Chapter 48. Valvular and Ischemic Heart Disease

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, surgery on the beating heart 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. Techniques for aortic valve replacement on the beating heart via a retrograde transvascular or transapical approach are now under investigation. 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 are discussed in other chapters. All are issues that the surgeon must consider when planning a 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 may 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 isolated valvular heart disease (Fig. 48-1). This complexity increases the need for careful preoperative assessment of myocardial function and an understanding of the impact on ventricular function of the changing afterload and preload associated with valve surgery. Therefore, in adult patients with combined valvular and ischemic heart disease, 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 laboratory tests, preoperative echocardiography is mandatory. Transesophageal echocardiography often is the diagnostic technique of choice for accurate planning when operative repair of the mitral valve is considered. It is also important to distinguish heart failure resulting from valvular disease from reversible or irreversible myocardial dysfunction owing to coronary ischemia. Dobutamine stress echocardiography may be useful in eliciting ventricular size and shape changes that occur under stress and that may exacerbate underlying pathology, especially of the mitral valve. 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) scans can help distinguish areas of viable myocardium with reversible ischemia and ischemic dysfunction from irreversibly scarred muscle. These assessments are important before embarking on combined valve and coronary artery surgery, for they are crucial in estimating operative risk and planning the operative approach.

The assessment of valve pathology is covered in detail in previous chapters on isolated valvular heart disease. As has been noted, 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, coronary angiography is usually performed in all patients greater than 40 years of age, and select younger patients with suggestive symptoms or significant risk factors.

With present technology and techniques, myocardial revascularization can be added to any valve procedure. What is needed are 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. The surgeon also must acknowledge and understand the potential and evolving roles of new techniques, such as coronary artery stenting, beating heart revascularization, and percutaneous aortic valve replacement in the management of patients with combined valve and coronary artery disease.3–7 At this time, none of these techniques represents the standard of care for patients who are candidates for a major cardiovascular surgical procedure.

Aortic stenosis is one of the more frequently encountered valvular lesions in adult populations. Because degenerative calcific aortic stenosis is most common in patients in their sixties, seventies, and eighties1,2 and because congenitally bicuspid valves that become stenotic are more frequent in men who are susceptible to CAD at an earlier age than are women,8 it is not surprising that the combination of aortic stenosis and CAD 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 because 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 usually 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 greater than 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 pressure, can be obtained. The transaortic valvular 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 the 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 function, especially renal function.

The optimal management of a patient with coronary artery disease and mild or moderate aortic stenosis presently remains a matter of some controversy. The dilemma is whether to subject a patient to the lifelong limitations of a valve replacement procedure that may not be necessary, or the prospect of a repeat cardiac operation, perhaps in only a few years, should the aortic stenosis progress. There is now evidence that favors valve replacement in patients with moderate aortic stenosis who are referred for surgical myocardial revascularization.9–12 In one study,9 survival rates at both 1 year and 8 years were superior for patients who underwent valve replacement for moderate aortic stenosis (gradient >30 mm Hg or gradient <40 mm Hg with valve area between 1.0 and 1.5 cm2). One-year survival was 90% in those having valve replacement compared to 85% in patients having coronary artery bypass graft (CABG) alone. Similarly, 8-year survival (55% versus 39%) was statistically significantly better (p < .001).

The rate of progression of aortic stenosis may also provide an indication for valve replacement even without hemodynamically critical disease.11 For slow progression (<3 mm Hg per year), isolated CABG is preferred for patients with valve gradients less than 50 mm Hg. In contrast, rapid progression (>10 mm Hg per year) favors valve replacement at the time of CABG surgery. One possible exception is in octogenarians with valve gradients less than 25 mm Hg. Of course, other individual patient characteristics (life expectancy and other significant comorbidity) may influence the decision to replace the aortic valve at the time of revascularization surgery.

Pathophysiology

Aortic stenosis produces obstruction to left ventricular emptying during systole, 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 CAD may itself lead to global ventricular dysfunction, which may be reversible with revascularization.

