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Schaff HV, Marsh DH. Multiple Valve Disease.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:10171045.

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Multiple Valve Disease

PATHOPHYSIOLOGY OF MULTIPLE VALVE DISEASE

????Primary Aortic Valve Disease with Secondary Mitral Regurgitation

????Tricuspid Valve Regurgitation Secondary to Other Valvular Disease

VALVE SELECTION FOR MULTIPLE VALVE REPLACEMENT

SURGICAL METHODS

????Aortic and Mitral Valve Replacement

????????CANNULATION

????????CARDIOPLEGIA

????????PROCEDURE

????Aortic Valve Replacement and Mitral Valve Repair

????Mitral Valve Replacement and Tricuspid Valve Replacement or Repair

????????PROCEDURE

????Tricuspid Valve Replacement and Pulmonary Valve Replacement for Carcinoid Heart Disease

????Triple Valve Replacement

RHEUMATIC HEART DISEASE AFFECTING MULTIPLE VALVES

????Rheumatic Mitral Stenosis with Rheumatic Aortic Regurgitation

????????DIAGNOSIS, SIGNS, AND SYMPTOMS

????????PATHOPHYSIOLOGY

????????OPERATIVE DECISION MAKING

????Rheumatic Mitral Stenosis with Rheumatic Aortic Stenosis

????????DIAGNOSIS, SIGNS, AND SYMPTOMS

????????PATHOPHYSIOLOGY

????????OPERATIVE DECISION MAKING

????Rheumatic Mitral Regurgitation with Rheumatic Aortic Regurgitation

????????DIAGNOSIS, SIGNS, AND SYMPTOMS

????????PATHOPHYSIOLOGY

????????OPERATIVE DECISION MAKING

MYXOMATOUS AND PROLAPSING VALVE DISEASE AFFECTING MULTIPLE VALVES

????Diagnosis, Signs, and Symptoms

????Operative Decision Making

????Myxomatous Mitral Regurgitation with Tricuspid Regurgitation

????????SENILE CALCIFIC AORTIC VALVE DISEASE WITH MULTIPLE VALVE INVOLVEMENT

????Patterns of Multiple Valve Involvement with Calcific Aortic Stenosis

????????CALCIFIC AORTIC STENOSIS WITH INFECTIVE ENDOCARDITIS OF THE MITRAL VALVE

????????CALCIFIC AORTIC STENOSIS WITH FUNCTIONAL MITRAL VALVE DISEASE

????????CALCIFIC AORTIC STENOSIS WITH CALCIFICATION OF THE MITRAL VALVE

????Diagnosis, Signs, and Symptoms

????????PHYSICAL FINDINGS

????????ELECTROCARDIOGRAPHY

????????ECHOCARDIOGRAPHY

INFECTIVE ENDOCARDITIS AFFECTING MULTIPLE VALVES

????Aortic Regurgitant Jet Lesion of the Mitral Valve

????Prosthetic Valve Endocarditis

????Tricuspid Valve with Left-Sided Valve Replacement

????Results

CARCINOID HEART DISEASE AFFECTING MULTIPLE VALVES

????Signs and Symptoms/Diagnosis

????Echocardiography

????Invasive Studies

????Pathophysiology

????Operative Decision Making

????????TIMING OF OPERATION

????????TRICUSPID VALVE OPERATION

????????PULMONARY VALVE OPTIONS

RARE CAUSES OF MULTIPLE VALVE DISEASE

RESULTS OF MULTIPLE VALVE SURGERY

????Long- and Short-Term Mortality

????Thromboembolism

????Anticoagulation-Related Hemorrhage

????Prosthetic Valve Infective Endocarditis

????Valve Performance

????????COMPARISON OF BIOPROSTHETIC VALVES TO MECHANICAL VALVES

????Results of Tricuspid Valve Procedures with Other Valve Procedures

????????RESULTS OF MITRAL AND TRICUSPID SURGERY

????????TRIPLE VALVE REPLACEMENT

????????DOUBLE VALVE REPLACEMENT AND TRICUSPID ANNULOPLASTY

????Other Results

SUMMARY

REFERENCES

	?? INTRODUCTION

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Repair of multiple lesions was necessary even in the early development of operative management of valvular heart disease (Table 41-1). The first triple valve replacement during a single operation was reported in 1960, and simultaneous replacement of all four valves was reported in 1992.^1,2

	?? PATHOPHYSIOLOGY OF MULTIPLE VALVE DISEASE

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Primary Aortic Valve Disease with Secondary Mitral Regurgitation

Isolated aortic valve lesions can cause secondary regurgitation of the mitral valve and, rarely, of the tricuspid valve. Severe aortic valve stenosis with or without left ventricular dilatation is frequently associated with some degree of mitral valve regurgitation. In one series, 67% of patients with severe aortic valve stenosis had associated mitral valve leakage.³

When the mitral valve is structurally normal, its regurgitation would be expected to improve with relief of left ventricular outflow obstruction⁴; mild mitral valve regurgitation would be expected to resolve almost completely following aortic valve replacement. Improvement in mitral valve regurgitation results both from decreased intraventricular pressure and ventricular remodeling.⁵ If mitral valve regurgitation is severe, some degree of persistent regurgitation is expected following aortic valve replacement, and mitral valve annuloplasty may be required. In contrast, with aortic valve stenosis and mitral valve regurgitation associated with a structurally abnormal mitral valve, repair or replacement of the mitral valve usually is necessary.

