the pathophysiology more complicated, and the surgical management more difficult.
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In patients with preserved ventricular function, the pathophysiology and management strategies are not significantly different from those for treatment of isolated mitral regurgitation or CAD. Of course, the operation is more complex and longer, and therefore, as has been described previously, a carefully conceived operative plan with special attention to myocardial preservation is important. However, the more interesting problems are in those patients with mitral insufficiency and CAD who do not have normal hearts, and in fact, most patients with this disease combination do not have normal ventricular function.
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Clinical Presentation
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The spectrum of clinical presentation ranges from patients who are asymptomatic to those who are moribund in cardiogenic shock. The patient may have no signs or symptoms of heart disease, or may have predominant symptoms of failure, ischemia, or both. Finally, patients may present with acute syndromes often related to myocardial infarction and the sudden development of mitral insufficiency. These patients are extremely ill when they present in congestive heart failure and cardiogenic shock. Management of these patients is the most difficult.
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Findings on physical examination obviously relate to the nature of the presentation, and can range from signs of mild mitral insufficiency to severe congestive failure or cardiogenic shock. An electrocardiogram may show evidence of ischemic heart disease. All patients should undergo echocardiography. The echocardiogram is particularly useful because it gives information both about the valve and about ventricular geometry and function. Transesophageal echocardiography is especially useful in the evaluation of mitral anatomy and function. Assessments of mitral valve leaflet structure and function, chordal anatomy, and functioning of the papillary muscles and adjacent ventricular wall via transesophageal echocardiography are invaluable. All these data are important in planning the operative approach to the mitral valve and assessing the risk of surgery. Cardiac catheterization is performed in these patients for the same reasons outlined for patients with aortic valve disease. Any patient with angina pectoris or a positive stress test and any patient greater than the age of 40 with mitral insufficiency should have coronary angiography before surgery. As noted, cardiac catheterization also provides information about hemodynamics that is important in planning the operation and estimating the risk.
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Mitral regurgitation increases left ventricular preload and decreases afterload at the expense of cardiac output. Ischemic damage causes ventricular dilatation with decreased contractility and an increase in left ventricular filling pressures. These lesions combined cause synergistic decompensation and can produce pulmonary hypertension and secondary tricuspid regurgitation. Cardiac output may be very low, especially in patients with acute mitral insufficiency. Mitral insufficiency may occur in association with CAD, but often the CAD is the cause of mitral insufficiency. The pathophysiology of primary mitral insufficiency can be caused by involvement of the valve leaflets, the annulus, the subvalvular apparatus, or some combination of all of these. A detailed understanding of the pathophysiology of primary mitral insufficiency is important for planning the operative approach.
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When CAD is the cause of mitral insufficiency by its effect on regional and global ventricular function, the pathophysiology is more complicated. Global ventricular dysfunction from CAD can produce ventricular dilatation with mitral annular dilatation and subsequent mitral insufficiency. The jet of mitral regurgitation is usually central and often can be managed with annuloplasty. Alternatively, regional wall motion abnormalities involving the papillary muscle and adjacent ventricular wall can produce dynamic changes that produce insufficiency of the mitral valve. These abnormalities are now becoming better understood and are discussed more completely in Chapter 40.
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Correction of mitral insufficiency either by valve repair or valve replacement produces an instantaneous increase in left ventricular afterload. The ventricle no longer has the low-impedance left atrial chamber into which to eject blood and must overcome systemic afterload in systole. Even when myocardial ischemia is reversible, recruitment of hibernating myocardium may take time. These factors in combination with the sudden increase in left ventricular afterload contribute to the difficulty and increased risk of managing this entity. Secondary right ventricular failure may be present or ensue because pulmonary hypertension does not decrease immediately after mitral valve repair or replacement, and CAD also may affect right ventricular function.