In patients with critical aortic stenosis and good ventricular function, valve replacement immediately reduces left ventricular afterload. Because most patients with aortic stenosis have hypertrophied and thick-walled ventricles, intraoperative subendocardial ischemia may be 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.13–16 This, of course, assumes more important pathophysiologic significance in patients with poor ventricular function preoperatively. Diastolic dysfunction may also occur, causing a less compliant left ventricle. The most extreme example of this was the so-called "stone heart" that plagued surgical pioneers who attempted aortic valve replacement surgery. Modern techniques of myocardial preservation have eliminated this feared complication.

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 myocardium10 with further enhancement of ventricular function.8

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 an arterial line (usually in the radial artery for blood pressure and blood gases) and a pulmonary artery catheter for measurement of pulmonary artery pressures, and 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. 48-2). 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 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.

A combination of antegrade and retrograde cardioplegia is optimal. The initial dose of cardioplegia usually is given both ways. 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 artery and vein saphenous bypass grafts after distal anastomoses are completed. This is especially important if a graft has been placed in the right coronary system, as retrograde cardioplegia is not well delivered to the right ventricle and may not protect it well.

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 used in the treatment of isolated valvular heart disease. Any type of prosthesis may be used, but 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 tolerate well 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 as described. The first step in the operation is performance of the distal radial artery and/or 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 anastomoses are performed when necessary. Alternatively, the proximal anastomoses can be performed with the aortic cross-clamp still in place. Although 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, because 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 the heart is resuscitated and de-airing is confirmed by transesophageal echocardiography, the left ventricular vent is removed. Of note, atrial-ventricular sequential activation is particularly important to optimize hemodynamic performance in patients with aortic stenosis. This is because as much as 30% of the cardiac output may be derived from atrial contraction as the hypertrophied and noncompliant ventricle that is typical of the patient with aortic stenosis does not fill completely during the earlier phases of diastole.

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 pay particular attention to keeping the poorly compliant left ventricle filled to ensure adequate preload and cardiac output.

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 after 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 CABG ranges from approximately 2 to 10%.8,17 Higher mortality is observed in patients with more severe symptoms of heart failure and impaired ventricular function preoperatively. The 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 50 to 75% at 8 years postoperatively (Fig. 48-3).18–23 By multivariate analysis, risk factors for 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. 48-4). Nonetheless, elderly patients have acceptable results following relief of aortic stenosis, even with redo valve surgery combined with coronary revascularization.24,25 As discussed, choice of valve type is a complex issue in combined valve–coronary 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. Similar consideration should apply to consideration of "hybrid" procedures such as coronary artery stenting followed by valve replacement.3,6 This approach has at least the one clear advantage of permitting aortic valve replacement through a smaller incision (partial sternotomy, anterior thoracotomy).

Significant aortic regurgitation occurs less often in older populations, and is also less often encountered with CAD. Most series of patients undergoing aortic valve replacement and CABG include a relatively small number (10 to 25%) of patients with aortic insufficiency.8,17–20 Although the operative management of patients with aortic regurgitation and CAD 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 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 caused by 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 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 CAD is no 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 difficult to detect. In addition, echocardiography gives important information regarding both ventricular contractile function and ventricular size. Because many patients with aortic regurgitation are asymptomatic, careful evaluation for changes in ventricular size or function is important, as 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 owing to a sudden increase in left ventricular end-diastolic pressure and decrease in net forward cardiac output. Global left ventricular dysfunction caused by CAD 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.13,16 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 to those described above, with emphasis on echocardiographic results. However, this evaluation is somewhat more difficult when CAD is also present, because the presence of coronary disease might have 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 caused by coronary artery obstructions are usually regional and can be distinguished from global dysfunction caused by volume overload from the insufficient valve. Making this distinction is of paramount importance in the preoperative assessment and risk stratification of these patients because regional abnormalities are likely to improve after myocardial revascularization. In difficult cases an evaluation of myocardial viability (with thallium or PET scanning) may be helpful in evaluating candidates for surgery. Decisions about timing of aortic valve surgery in the presence of CAD are different from those in cases of isolated valvular disease, with the usual result that the valve is replaced earlier in the course of the disease.

