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LeBoutillier M III, DiSesa VJ. Valvular and Ischemic Heart Disease.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:10571074.

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Chapter 43

Valvular and Ischemic Heart Disease

Martin LeBoutillier, III/ Verdi J. DiSesa

AORTIC STENOSIS AND CORONARY ARTERY DISEASE
????Clinical Presentation
????Pathophysiology
????Operative Management
????Results
AORTIC REGURGITATION AND CORONARY ARTERY DISEASE
????Clinical Presentation
????Pathophysiology
????Operative Management
????Results
MITRAL REGURGITATION AND CORONARY ARTERY DISEASE
????Clinical Presentation
????Pathophysiology
????Operative Management
????Results
MITRAL STENOSIS AND CORONARY ARTERY DISEASE
????Clinical Presentation
????Pathophysiology
????Operative Management
????Results
AORTIC STENOSIS, MITRAL REGURGITATION, AND CORONARY ARTERY DISEASE
????Clinical Presentation
????Pathophysiology
????Operative Management
????Results
AORTIC AND MITRAL REGURGITATION AND CORONARY ARTERY DISEASE
????Clinical Presentation
????Pathophysiology
????Operative Management
????Results
SUMMARY
REFERENCES

?? INTRODUCTION
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In recent years, there has been a great deal of progress in coronary artery surgery, nonsurgical treatment of coronary artery disease, and the surgical treatment of valvular heart disease. As thoroughly described in previous chapters, beating heart surgery has become commonplace. Interventional therapies for coronary artery obstruction have extended to multivessel disease and continue to change the number and the nature of patients referred for bypass surgery. The options for treatment of valvular disease have continued to expand with advances in techniques for repair of aortic and mitral valves as well as increases in the choices of valve type for replacement. Other areas of rapidly growing interest are surgical treatment of atrial arrhythmias and the surgical approach to the failing ventricle in dilated ischemic cardiomyopathy. Some of these topics will be discussed in subsequent chapters. All are issues that the surgeon must consider when planning strategy for the treatment of the patient with combined valvular and coronary artery disease. More patients are now presenting with increasingly complex pathology. It is less often that the surgeon sees a patient with simple aortic stenosis and proximal coronary artery disease. Rather, that patient now may have been managed with more aggressive medical therapy or even catheter interventions and is referred at an older age and is sicker, with more diffuse disease, arrhythmias, and worsening ventricular function. As a result those patients who present for surgery have a higher risk profile than was previously the case, and require a more flexible and thoughtful approach.

The interaction between the pathophysiologies of valvular heart disease and coronary artery disease is complex. Valvular heart disease alters ventricular function. Coronary artery disease may have an additional impact because of its potential to affect ventricular morphology and physiology. In addition to decreases in contractile strength, regional myocardial infarction may lead to distortion of ventricular shape with resulting effects not only on ventricular function but also on mitral valve performance. In patients with valvular heart disease, coronary obstructions may be symptomatic or asymptomatic, but the decision to intervene surgically is often made regardless of the presence of symptoms and in order to have a positive effect on the pathophysiology of both diseases.

Under most circumstances, surgeons attempt to treat both valvular and coronary artery diseases simultaneously. At the least, this makes for a longer and more complicated operation with longer myocardial ischemia times. Because of this, combined coronary artery and valve operations usually have a higher risk for early and late mortality than operations for valvular heart disease alone (Fig. 43-1). The increased complexity increases the need for careful preoperative assessment of myocardial function and an understanding of the impact of changing afterload and preload associated with valve surgery on ventricular function. In adult patients with combined valvular and ischemic heart disease, therefore, the assessment of intrinsic left ventricular function assumes paramount importance. Clinical signs and symptoms of left ventricular failure should be sought. In addition to history, physical examination, and routine lab tests, preoperative echocardiography is mandatory. Transesophageal echocardiography allows for accurate planning when operative repair is considered. It is also important to distinguish heart failure due to valvular disease from reversible or irreversible myocardial dysfunction due to coronary ischemia. Dobutamine stress echocardiography may be useful in eliciting ventricular size and shape changes that occur under stress and any resultant exacerbation of underlying valve pathology. At cardiac catheterization, left ventricular end-diastolic pressure and pulmonary pressures give additional information about left and right ventricular function and supplement noninvasive evaluation of valve function and coronary anatomy. In centers where it is available, positron-emission tomography (PET) helps detect areas of viable myocardium with reversible ischemia and ischemic dysfunction as distinguished from irreversibly scarred muscle. These assessments are important prior to embarking on combined valve and coronary artery surgery, for they are crucial in estimating operative risk and planning the operative approach.



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FIGURE 43-1 Survival after aortic or mitral valve replacement in patients with and without coronary artery disease. In both cases, long-term survival is significantly worse in patients with coronary disease. (Adapted with permission from Jones EL, Weintraub WS, Craver JM, et al: Interaction of age and coronary disease after valve replacement: implications for valve selection. Ann Thorac Surg 1994; 58:378.)

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The assessment of valve pathology is covered in detail in previous chapters on isolated valvular heart disease. As has been noted earlier, coronary angiography is not necessarily required in all patients with valvular pathology who are about to undergo valve surgery. However, given the prevalence of coronary artery disease in aging Western populations, a high index of suspicion leads to the generalized use of coronary angiography in all patients over 40 years of age, and in select younger patients as well.

With present technology and techniques, myocardial revascularization can be added to any valve operation. For the most part, all that is needed is a rational approach, more time, and good myocardial protection. Because of the wide pathophysiologic spectrum of valvular and coronary artery diseases, several frequently encountered valve and coronary artery combinations are considered in this chapter, including (1) aortic stenosis with coronary artery disease (CAD), (2) aortic regurgitation plus CAD, (3) mitral regurgitation plus CAD, (4) mitral stenosis plus CAD, (5) aortic stenosis and mitral regurgitation plus CAD, and (6) aortic regurgitation and mitral regurgitation plus CAD. Of course, patients may have combined lesions of stenosis and insufficiency, but to avoid unproductive complexity, and because one lesion usually dominates, the somewhat arbitrary categorization noted above will be maintained during the ensuing discussion. For each entity, the clinical presentation, the pathophysiology of the disease state and its correction, the operative and management approach, and short- and long-term results are discussed.


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Aortic stenosis is one of the more frequently encountered valvular lesions in adult populations. Since degenerative calcific aortic stenosis is most common in patients in their 60s, 70s, and 80s,1,2 and since congenitally bicuspid valves that become stenotic are more frequent in men who are susceptible to coronary artery disease at an earlier age,3 it is not surprising that the combination of aortic stenosis and coronary artery disease is encountered frequently. This disease combination is usually gratifying to treat because the response to surgical relief of aortic stenosis and coronary artery obstructions is significant, immediate, and relatively durable.