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Symptomatic mitral insufficiency and symptomatic CAD are the usual indicators for combined surgery. As noted, patients with acute illnesses may be in extremis. Ventricular dysfunction is not per se a contraindication to surgery, especially if it is caused by reversible ischemia. Patients with global irreversible cardiomyopathy and mitral insufficiency should not be operated on because the ventricle tolerates the increase in afterload poorly and results are unsatisfactory. Estimation of the viability of the myocardium and demonstration of reversible ischemia using thallium or PET scanning therefore are important. With the left atrial enlargement that is common, patients often present with chronic or recent-onset atrial fibrillation. This condition often contributes to the reduction in cardiac output and ablation of the arrhythmia at the time of surgery may confer additional benefit. Finally a hybrid approach with catheter-based treatment of coronary disease followed by mitral surgery through a less invasive approach may be an attractive option.3,6
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One important preoperative decision in patients with mitral regurgitation and CAD is whether there is, in fact, any need for valve surgery. Because mitral regurgitation in the presence of CAD may be functional and caused by reversible myocardial ischemia, revascularization alone may improve mitral regurgitation. It is important, therefore, to distinguish organic from functional mitral insufficiency. Intraoperative transesophageal echocardiography is an essential tool for assessment of mitral valve function in this setting.31 Patients with no preoperative congestive heart failure, absent or only transient murmurs of mitral insufficiency, normal pulmonary pressures in the operating room, and trace to mild mitral insufficiency by transesophageal echocardiography after induction of anesthesia probably do not need mitral valve surgery at all.32 Many of these patients will appear to have more mitral regurgitation and higher pulmonary pressures at catheterization or when they are ischemic than when they are under anesthesia. On the other hand, many, if not all, patients with moderate to severe insufficiency will need to have the valve regurgitation addressed.5,33 If the patient has no symptoms of mitral valve disease and the morphology of the valve is normal, it is often unclear whether a valve repair operation is necessary. Myocardial revascularization itself, by its effect on ventricular function, may be associated with or is likely often the cause in improvement of mitral valve function even in the absence of a procedure on the valve itself. This may be a situation in which a staged hybrid procedure is particularly useful. For example, percutaneous coronary artery stenting, perhaps of multiple vessels, can be performed in association with expectant treatment of the moderate mitral valve insufficiency. If revascularization also contributes to amelioration of valve function, the patient may avoid an intracardiac procedure without sacrificing long-term benefit.34
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Several recent studies suggest that the quality of modern surgical results justifies a more aggressive approach to valve repair in patients with moderate mitral insufficiency and CAD.35–39 Some patients with ventricular enlargement and annular dilation secondary to CAD and/or mitral insufficiency may be managed with annuloplasty alone. Patients with organic mitral valve disease such as leaflet prolapse, chordal rupture, or chordal elongation need primary repair. Restricted leaflet motion is frequently a complication of ischemic changes in ventricular shape. In other cases, standard leaflet resection techniques for posterior flail segments may be indicated. In sicker patients, and those with restricted leaflet motion or more complex lesions (severe myxomatous degeneration), an edge-to-edge leaflet approximation (the "Alfieri stitch") may be appropriate.40 This is especially true in patients with extensive calcification of the posterior annulus or severely restricted posterior leaflet motion.41 As noted elsewhere, results of mitral repair and CABG are superior to those of mitral valve replacement, which should be avoided except in the setting of acute, severe mitral insufficiency caused by papillary muscle rupture.42
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Anesthetic considerations are similar to those described previously, although it must be recognized that these patients are in general sicker than patients with aortic valve disease and in some cases are among the sickest patients treated. Monitoring includes a radial artery line and a pulmonary artery catheter. As suggested earlier, intraoperative transesophageal echocardiography is particularly important in this group of patients for operative planning, intraoperative monitoring, and post-repair assessment of valve function. Setup for cardiopulmonary bypass is similar to that described earlier. However, both venae cavae are cannulated for venous return (Fig. 48-5). This is usually accomplished by introducing the cannulas through pursestrings in the superior vena cava and low in the right atrium. Vena caval tourniquets may be used to establish total cardiopulmonary bypass and facilitate visualization of the mitral valve and subvalvar apparatus. After clamping the aorta, cardioplegia is administered antegrade and then retrograde. Subsequent doses of cardioplegia are given retrograde. As with aortic disease, special attention must be paid to protecting the right ventricle during periods of prolonged retrograde cardioplegia.
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The most common incision providing access to the mitral valve is in the wall of the left atrium anterior to the right pulmonary veins. Preparative dissection of the interatrial groove facilitates exposure using this incision. Another choice for exposure of the mitral valve is the transseptal approach with the primary incision in the right atrium. This allows for direct visual insertion of the retrograde cardioplegia catheter through a pursestring, and affords an excellent view of the mitral valve, especially if the left atrium is not enlarged, without excessive stretching of the right atrium or the cavae. If necessary, the incision can be carried up into the dome of the left atrium for even greater exposure. This approach is particularly useful when a procedure on the tricuspid valve is indicated as well. Other incisions are discussed in the section on mitral valve disease.