Operative Management

The operation is conducted in a fashion similar to that described for aortic stenosis and CAD. 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, especially on the right, 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. Therefore, successful perioperative management of these patients requires careful attention to adjustments in preload and afterload. In patients with volume-overloaded ventricles caused by 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 device—the intra-aortic balloon pump—also 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 CAD include an expected hospital mortality rate of less than 10%.8,17 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 CAD (see Fig. 48-3).18–23 Despite the impression that patients with aortic insufficiency and CAD do not do as well as those with aortic stenosis, aortic insufficiency has not been an independent risk factor for early or late mortality.8 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. Although some improvement of function can occur with elimination of the volume overload and 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. This observation is the primary reason that valve replacement is recommended before changes in ventricular morphology and function have occurred. 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.

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.

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.

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 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.

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 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.

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.

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.

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

Operative Management

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

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

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.

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.

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.

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.

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.

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.

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.

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

Results

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

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).

Patients with mitral stenosis and CAD usually have good left ventricular function and often are a relatively easy group of patients to take care of because the mitral stenosis does not subject the left ventricle to abnormal hemodynamic loads. CAD may cause left ventricular dysfunction, but this is unusual. A more usual concern is right ventricular dysfunction postoperatively, because pulmonary hypertension, with its potential to produce right ventricular failure and tricuspid insufficiency, is often encountered in patients with mitral stenosis.

Clinical Presentation

As implied earlier, mitral stenosis is usually the dominant lesion in patients with mitral stenosis and CAD; therefore, symptoms are typically caused by the valvular lesion. Patients may have congestive heart failure with shortness of breath, orthopnea, and fatigue. Atrial fibrillation is a common presenting symptom with mitral stenosis. Patients with mitral stenosis and CAD 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 greater than age 40 in whom mitral valve surgery is anticipated.

Pathophysiology

Unlike the other entities described, mitral stenosis and CAD do not have significantly synergistic pathologic effects on the heart. CAD 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 CAD on right ventricular function in adults is usually not significant. In the rare patient with diffuse CAD and ischemic cardiomyopathy, the risk of surgery is enhanced because of global ventricular dysfunction.

The indications for surgery, not surprisingly, are usually determined 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 CAD is present. A rare patient may have significant CAD and mild mitral stenosis detected incidentally. These patients may be managed with CABG and mitral commissurotomy if this is technically feasible. Another alternative in the modern era is the combination of percutaneous revascularization with stents and balloon mitral valvuloplasty. The number of patients suitable for the latter procedure is relatively small and thus far there are no definitive data supporting this kind of hybrid transcatheter approach to these lesions.

Operative Management

Monitoring, perfusion setup, and operative sequence are identical to those described for treatment of mitral regurgitation and CAD. 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 subvalvular 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, the potential benefits of an ablation procedure (as discussed) within the left and right atria also may have an impact on prosthetic choice. Particular attention must be directed to preservation of the right ventricle. In practice, this means that initial and subsequent doses of cardioplegia should be given antegrade as well as retrograde because the latter approach usually offers relatively poor distribution of cardioplegia to the right ventricle.

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 important components of the clinical syndrome. Drugs such as isoproterenol, dobutamine, and especially milrinone (the latter often in combination with norepinephrine or other catecholamine) 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 usually are sufficient to restore 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 once the acute phase is past, 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 CAD is approximately 8%.18–21,26,37 This is not significantly different from results of surgery in lower-risk patients with mitral regurgitation and CAD. 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.21–23,27–29,47 Interestingly, long-term survival of patients with myxoid degeneration of the mitral valve and CAD (65%) was significantly better than survival of the patients with rheumatic or ischemic mitral valve disease and CAD in at least one series (see Fig. 48-7).27 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. 48-8). These data lend support to the hypothesis that biologic valves may be appropriate for mitral replacement in older patients and those with CAD, whose expected life span may be shorter than the anticipated durability of the replacement device.43

Patients with aortic stenosis, mitral regurgitation, and CAD 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 surgery.