Clinical Presentation

Patients with aortic stenosis are asymptomatic initially but eventually present with angina pectoris, congestive heart failure, syncope, or some combination of these. When significant coronary artery obstructions are present in addition to valvular obstruction, angina pectoris is almost always present. However, angina pectoris can occur in the absence of significant coronary artery obstructions. It is relatively easy to identify symptoms of myocardial ischemia or congestive heart failure in these patients. Neurologic symptoms may be more difficult to elicit, and careful questioning regarding transient symptomatology is required. Symptoms suggestive of carotid artery obstruction should be sought. Specific studies of the carotid arteries may be necessary, especially since the murmur of aortic stenosis may radiate into the carotids and obscure the detection of bruits.

Prominent findings on physical examination include the typical crescendo/decrescendo systolic murmur heard in the aortic area. Signs of congestive heart failure with rales and edema may be present. The electrocardiogram may show left ventricular strain. If the patient suffered recent or old myocardial infarction, electrocardiographic abnormalities typical of infarction also may be present. The echocardiogram typically shows calcified and immobile aortic valve leaflets producing a constricted aortic orifice with the resultant hypertrophied left ventricle. All patients with angina pectoris and all patients with aortic valve disease who are over 40 years of age should have coronary angiography to define coronary anatomy. Right- and left-sided heart catheterization should be performed simultaneously so that complete evaluation of myocardial performance, including measurement of left ventricular end-diastolic pressure and the pulmonary artery pressures, can be obtained. Transaortic valvar gradient also can be determined at catheterization.

The preoperative evaluation of patients with aortic stenosis, coronary artery disease, and poor ventricular function is complicated. Patients with poor ventricular function often generate relatively low transaortic valve gradients. This renders the calculation of valve area and the assessment of critical aortic stenosis less accurate. The morphology of the valve with immobile leaflets and heavy calcification as seen on echocardiography is often an important confirmatory sign that critical aortic stenosis is present. Even in the presence of a small gradient, if echocardiographic signs of significant valve stenosis are present, and if left ventricular intracavitary pressure exceeds 120 mm Hg in systole, mortality rates are acceptable, and response to valve replacement surgery is usually good. A poorly contractile, thinned-out ventricle with low transvalvular gradient and low intracavitary systolic pressure usually suggests that operation is of high risk and may be of limited or no benefit. A poorly contractile ventricle with normal or increased wall thickness may recover contractile force if a substantial amount of reversibly ischemic myocardium is present and if the degree of aortic stenosis is significant. In addition to ventricular function, other important determinants of the risks and advisability of surgery include patient age, presence of previous cardiac operations, and overall organ functions, especially renal function.

Pathophysiology

Aortic stenosis produces high ventricular afterload, which ultimately is the source of all the symptoms and signs of aortic stenosis. Most patients with aortic stenosis have hypertrophied and thick-walled left ventricles. Contractile function is initially good, and ejection fraction may be maintained. In later stages of the disease, the ventricle begins to fail with enlargement and global diminution of contractile function. At any stage of the disease, the presence of critical coronary artery obstruction can cause regional wall motion abnormalities. Significant three-vessel coronary artery disease of long-standing duration may itself lead to global ventricular dysfunction.

In patients with critical aortic stenosis and good ventricular function, the increased left ventricular afterload is immediately reduced by valve replacement. Since most patients with aortic stenosis have hypertrophied and thick-walled ventricles, intraoperative subendocardial ischemia is more difficult to avoid during aortic cross-clamping. Although revascularization should not decrease left ventricular contractility and may increase it, some myocardial stunning with a temporary decrease in global and regional left ventricular contractility inevitably results from the surgical procedure.47 This, of course, assumes more important pathophysiologic significance in patients with poor ventricular function preoperatively.

Postoperatively, patients may have dramatic improvement in symptoms. Relief of left ventricular outflow obstruction immediately leads to enhanced cardiac output and perfusion of vital organs. In addition, left ventricular function improves both immediately and over time after relief of outflow obstruction and as remodeling ensues. Correction of myocardial ischemia can lead to recruitment of formerly hibernating myocardium7 with further enhancement of ventricular function.3

Operative Management

Monitoring for surgery of the aortic valve and coronary arteries includes catheters and measurements that have become standard for most cardiac surgical operations. These include arterial lines (usually in the radial artery for blood pressure and blood gases), and a pulmonary artery catheter for measurement of pulmonary artery pressures, cardiac output by thermodilution, with optical sensors for continuous estimation of mixed venous oxygen saturation. While the pulmonary artery catheter has a balloon at its tip, occlusion wedge pressure is rarely measured in the perioperative period because of the danger of pulmonary artery rupture. Particularly useful information is provided by continuous measurement of mixed venous oxygen saturation.

The perfusion setup is standard and similar to that for isolated coronary artery bypass (Fig. 43-2). A single aortic cannula is ordinarily placed in the distal ascending aorta. A single two-stage venous cannula is placed via the right atrial appendage with its tip positioned in the inferior vena cava. After establishment of cardiopulmonary bypass, the patient is usually cooled to 32?C to 34?C, during which time a left ventricular vent is positioned via the right superior pulmonary vein. With the heart well emptied, the aortic cross-clamp is applied during a temporary reduction in pump flow. Thereafter, the heart is arrested with cold (4?C) potassium blood cardioplegia and topical irrigation is applied with iced saline solution. After the aorta is opened, the endocardium is intermittently irrigated with iced saline solution to enhance myocardial cooling.



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FIGURE 43-2 Operative sequence for aortic valve replacement and coronary artery bypass grafting: (1) aorta is cross-clamped and cardioplegia administered antegrade and retrograde, (2) distal graft anastomoses are performed, (3) the aortotomy is made with an oblique incision into the noncoronary sinus of Valsalva, (4) aortic valve replacement is carried out using the prosthesis of choice, (5) the aortotomy is closed, (6) the distal mammary artery anastomosis is performed, and (7) the proximal graft anastomoses are done. In this case, the proximal anastomoses are done with the aortic cross-clamp in place.

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A combination of antegrade and retrograde cardioplegia is optimal. The initial dose of cardioplegia usually is given both ways, half antegrade and half retrograde. Approximately 15 mL/kg is given as the initial dose. Subsequent doses of cardioplegia are given retrograde throughout the operation. This is particularly convenient because retrograde cardioplegia can be given even after the aortic root is opened without significantly disrupting the flow of the operation. Cardioplegia may also be given antegrade via radial and vein grafts after they are attached. This is especially important if a graft has been placed in the right coronary system, as retrograde cardioplegia may not fully protect the right ventricle.

The left internal mammary artery is almost always used to graft the left anterior descending artery when it has a significant obstruction. In general, reversed greater saphenous veins and radial arteries are used for other bypass grafts. The reasoning behind the choice of valve prosthesis is nearly identical to that in the treatment of isolated valvular heart disease. Any type of prosthesis may be used. However, several issues must be considered. The indications for all types of tissue valves are stronger as these patients' life expectancies are often shorter. However, these sicker patients may not well tolerate the longer clamp times necessary for the more complex implantation of nonstented tissue valves.