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The first choice in surgery for mitral insufficiency is valve repair. When valve repair is impossible, valve replacement follows the same guidelines set forth in Chapter 42. However, in patients with the combination of coronary artery and mitral valve disease and an abbreviated life expectancy, a stronger rationale for use of a tissue prosthesis may exist.43 Regardless of the type of prosthesis, an effort should be made to retain continuity between the papillary muscles and the mitral annulus. The attachments to the posterior leaflet usually can be retained in their entirety without interfering with prosthesis function. The anterior leaflet must be resected either in whole or in part to avoid left ventricular outflow tract obstruction or interference with mechanical valve function. However, major chordal attachments may still be preserved and incorporated into the annular suture line. Regardless, standard practice is to retain continuity between the mitral annulus and the subvalvular apparatus whenever the mitral valve is replaced. Short- and long-term ventricular function has been demonstrated to be superior when this is done. Obviously, in this clinical setting, in which ventricular function has a significant impact on short- and long-term results, all steps should be taken to ensure optimal myocardial performance postoperatively.
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Patients with papillary muscle rupture caused by infarction are usually extremely sick. Valve replacement is almost always required. Some surgeons have reported success with reimplantation of the papillary muscle. This strategy is risky in these sick patients because the operation must be both expeditious and effective. Multiple attempts to achieve mitral valve competence are tolerated poorly. A reimplanted, infarcted papillary muscle does not necessarily restore mitral valve competence and also may be subject to early or late breakdown.
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As in combined aortic valve and coronary artery surgery, distal graft anastomoses are performed first (see Fig. 48-5). At this point, after the atrium has been opened, it may be prudent to undertake an arrhythmia ablation procedure in selected patients with atrial fibrillation. Radiofrequency or cryoablation probes can be used to create a lesion set within the left and right atria, as described in Chapter 58. The left atrial appendage should be oversewn. Valve repair or replacement is then carried out, followed by performance of the mammary artery anastomosis. Proximal graft anastomoses can be done either after release of the cross-clamp and application of a partially occluding clamp or with the cross-clamp in place.
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Weaning from cardiopulmonary bypass is similar to that in patients with aortic insufficiency and CAD. Again, in this group of patients, afterload reduction using drugs or the intra-aortic balloon pump may be required. Inotropic drugs with afterload-reducing capabilities such as dobutamine and milrinone may be indicated. The surgeon should have a low threshold for adding a drug such as milrinone to catecholamine agents because this combination has some theoretical advantages as a result of positive inotropic and unloading effects, as well as a reduction in pulmonary artery pressures. Alternatively dobutamine, which has both central inotropic and peripheral afterload-reducing effects, may be a first-choice drug. Because some of these patients are particularly sick, little time should be wasted in futile attempts to wean from cardiopulmonary bypass on medications and without the intra-aortic balloon. There should be a low threshold for insertion of the intra-aortic balloon in patients whose hemodynamics may be quite tenuous for hours to days after surgery, especially when the operation is an emergency.
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Another consideration for a select subset of patients with this disease is the incorporation of ventricular remodeling into the operation. There now is evidence that patients with anterior infarctions and dilated cardiomyopathy, mitral insufficiency, and CAD will benefit from exclusion of the infarcted area and remodeling of the left ventricle so as to restore an elliptical shape.44 This can be performed safely, along with mitral repair and coronary revascularization, in carefully selected patients. The result can be an increase in ejection fraction with improved postoperative function.
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Strict attention must be paid to right ventricular function and therefore to right ventricular myocardial protection in this group of patients, although right ventricular failure is more common in the setting of mitral stenosis. Right ventricular failure must be anticipated and correctly diagnosed and managed. The presence of a falling systemic blood pressure and cardiac output with falling pulmonary artery pressure and/or pulmonary capillary wedge pressure should prompt a search for right ventricular failure, which is manifested by a rising central venous pressure. Failure to recognize this and inappropriate administration of fluid can lead to irreversible right ventricular failure. As noted, less invasive approaches to mitral valve repair and coronary revascularization may become increasingly useful in these patients.45
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Hospital mortality for this group of patients is higher than that for most other forms of acquired heart disease. Early mortality rates range from 3% in good-risk patients to 60% in the sickest patients.21–23,26–29,46 The higher mortality is seen in patients with acute ischemic mitral valve disease and severe ventricular dysfunction who require emergency surgery. Incremental risk factors for early death include age, functional class, ventricular function, elevated pulmonary pressures, and cardiogenic shock. Late survival in patients with this entity is 55 to 85% at 5 years and 30 to 45% at 10 years (Fig. 48-6).21–23,26–29,47–50
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In general, patients who survive surgery have good relief of symptoms, although recurrent mitral insufficiency remains an issue for some patients who have undergone restrictive annuloplasty.51 The risk factors for this complication remain incompletely identified, although abnormal ventricular morphology and regional function appear to play a role. Significant risk factors for late death include preoperative functional class, left ventricular function, and an ischemic as opposed to a degenerative etiology for mitral insufficiency (Fig. 48-7).
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