Clinical Presentation

Patients with these diseases often present identically with patients with aortic stenosis and CAD, 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 resulting from 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, because improvement in mitral insufficiency is expected after aortic valve replacement and relief of left ventricular outflow obstruction.52 It is critical to determine whether or not the mitral valve has anatomical abnormalities that might not reverse with aortic surgery alone.53 Of course, cardiac catheterization is required, as it is for the other disease entities described.

Pathophysiology

Aortic stenosis increases left ventricular afterload and therefore can contribute to increasing the amount of mitral regurgitation. Because the combined lesions may cause patients to present earlier in the course of the disease, the left ventricle may be better preserved in this setting than in patients with isolated mitral insufficiency and CAD. 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 CAD. Critical aortic stenosis, when documented, requires valve replacement; if significant CAD 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 anatomical abnormalities of the valve are detected. End-stage ventricular dysfunction with ventricular dilatation and myocardial thinning are the primary cardiac contraindications 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 structure and function before and after bypass is critical. The choice of valve for aortic replacement is the same as described previously. In most situations, however, bioprosthetic valves should be considered, especially if the mitral valve is to be repaired.

Under almost all circumstances in which anatomical 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 results from annular dilatation and the insufficiency is symmetric and central. 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 should be repaired or replaced. This is technically more difficult after the aortic valve has been replaced, because 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. 48-9). 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, because of the fibrous continuity between the aortic and mitral valves, sutures used for mitral valve repair or replacement, if placed first, 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. It is conceivable that at some point in the future patients with this combination of lesions may undergo catheter-based coronary revascularization, catheter-based aortic valve replacement, and catheter-based mitral valve repair.54,55 That day, however, has not arrived yet.

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%.56,57 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 CAD. Late survival is approximately 60% at 72 months (Fig. 48-10). Multivariate predictors of late mortality include advanced symptoms of heart failure and increased severity of mitral insufficiency.

Relatively few patients have insufficiency of both the aortic and mitral valves combined with CAD. Those patients who do usually have rheumatic heart disease and present early in the course of the valvular heart disease. Aortic regurgitation may be the predominant valve pathology in a patient with simultaneous significant CAD. The mitral valve problem may be secondary to left ventricular dilatation from the aortic lesion and/or from ischemia resulting from the coronary obstructions. Morphologic mitral valve disease may not be present. Because of the interaction of the valve and coronary pathologies, assessment of left ventricular contractility may be difficult for the reason that both preload and afterload are altered. In addition, the presence of reversible ischemia may obscure accurate measurement of ventricular function and reserve. Therefore, assessment of myocardial viability in these patients is often important.

Clinical Presentation

Most patients with this combination of cardiac lesions present with congestive heart failure. It is unusual to see a patient who has significant insufficiency of both the aortic and mitral valves present with angina as the primary symptom. 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 may be seen on electrocardiogram and echocardiogram. 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 and/or diffuse CAD. Cardiac catheterization defines the coronary anatomy and helps to assess 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 insufficient aortic and mitral valves and the potential contribution of dysfunctional myocardium from ischemia make it very difficult to get an accurate estimation 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 significant ischemia, mitral regurgitation is more 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 should improve output further. Hence, forward flow will 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 after 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 hand-held ostial cannulas to deliver cardioplegia antegrade. For the reasons enunciated, excellent myocardial protection is important in these patients. 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 as the ventricle remodels 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.56,57 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 CAD.

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

Rather than concentrating 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 among valve function, myocardial perfusion, and ventricular performance. Dysfunction of the aortic and mitral valves has secondary effects on ventricular function, and the addition of CAD can make this interaction more complex. Therefore, the pathophysiology of these disease states can be complicated. 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 anatomical 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. 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 and the benefits of avoiding long-term anticoagulation. The ultimate role of catheter-based therapies for valvular and coronary artery disease in these patients remains to be defined. It is a certainty, however, that as these techniques are perfected, they will be applied to more patients, some of whom may have been considered at too high a risk for direct surgical therapy.

Finally, the complex interaction among ventricular function, valvular function, and coronary ischemia requires that the operation be well planned with attention paid to expeditious surgery, 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.