The multiple steps in the combined operation follow a logical sequence. After establishment of cardiopulmonary bypass and insertion of the left ventricular vent, the aorta is clamped and the heart arrested with antegrade and retrograde cold blood cardioplegia and topical hypothermia with iced saline. The first step in the operation is performance of the distal radial artery and saphenous vein bypass grafts. When these are complete, the ventricles may be wrapped in a cooling pad after which the aorta is opened, and aortic valve replacement is carried out using the prosthesis of choice. The aorta is closed completely at this point. The distal anastomosis of the internal mammary artery graft is then made. Following completion of this, air is evacuated from the heart and the aortic cross-clamp is released. A partially occluding clamp is applied to the aorta, and proximal anastamoses are performed, when necessary. Alternatively, the proximal anastomoses can be performed with the aortic cross-clamp still in place. While this prolongs the ischemia time, it avoids application of a second clamp to the aorta with the potential for disruption of atheromatous debris or injury to the aortic suture line. This consideration is particularly important in patients undergoing reoperations, since the presence of previous bypass grafts can make application of a partially occluding clamp on the aorta difficult. Coordinated sinus rhythm is established after temporary atrial and ventricular pacing wires are positioned. After de-airing is confirmed by TEE, the left ventricular vent is removed. Of note, atrial-ventricular sequential activation is particularly important to optimize hemodynamic performance in patients with aortic stenosis because as much as 30% of the cardiac output may be derived from atrial kick as a result of the hypertrophied and noncompliant ventricle that is typical of the patient with aortic stenosis.

Weaning from cardiopulmonary bypass is performed gradually with stepwise diminution of pump flow and increased left ventricular filling. Simultaneous monitoring of the appearance of the heart, pulmonary artery and systemic blood pressures, and mixed venous oxygen saturation is done during weaning. In patients with hypertrophied ventricles, it may be important to keep the left ventricle filled to prevent excessive left ventricular outflow tract obstruction in systole and to provide adequate preload in the noncompliant heart.

In patients with particularly severe ventricular dysfunction who do not wean from bypass, the intra-aortic balloon pump may be used. Two to three attempts to wean from cardiopulmonary bypass using inotropic drugs should be made over a period of 20 to 30 minutes. If weaning from cardiopulmonary bypass is not successful at this point, an intra-aortic balloon pump should be inserted. In some patients, a ventricular assist device is required. Persistent attempts to wean from bypass without mechanical support may be counterproductive because complications from prolonged cardiopulmonary bypass may ensue beyond 30 minutes of elapsed time. As the hypertrophied heart recovers following the ischemic insult, inotropic and mechanical support often can be weaned rapidly. In patients with more impaired ventricular function, weaning, of necessity, occurs more gradually and may take days.

Results

Early hospital mortality after aortic valve replacement and coronary bypass grafting ranges from approximately 2% to 10%.3,8 Higher mortality is observed in patients with more severe symptoms of heart failure and impaired ventricular function preoperatively. Most frequent causes of operative death are low-output cardiac failure, myocardial infarction, and arrhythmia. Incremental risk factors for hospital death include patient age, functional class, and several measures of ventricular function. In a number of studies, late survival has ranged from 60% to 80% at 5 years and from 50% to 75% at 8 years postoperatively (Fig. 43-3).914 By multivariate analysis, variables leading to reduced late survival include older age, cardiac enlargement, and more severe preoperative clinical symptoms. The use of a mechanical prosthesis at valve replacement has been associated with lower long-term survival and lower long-term event-free survival (Fig. 43-4). As discussed earlier, choice of valve type is a complex issue in combined valvecoronary artery surgery. This is a decision that cannot be made without consultation with the patient. A frank discussion of the advantages and drawbacks of each approach continues to be an important component of the preoperative evaluation and planning for this type of surgery.



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FIGURE 43-3 Long-term survival and event-free survival after aortic valve replacement and coronary artery bypass grafting in 471 patients. Adapted with permission from Lytle BW, Cosgrove DM, Gill CC, et al: Aortic valve replacement combined with myocardial revascularization. J Thorac Cardiovasc Surg 1988; 95:402.)

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FIGURE 43-4 Long-term survival advantage for patients undergoing aortic valve replacement and coronary artery bypass grafting using a bioprosthesis (n = 218) versus a mechanical valve (n = 253). (Adapted with permission from Lytle BW, Cosgrove DM, Gill CC, et al: Aortic valve replacement combined with myocardial revascularization. J Thorac Cardiovasc Surg 1988; 95:402.)

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Significant aortic regurgitation occurs less often in older populations, and is also less often encountered with coronary artery disease. Most series of patients undergoing aortic valve replacement and coronary artery bypass surgery include a relatively small number (10% to 25%) of patients with aortic insufficiency3,811 While the operative management of patients with aortic regurgitation and coronary artery bypass surgery is similar to that previously described, aortic insufficiency produces different pathophysiology that has implications for perioperative management, and the presence of an incompetent aortic valve introduces subtle nuances to the intraoperative management of these patients.

Clinical Presentation

Patients with aortic regurgitation and coronary artery disease usually present in one of three ways. The aortic regurgitation may be asymptomatic and detected incidentally during evaluation for symptomatic coronary disease. Second, the patient may be asymptomatic, yet a routine physical examination reveals a murmur of aortic insufficiency that leads to cardiac evaluation and detection of coronary disease. Finally, patients may present relatively late in the course of valvular heart disease with congestive heart failure due to decompensation of the volume-overloaded left ventricle or ischemic damage or both. Patients therefore may present with no symptoms and essentially normal physiology, a classic ischemic syndrome, or congestive heart failure. The physical signs also will depend on the nature of the presentation. In general, all patients with aortic insufficiency have an audible early diastolic blowing murmur. In late stages of the disease, signs of congestive heart failure, including rales and peripheral edema, may be present.

The preoperative evaluation of a patient with aortic insufficiency and coronary artery disease is not different from that previously described for patients with aortic stenosis and ischemic heart disease. Echocardiography is particularly useful in detecting aortic regurgitation because the murmur is sometimes subtle and difficult to detect. In addition, echocardiography gives important information regarding both ventricular contractile function and ventricular size. Since many patients with aortic regurgitation are asymptomatic, careful evaluation for changes in ventricular size or function is important because the presence of these changes may constitute an indication to proceed with surgical intervention in the absence of symptoms.

Pathophysiology

Aortic regurgitation increases left ventricular preload and causes left ventricular dilatation. Dilatation does not occur acutely, and patients with acute aortic insufficiency are often severely symptomatic due to a sudden increase in left ventricular end-diastolic pressure and decrease in net forward cardiac output. Left ventricular dysfunction due to coronary artery disease also can produce left ventricular dilatation. Valve replacement relieves some of the preload but does not immediately result in improved left ventricular contractility. Revascularization may produce improved contractility by recruitment of hibernating myocardium.4,7 This operation does not increase left ventricular afterload.

The indications for surgery in aortic regurgitation continue to be somewhat controversial, and are reviewed in depth in the section on aortic valve disease. The evaluation of valvular pathology proceeds along similar lines as described above, with emphasis on echocardiographic results. However, this evaluation is somewhat more difficult when coronary artery disease is also present, because there might be an impact on ventricular function that revascularization may or may not improve. Nevertheless, except in advanced stages of diffuse three-vessel coronary artery disease, myocardial abnormalities due to coronary artery obstructions are usually regional and can be distinguished from global dysfunction due to volume overload from the insufficient valve. Making this distinction is of paramount importance in the preoperative assessment and risk stratification of these patients. Again, decisions about timing of aortic valve surgery in the presence of coronary artery disease are different than in cases of isolated valvular disease, with emphasis on fixing the valve earlier in the course of the disease.

Operative Management

The operation is conducted in a fashion similar to that described for aortic stenosis and coronary artery disease. However, in the presence of aortic insufficiency, antegrade cardioplegia in the aortic root cannot be given because the cardioplegia solution leaks into the left ventricle. In general, retrograde cardioplegia is used under these circumstances with doses of antegrade cardioplegia given into the coronary ostia with hand-held catheters after the aorta has been opened.

Considerations in weaning from cardiopulmonary bypass are somewhat different from those described for aortic stenosis. Patients with aortic regurgitation are more likely to have dilated ventricles that tolerate increases in afterload poorly. Successful perioperative management of these patients, therefore, requires careful attention to adjustments in preload and afterload. In patients with volume-overloaded ventricles due to aortic insufficiency, vasodilators may be an important component of postoperative management. Drugs such as milrinone and dobutamine have a role because they provide both inotropic support and ventricular unloading. The mechanical ventricular unloading devicethe intra-aortic balloon pumpalso may be used. It is rare that mechanical circulatory assistance with a ventricular assist device is required. Its use should be reserved for younger patients without comorbid conditions in whom prompt improvement in ventricular function is anticipated.

Results

Early results after operation for aortic regurgitation and coronary artery disease include an expected hospital mortality rate of less than 10%.3,8 Incremental risk factors for hospital death are similar to those described previously, with advanced age and poor ventricular function having the greatest impact. Late survival after this operation is similar to that for aortic stenosis and coronary artery disease (see Fig. 43-3).914 Despite the impression that patients with aortic insufficiency and coronary artery disease do not do as well as those with aortic stenosis, aortic insufficiency has not been an independent risk factor for early or late mortality.3 Interestingly, recovery of ventricular ejection fraction does have a favorable impact on late mortality. When ventricular dilatation and diminution in ventricular systolic function occur in the setting of aortic regurgitation, these often are irreversible changes. While some improvement of function can occur with elimination of the volume overload and with revascularization in patients with combined valvular and coronary artery diseases, there may be less recovery of ejection fraction in patients with aortic insufficiency compared with aortic stenosis. Failure of recovery of ventricular function in this setting may have an impact on long-term survival but not one so great as to render aortic insufficiency an independent risk factor for late death.


?? MITRAL REGURGITATION AND CORONARY ARTERY DISEASE
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Successful management of patients with mitral regurgitation and coronary artery disease 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.1,1518 This is almost certainly because of the complex interaction between the left ventricle and 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 coronary artery disease and mitral valve disease to interact, making the patient sicker, the pathophysiology more complicated, and the surgical management more difficult.

In patients with preserved ventricular function, the pathophysiology and management strategies are not significantly different from those for treatment of isolated mitral regurgitation or coronary artery disease. 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 coronary artery disease who do not have normal hearts, and in fact, most patients with this disease combination do not have normal ventricular function.

Clinical Presentation

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.

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 function. Assessments of mitral valve leaflet structure and function, chordal anatomy, and functioning of the papillary muscles and adjacent ventricular wall via TEE 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 with mitral insufficiency over the age of 40 should have coronary angiography before surgery. As noted previously, cardiac catheterization also provides information about hemodynamics that is important in planning the operation.

Pathophysiology

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 coronary artery disease, but often the coronary artery disease is the cause of mitral insufficiency. The pathophysiology of primary mitral insufficiency can be due to involvement of the valve leaflets, the annulus, the subvalvular apparatus, or some combination of all of the above. A detailed understanding of the pathophysiology of primary mitral insufficiency is important for planning the operative approach.

When coronary artery disease is the cause of mitral insufficiency by its effect on regional and global ventricular function, the pathophysiology is more complicated. Global ventricular dysfunction from coronary artery disease 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 the 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 36.

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 in 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 are responsible for 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 coronary artery disease also may affect right ventricular function.

Symptomatic mitral insufficiency and symptomatic coronary artery disease 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 due to 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.

Finally, with the left atrial enlargement that is common in these patients, they often present with chronic or recent onset atrial fibrillation. This further acts to reduce cardiac output and may also benefit from being addressed at the time of surgery by ablation therapy.

Operative Management

One important preoperative decision in patients with mitral regurgitation and coronary artery disease is whether there is, in fact, any need for valve surgery. Since mitral regurgitation in the presence of coronary artery disease may be functional and due to 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.19 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.20 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. Clearly, however, those with moderate to severe insufficiency will need to have the valve regurgitation addressed.21 Some patients with ventricular enlargement and annular dilation secondary to coronary artery disease 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. Standard leaflet resection techniques for posterior flail segments are 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.22 This is especially true in patients with extensive calcification of the posterior annulus or severely restricted posterior leaflet motion.23 As noted elsewhere, results of mitral repair and coronary artery bypass surgery are superior to those of mitral valve replacement, which should be avoided except in the setting of acute, severe mitral insufficiency due to papillary muscle rupture.24

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, transesophageal echocardiography is particularly important in this group of patients. Setup for cardiopulmonary bypass is similar to that described. However, both venae cavae are cannulated for venous return (Fig. 43-5). This is usually accomplished by introducing the cannulas through purse strings in the superior vena cava and low in the right atrium. 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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FIGURE 43-5 Operative sequence for mitral valve replacement and coronary artery bypass grafting: (1) cannulation and cross-clamping of the aorta with antegrade and retrograde cardioplegia, (2) distal vein graft anastomoses are performed, (3) left atriotomy is performed after dissection in the interatrial groove, (4) mitral valve repair or replacement with the prosthesis of choice, (5) closure of left atriotomy, (6) distal anastomosis using the mammary artery is performed, and (7) proximal graft anastomosis is done. In this case, the cross-clamp has been removed and a partially occluding aortic clamp used.

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The most common incision is in the wall of the left atrium anterior to the right pulmonary veins. Preparative dissection of the interatrial groove usually facilitates exposure using this incision. Another choice for exposure of the mitral valve is the trans-septal approach. This allows for direct visual insertion of the retrograde cardioplegia catheter through a purse string, 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. Other incisions are discussed in the section on mitral valve disease. Choice of coronary artery grafts is similar to that for aortic disease.

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 38. However, in patients with this disease combination and an abbreviated life expectancy, a stronger rationale for use of a tissue prosthesis may exist.25 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 functions appear to be better when this is done. Obviously, in this clinical setting where ventricular function has a significant impact on short- and long-term results, all steps should be taken to ensure optimal myocardial performance postoperatively.

Patients with papillary muscle rupture due to 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 late breakdown.

As in combined aortic valve and coronary artery surgery, distal graft anastomoses are performed first (see Fig. 43-5). At this point, after the atrium has been opened, it may be prudent to undertake an arrhythmia ablation procedure in selected patients. Radiofrequency or cryoablation probes can be used to create a lesion set within the left and right atria, as described elsewhere in this text (Chapter 53). The left atrial appendage may be oversewn as necessary. 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. Weaning from cardiopulmonary bypass is similar to that in patients with aortic insufficiency and coronary artery disease. 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 particularly indicated. The surgeon should have a low threshold for adding a drug such as milrinone to epinephrine 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. Since 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.

Another consideration for a select subset of patients with this disease is the incorporation of ventricular remodeling into the operation. A large body of work is now emerging indicating that patients with anterior infarctions and dilated cardiomyopathy, mitral insufficiency, and coronary artery disease will benefit from exclusion of the infarcted area and remodeling of the left ventricle with return to elliptical shape.26 This can be performed safely, along with mitral repair and coronary revascularization, in carefully selected patients. The result can be a dramatic increase in ejection fraction with greatly improved postoperative function.

Strict attention must be paid to right ventricular function 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.

Results

Hospital mortality for this group of patients is higher than for most other forms of acquired heart disease. Early mortality rates range from 3% in good-risk patients to 60% in the sickest patients.1214,1518,27 The higher mortality is seen in patients with acute ischemic mitral valve disease and severe ventricular dysfunction who require emergency operation. Incremental risk factors for early death include age, functional class, ventricular function, pulmonary pressures, and cardiogenic shock. Late survival in this entity is 55% to 85% at 5 years and 30% to 45% at 10 years (Fig. 43-6).1214,1518,28 In general, patients who survive surgery have good relief of symptoms. 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. 43-7).



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FIGURE 43-6 Survival and event-free survival after mitral valve replacement combined with coronary artery bypass grafting in 278 patients. (Adapted with permission from Lytle BW, Cosgrove DM, Gill CC, et al: Mitral valve replacement combined with myocardial revascularization: early and late results for 300 patients, 1970 to 1983. Circulation 1985; 71:1179.)

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FIGURE 43-7 Survival after mitral valve replacement and coronary artery bypass grafting based on the etiology of mitral valve disease. A survival advantage for patients with myxoid degeneration of the mitral valve is demonstrated. (Adapted with permission from Lytle BW, Cosgrove DM, Gill CC, et al: Mitral valve replacement combined with myocardial revascularization: early and late results for 300 patients, 1970 to 1983. Circulation 1985; 71:1179.)

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?? MITRAL STENOSIS AND CORONARY ARTERY DISEASE
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Patients with mitral stenosis and coronary artery disease usually have good left ventricular function and often are a relatively easy group of patients to take care of because the mitral stenosis protects the left ventricle from hemodynamic loads. Coronary artery disease may cause left ventricular dysfunction, but this is unusual. A more usual concern is right ventricular dysfunction postoperatively, since in patients with mitral stenosis, pulmonary hypertension, with its potential to produce right ventricular failure and tricuspid insufficiency, is often encountered.

Clinical Presentation

As implied earlier, mitral stenosis is usually the dominant lesion in patients with mitral stenosis and coronary artery disease. Therefore, symptoms usually are due to the valvular lesion. Patients may have congestive heart failure with shortness of breath and orthopnea and fatigue. Atrial fibrillation is a common presenting symptom with mitral stenosis. Patients with mitral stenosis and coronary artery disease infrequently have angina as a presenting symptom. The electrocardiogram may show evidence of right ventricular strain and hypertrophy. Transesophageal echocardiography confirms the diagnosis of mitral stenosis and usually shows a small left ventricle with preserved contractile function. The right ventricle may be enlarged and hypertrophied. Cardiac catheterization further confirms the diagnosis by showing a gradient across the mitral valve. Other important information gleaned from invasive catheterization includes a measurement of the pulmonary artery pressures and central venous pressure. The degree of pulmonary hypertension is a marker of the severity and duration of mitral stenosis and alerts the surgeon to the potential for right ventricular failure postoperatively. An elevated central venous pressure is a potential sign that right ventricular decompensation has already occurred. Coronary angiography should be done in all patients with angina pectoris and, as noted before, in any patient over age 40 in whom mitral valve surgery is anticipated.

Pathophysiology

Unlike the other entities described, mitral stenosis and coronary artery disease do not have significantly synergistic pathologic effects on the heart. Coronary artery disease usually has more profound effects on the left ventricle, which remains protected in patients with mitral stenosis until late in the disease. The right ventricle is the chamber most vulnerable to the effects of long-standing mitral stenosis, as noted. However, even with right ventricular hypertension, the potential impact of coronary artery disease on right ventricular function in adults is relatively insignificant. In the rare patient with diffuse coronary artery disease and ischemic cardiomyopathy, the risk of surgery is enhanced because of global ventricular dysfunction. The indications for surgery, not surprisingly, are determined usually by the severity of the mitral stenosis. Patients with significant heart failure and low cardiac output from mitral stenosis whose calculated valve area is less than 1 cm2 should have a mitral valve operation and associated bypass grafting if significant coronary artery disease is present. A rare patient may have significant coronary artery disease and mild mitral stenosis detected incidentally. These patients may be managed with coronary artery bypass surgery and mitral commissurotomy if this is technically feasible.

Operative Management

Monitoring, perfusion setup, and operative sequence are identical to those described for treatment of mitral regurgitation and coronary artery disease. Transesophageal echocardiography is useful to assess both the feasibility of mitral commissurotomy (or more extensive mitral repair) and the results of valvuloplasty. In most patients with mitral stenosis, valve replacement is required because irreversible damage to the leaflets and subvalvar apparatus is usually extensive. A mechanical prosthesis is used most often because the majority of patients have chronic atrial fibrillation from left atrial enlargement, and long-term anticoagulation is indicated. However, an ablation procedure (as discussed above) within the left and right atria may be indicated, which also may have an impact on prosthetic choice.

Transesophageal echocardiography is often important in monitoring both right and left ventricular function postoperatively. The early differentiation between left and right ventricular failure is facilitated by the use of this modality during weaning from cardiopulmonary bypass. If inotropic drugs are required, their selection should be based in part on the consideration that pulmonary hypertension and right ventricular failure might be an important component of the clinical syndrome postoperatively. Drugs such as isoproterenol, dobutamine, and especially milrinone (the latter often in combination with norepinephrine) may be indicated for their combined beneficial effects on right ventricular contractility and pulmonary vascular resistance. Judicious use of inotropic drugs and careful administration of fluid should result in optimal cardiac output. The intra-aortic balloon is almost never useful in these patients because right ventricular problems predominate, and the intra-aortic balloon has little direct effect on right ventricular function. Temporary support with a right ventricular assist device may be employed because mitral valve replacement can lead to dramatic decreases in pulmonary artery pressures and subsequent recovery of right ventricular function.

Results

Early mortality after combined surgery for mitral stenosis and coronary artery disease is approximately 8%.1214,1518,27 This is not significantly different from results of surgery in better-risk patients with mitral regurgitation and coronary artery disease. Long-term probability of survival is approximately 50% at 7 years and in one series was not significantly different from that for patients with ischemic mitral insufficiency.1214,1618,28 Interestingly, long-term survival of patients with myxoid degeneration of the mitral valve and coronary artery disease (65%) was significantly better than survival of the patients with rheumatic or ischemic mitral valve disease and coronary artery disease in at least one series (see Fig. 43-7).16 As implied, rheumatic valve pathology is a risk factor for late death, as is poor preoperative left ventricular function and the presence of ventricular arrhythmias. Interestingly, the use of a bioprosthesis without anticoagulants confers both a survival advantage and an event-free survival advantage in these patients (Fig. 43-8). These data lend support to the hypothesis that biologic valves may be appropriate for mitral replacement in older patients and in those with coronary artery disease, whose expected life span may be shorter than the expected durability of the replacement device.25



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FIGURE 43-8 Comparative survival after mitral valve replacement and coronary artery bypass grafting for patients having mitral valve replacement with a bioprosthesis (n = 82) or mechanical valve (n = 100). (Adapted with permission from Lytle BW, Cosgrove DM, Gill CC, et al: Mitral valve replacement combined with myocardial revascularization: early and late results for 300 patients, 1970 to 1983. Circulation 1985; 71:1179.)

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?? AORTIC STENOSIS, MITRAL REGURGITATION, AND CORONARY ARTERY DISEASE
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Patients with aortic stenosis, mitral regurgitation, and coronary artery disease often present with aortic stenosis as the predominant lesion. It is important to note that functional mitral regurgitation may improve after relief of aortic stenosis with concomitant reduction in left ventricular systolic pressure. If the mitral valve is not intrinsically diseased, it may not require operation.

Clinical Presentation

Patients with these diseases often present identically to patients with aortic stenosis and coronary artery disease but may do so earlier because of the combined valvular lesions. Angina, congestive heart failure, and syncope may be presenting symptoms alone or together. It is relatively uncommon for symptoms due to mitral insufficiency to be predominant. Echocardiography is an extremely important tool in this disease combination. Careful evaluation of the mitral valve, often using transesophageal echocardiography, is necessary to determine the degree of intrinsic mitral valve disease, since improvement in mitral insufficiency is expected after aortic valve replacement and relief of left ventricular obstruction. It is critical to determine whether or not anatomic abnormalities of the mitral valve are present that might not reverse with aortic surgery alone. Of course, cardiac catheterization is required, as it is for the other disease entities described.

Pathophysiology

Aortic stenosis increases left ventricular afterload and the potential amount of mitral regurgitation. The left ventricle may be better preserved in this setting than in patients with isolated mitral insufficiency and coronary artery disease. Also as noted, the mitral valve may not be structurally diseased. Because of earlier presentation, pulmonary hypertension and subsequent right ventricular failure and tricuspid valve incompetence are usually not prominent features. Because relief of outflow obstruction helps left ventricular function immediately, these patients often do quite well.

The indications for surgery are usually the same as for aortic stenosis and coronary artery disease. Critical aortic stenosis, when documented, requires valve replacement; if significant coronary artery disease is present, coronary artery bypass grafts are also done. Mitral valve repair is almost always necessary and possible when mitral insufficiency is moderate to severe and/or anatomic abnormalities of the valve are detected. If absolutely necessary, valve replacement may be performed. End-stage ventricular dysfunction with ventricular dilatation and myocardial thinning is the only cardiac contraindication to surgery.

Operative Management

Anesthesia and perfusion setup are identical to those described for mitral valve and coronary artery surgery. In this entity, intraoperative transesophageal echocardiographic monitoring plays an important role because the intraoperative assessment of mitral valve function before and after bypass is critical. The choice of valves for aortic replacement is the same as described previously. In almost all situations, however, bioprosthetic valves should be considered, especially if the mitral valve is to be repaired.

Under almost all circumstances in which anatomic abnormalities of the mitral valve are detected or in which mitral insufficiency is severe, mitral valve repair should be considered. Annuloplasty may be all that is required if the mitral insufficiency is due to annular dilatation and there is a symmetric central jet of regurgitation. More complex disease may require more extensive repair or even replacement of the mitral valve. When the decision is made not to operate on the mitral valve, transesophageal echocardiography is done to assess residual mitral valve dysfunction following aortic valve replacement and coronary artery bypass surgery. If moderate or severe mitral regurgitation remains, the valve is repaired or replaced. This is technically more difficult after the aortic valve has been replaced, since the prosthesis in the aortic position hinders exposure of the mitral valve. Therefore, every effort must be made to assess mitral valvular morphology and function before starting cardiopulmonary bypass.

As in the other entities described, distal graft anastomoses are performed first (Fig. 43-9). After these grafts are completed, the aorta is opened, and the aortic valve is resected. Replacement of the aortic valve, however, is deferred until after the mitral valve operation. However, it is important to resect the aortic valve before replacing the mitral valve to improve exposure of the latter. In addition, sutures used for mitral valve repair or replacement may become disrupted during resection or debridement of the aortic valve and annulus. After resection of the aortic valve, the atrium is opened, and the mitral operation is performed. The atrium is closed with a vent across the mitral valve. The aortic valve is then replaced, and the aorta is closed. The internal mammary artery graft is done last. Proximal graft anastomoses can be done with the aortic cross-clamp in place or after removal of the cross-clamp and placement of a partially occluding clamp, as described previously.



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FIGURE 43-9 Operative sequence for aortic valve replacement, mitral valve replacement, and coronary artery bypass grafting: (1) cannulation with cross-clamping of the aorta and administration of antegrade and retrograde cardioplegia, (2) distal graft anastomoses are performed, (3) aortotomy with standard oblique incision, (4) aortic valve is resected but not replaced, (5) standard left atriotomy after dissection in the interatrial groove, (6) mitral valve repair or replacement with the prosthesis of choice, (7) closure of left atriotomy, (8) aortic valve replacement with prosthesis of choice, (9) closure of aortotomy and performance of distal anastomosis with the internal mammary artery, and (10) proximal graft anastomoses performed. In this illustration, a partially occluding clamp has been applied to the aorta.

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As noted, this group of patients may have preserved ventricular function, and weaning from cardiopulmonary bypass may be relatively easy. Inotropic drugs and the intra-aortic balloon can be used as indicated.

Results

Early hospital mortality is 12% to 16%.29,30 Not surprisingly, predictors of early death include severe mitral regurgitation, lower ejection fraction with more severe symptoms of heart failure, and the presence of triple-vessel coronary artery disease. Late survival is approximately 60% at 72 months (Fig. 43-10). Multivariate predictors of late mortality include advanced symptoms of heart failure and increased severity of mitral insufficiency.



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FIGURE 43-10 Long-term survival after combined aortic and mitral valve replacement and coronary artery bypass grafting. (Adapted with permission from Akins CW, Buckley MJ, Daggett WM, et al: Myocardial revascularization with combined aortic and mitral valve replacements. J Thorac Cardiovasc Surg 1985; 90:272.)

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?? AORTIC AND MITRAL REGURGITATION AND CORONARY ARTERY DISEASE
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Not many patients have regurgitation of both the aortic and mitral valves and coronary artery disease. These patients usually have rheumatic heart disease and present early in the course of the disease. Aortic regurgitation may be the primary valve pathology in a patient with significant coronary artery disease. Patients may have mitral disease secondary to left ventricular dilatation from ischemia as well as from aortic regurgitation. Organic mitral valve disease may not be present. Assessment of left ventricular contractility may be difficult because of the alterations in preload and afterload produced by this combination of lesions. In addition, the presence of reversible ischemia may obscure accurate assessment of ventricular function. Therefore, assessment of myocardial viability is important.

Clinical Presentation

Most patients with this combination of cardiac lesions present with congestive heart failure. It is unusual to see a patient with angina as the primary symptom who also has significant insufficiency of both the aortic and mitral valves. Typical murmurs of aortic and mitral insufficiency are present, and the patient may have other signs of chronic congestive heart failure, including rales and peripheral edema. If myocardial infarction is a significant component of the pathophysiology and presentation of the disease, evidence of it on electrocardiogram and echocardiogram may be seen. On echocardiography, patients may have regional wall motion abnormalities if infarction has occurred, as well as global ventricular dilatation and dysfunction from the combined valvular lesions. Cardiac catheterization defines the coronary anatomy, and helps define the severity of the valvular insufficiency and ventricular dysfunction. Accurate assessment of true left ventricular function is difficult in this entity. Mitral insufficiency may abnormally inflate visual measurements of ejection fraction because the ventricle can eject into the low-pressure pulmonary venous circuit. The misleading ejection fraction combined with the multiple volume overloads of leaking aortic and mitral valves and the potential contribution of dysfunctional myocardium from ischemia make it very difficult to get an accurate perception of preoperative left ventricular function. Thallium or PET scans may be useful to assess which areas of dysfunctional myocardium may be viable and potentially recruitable after revascularization.

Pathophysiology

Symptoms and signs of left ventricular failure develop as the left ventricle dilates. In patients with rheumatic disease with both valves intrinsically damaged, ischemic disease may be minimal. In the more common setting of patients with aortic regurgitation and severe ischemia, mitral regurgitation is likely to be secondary to both of these processes, and valve repair should be possible. Correction of aortic regurgitation reduces preload, whereas correction of mitral insufficiency increases afterload. The dilated myopathic ventricle may not have sufficient reserves to maintain adequate output under these circumstances. Higher postoperative preload may need to be maintained while afterload is reduced. Any additional contractility as a result of revascularization, given a smaller left ventricle, should further improve output. Hence, forward flow should improve if ventricular contractility is maintained or increased. However, because of the multiple, uncontrollable variables that inhibit preoperative assessment of ventricular function, prediction of expected improvement from this operation is difficult.

This consideration is extremely important. Patients with severe and irreversible ischemic myocardial disease and poor ventricular function will not do well with operative treatment of this entity. Therefore, preoperative assessments of myocardial viability and reversible ischemia are important. It is also important to assess whether organic mitral valve disease is present. The best results in these patients are in those in whom no mitral operation, or at most annuloplasty, is required.

Operative Management

Details of the operative technique are similar to those described previously. Because of the presence of aortic insufficiency, retrograde cardioplegia must be used in conjunction with handheld antegrade ostial cannulae as necessary. Transesophageal echocardiography is required in the operating room for the assessment of mitral valve function. Residual 1+ to 2+ mitral regurgitation may be acceptable in certain patients because relief of aortic regurgitation can be expected to reduce ventricular size, which may lead to improvement of mitral regurgitation with time. Similarly, myocardial revascularization also may lead to ultimate improvement in ventricular and mitral valve function.

In weaning from cardiopulmonary bypass, afterload reduction is extremely important because of the large preoperative volume overload of the heart. Drugs that reduce ventricular afterload, including vasodilators and inotropic drugs such as milrinone, may be particularly appropriate. The intra-aortic balloon pump may be needed.

Results

Early hospital mortality in this group of patients may be high, and if myocardial failure is severe, overall mortality rates exceed the range already noted for double-valve and coronary artery surgery.29,30 Important determinants of risk in these patients are the familiar ones. In several series, predictors of hospital death and late events included severe mitral regurgitation, lower ejection fraction, more severe symptoms of congestive heart failure, and severe triple-vessel coronary artery disease.


?? SUMMARY
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This chapter has reviewed the management of patients with valvular and ischemic heart disease. The discussion has focused on management of disease of the aortic and mitral valves, since these are the valves most frequently affected in adults who present with these combined diseases.

Rather than concentrate on the details of the technical aspects of valve implantation or coronary artery grafting, the discussion has focused on the particular problems for surgical management that the combined pathophysiology of valvular and ischemic heart disease produces. As has been noted often during the discussion, there is usually an interaction between valve function, myocardial perfusion, and ventricular performance. Dysfunction of the aortic and mitral valves has secondary effects on ventricular function, and the addition of coronary artery disease can make this interaction more complex. Therefore, the pathophysiology of these disease states can be complicated. In order to manage these entities successfully, this pathophysiology must be understood so that accurate estimates of risk and reasonable expectations for results can be achieved.

In almost every case, ventricular function and severity of mitral incompetence are important short- and long-term risk factors. Also, functional mitral insufficiency in the absence of anatomic abnormalities of the mitral valve may resolve after aortic and/or coronary artery surgery, and therefore an operation on the mitral valve may not be required. Finally, data from several sources suggest that patients with both coronary artery and valvular heart disease should be considered for a tissue prosthesis because of reduced life expectancy.

In addition, the complex interaction between ventricular function, valvular function, and coronary ischemia requires that the operation be well planned with attention paid to expeditious surgery with short myocardial ischemia times and good myocardial preservation. Much of the discussion in this chapter, therefore, has focused on the operative plan and the development of a rational approach to intraoperative and postoperative management of these patients.


?? REFERENCES
 Top
?
  1. Davis EA, Gardner TJ, Gillinov AM, et al: Valvular disease in the elderly: influence on surgical results. Ann Thorac Surg 1993; 55:333.[Abstract]
  2. Freeman WK, Schaff HV, O'Brien PC, et al: Cardiac surgery in the octogenarian: perioperative outcome and clinical follow-up. J Am Coll Cardiol 1991; 18:29.[Abstract]
  3. Morris JJ, Schaff HV, Mullany CJ, et al: Determinants of survival and recovery of left ventricular function after aortic valve replacement. Ann Thorac Surg 1993; 56:22.[Abstract]
  4. Ren JF, Panidis IP, Kotler MN, et al: Effect of coronary bypass surgery and valve replacement on left ventricular function: assessment by intraoperative two-dimensional echocardiography. Am Heart J 1985; 103:281.
  5. Braunwald E, Kloner RA: The stunned myocardium: prolonged postischemic ventricular dysfunction. Circulation 1982; 66:1146.[Medline]
  6. Braunwald E: The stunned myocardium: newer insights into mechanisms and clinical applications. J Thorac Cardiovasc Surg 1990; 100:310.[Medline]
  7. Marban E: Myocardial stunning and hibernation: the physiology behind the colloquialisms. Circulation 1991; 83:681.[Medline]
  8. Shahle E, Bergstrom R, Nystrom SO, Hansson HE: Early results of aortic valve replacement with or without concomitant coronary artery bypass grafting. Scand J Thorac Cardiovasc Surg 1991; 25:29.[Medline]
  9. Lytle BW, Cosgrove DM, Gill CC, et al: Aortic valve replacement combined with myocardial revascularization. J Thorac Cardiovasc Surg 1988; 95:402.[Abstract]
  10. Kay PH, Nunley D, Grunkemeier GL, et al: Ten-year survival following aortic valve bypass as a risk factor: a multivariate analysis of coronary replacement. J Cardiovasc Surg 1986; 27:494.[Medline]
  11. Mullany CJ, Elveback LR, Frye FL, et al: Coronary artery disease and its management: influence on survival in patients undergoing aortic valve replacement. J Am Coll Cardiol 1987; 10:66.[Abstract]
  12. Kirklin JK, Nartel DC, Blackstone EH, et al: Risk factors for mortality after primary combined valvular and coronary artery surgery. Circulation 1989; 79(suppl I):I-180.
  13. Karp RB, Mills N, Edmunds LH Jr: Coronary artery bypass grafting in the presence of valvular disease. Circulation 1989; 79(suppl I): I-182.
  14. Tsai TP, Matloff JM, Chaux A, et al: Combined valve and coronary artery bypass procedures in septuagenarians and octogenarians: results in 120 patients. Ann Thorac Surg 1986; 42:681.[Abstract]
  15. Andrade IG, Cartier R, Panisi P, et al: Factors influencing early and late survival in patients with combined mitral valve replacement and myocardial revascularization and in those with isolated replacement. Ann Thorac Surg 1987; 44:607.[Abstract]
  16. Lytle BW, Cosgrove DM, Gill CC, et al: Mitral valve replacement combined with myocardial revascularization: early and late results for 300 patients, 1970 to 1983. Circulation 1985; 71:1179.[Medline]
  17. Ashraf SS, Shaukat N, Odom N, et al: Early and late results following combined coronary bypass surgery and mitral valve replacement. Eur J Cardiothorac Surg 1994; 8:57.[Abstract]
  18. Szecsi J, Herrijgers P, Sergeant P, et al: Mitral valve surgery combined with coronary bypass grafting: multivariate analysis of factors predicting early and late results. J Heart Valve Dis 1994; 3:236.[Medline]
  19. Sheikh KH, Bengtson JR, Rankin JS, et al: Intraoperative transesophageal Doppler color flow imaging used to guide patient selection and operative treatment of ischemic mitral regurgitation. Circulation 1991; 84:594.[Medline]
  20. Dion R: Ischemic mitral regurgitation: when and how should it be corrected? J Heart Valve Dis 1993; 2:536.[Medline]
  21. Aklog L, Filsoufi F, Flores KQ, et al: Does coronary artery bypass grafting alone correct moderate ischemic mitral regurgitation? Circulation 2001; 75:I-68.
  22. Maisano F, Schreuder JJ, Oppizzi M, et al: The double-orifice technique as a standardized approach to treat mitral regurgitation due to severe myxomatous disease: surgical technique. Eur J Cardiothorac Surg 2000; 17:201.[Abstract/Free?Full?Text]
  23. Alfieri O, Maisano F, DeBonis M, et al: The double-orifice technique in mitral valve repair: a simple solution for complex problems. J Thorac Cardiovasc Surg 2001; 122:674.[Abstract/Free?Full?Text]
  24. Cohn LH, Kowalker W, Bhatia S, et al: Comparative morbidity of mitral valve repair versus replacement for mitral regurgitation with and without coronary artery disease. Ann Thorac Surg 1988; 45:284.[Abstract]
  25. Jones EL, Weintraub WS, Craver JM, et al: Interaction of age and coronary disease after valve replacement: implications for valve selection. Ann Thorac Surg 1994; 58:378.[Abstract]
  26. Cox JL, Buckberg GD: Ventricular shape and function in health and disease. Semin Thorac Cardiovasc Surg 2001; 13:298.[Medline]
  27. Cohn LH, Couper GS, Kinchla NM, Collins JJ Jr: Decreased operative risk of surgical treatment of mitral regurgitation with or without coronary artery disease. J Am Coll Cardiol 1990; 16:1575.[Abstract]
  28. Kay PH, Nunley DL, Grunkemeier GL, et al: Late results of combined mitral valve replacement and coronary bypass surgery. J Am Coll Cardiol 1985; 5:29.[Abstract]
  29. Akins CW, Buckley MJ, Daggett WM, et al: Myocardial revascularization with combined aortic and mitral valve replacements. J Thorac Cardiovasc Surg 1985; 90:272.[Abstract]
  30. Johnson WD, Kayser KL, Pedraza PM, Brenowitz JB: Combined valve replacement and coronary bypass surgery: results in 127 operations stratified by surgical risk factors. Chest 1986; 90:338.[Abstract/Free?Full?Text]




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