Thus, determination of the morphology and pathophysiologic severity of each valve lesion is critically important in planning surgical management, and preoperative and intraoperative echocardiographic studies are necessary in all patients suspected of having multiple valve disease. Often, transthoracic echocardiography can define the etiology of mitral and tricuspid valvular regurgitation. When valve regurgitation is entirely secondary, the mitral valve leaflets will appear thin and freely mobile, without prolapsing segments. Mitral (and tricuspid) valve regurgitation secondary to rheumatic disease is readily identified when leaflets are thickened and chordae are shortened; fibrosis of these structures restricts leaflet mobility. Leaflet prolapse with or without ruptured chordae tendineae may also cause atrioventricular valve regurgitation.

Transesophageal echocardiography images the heart from a retrocardiac position, which avoids interference from interposed ribs, lungs, and subcutaneous tissue. A high-frequency (5-MHz) transducer is employed, which yields better resolution than that of images obtained with routine transthoracic imaging utilizing 2.25- to 3.5-MHz transducers.⁶ Thus, transesophageal echocardiography provides the best image of the mitral and tricuspid valves and may be obtained preoperatively. Intraoperative transesophageal Doppler echocardiography should be employed in all patients having valve replacement or repair, and the technique is especially important for assessment of response of mitral regurgitation to relief of left ventricular outflow obstruction.⁷ In some cases, preoperative left ventriculography may help to quantify left atrioventricular valve leakage. Right ventricular angiocardiography also can be useful in determining the degree of tricuspid valve dysfunction, but it is rarely employed in current practice.⁸

Tricuspid Valve Regurgitation Secondary to Other Valvular Disease

Secondary tricuspid valve regurgitation commonly is associated with rheumatic mitral valve stenosis, and the exact cause is unknown.^9,10 Some authors believe that secondary tricuspid valve regurgitation is a result of pulmonary artery hypertension and right ventricular dilatation.¹¹ As with the mitral valve, tricuspid valve annular dilatation is asymmetrical. Most enlargement occurs in the annulus subtended by the free wall of the right ventricle, and there is little dilatation of the annulus adjacent to the septal leaflet of the tricuspid valve.^12,13

Although pulmonary artery hypertension with secondary enlargement of the right ventricle and tricuspid valve annulus may be an important contributing factor in secondary tricuspid regurgitation, it is not the sole mechanism. For example, congenital heart lesions such as tetralogy of Fallot produce systemic pressure in the right ventricle, yet severe tricuspid valve regurgitation rarely is seen in these patients. Similarly, important tricuspid valve regurgitation is uncommon in children with ventricular septal defects who have enlargement of the right ventricle associated with variable degrees of pulmonary hypertension.

Furthermore, clinical experience suggests that other mechanisms must play a role in development of secondary tricuspid valve regurgitation. Patients who have had mitral valve replacement for rheumatic mitral valve stenosis may develop regurgitation of their native tricuspid valve years after initial operation, and many patients have only modest elevation of pulmonary artery pressure.^14,15

It is useful to classify secondary mitral and tricuspid valve regurgitation as mild, moderate, and severe.¹³ Usually, patients with mild tricuspid valve regurgitation do not have clinical signs and symptoms of right heart failure. Also, mild tricuspid regurgitation demonstrated by preoperative echocardiography may appear even less severe in the operating room under general anesthesia. In most instances, mild secondary tricuspid regurgitation does not require intervention.

Patients with echocardiographic evidence of significant regurgitation who do not have symptoms or have their symptoms controlled by medical treatment can be classified as having moderate tricuspid regurgitation. These patients usually are managed with a deVega suture annuloplasty or a partial ring annuloplasty.¹⁶ Patients with severe secondary tricuspid regurgitation and clinical evidence of right heart failure (pulsatile liver, distended neck veins, and peripheral edema with or without ascites) are managed by concomitant ring annuloplasty or tricuspid valve replacement.

The degree of pulmonary hypertension may influence surgical management of secondary tricuspid valve regurgitation. Kaul et al grouped 86 patients with functional tricuspid regurgitation in association with rheumatic mitral valve disease according to the degree of pulmonary hypertension. One group had severe pulmonary hypertension (mean pulmonary pressure 78 mm Hg), and a second group had moderate pulmonary hypertension (mean pulmonary artery pressure 41 mm Hg). Patients with moderate pulmonary hypertension preoperatively had more advanced right heart failure and right ventricular dilatation, and many of these patients continued to have tricuspid valve regurgitation following mitral valve surgery without tricuspid valve surgery. The patients with severe pulmonary hypertension all showed regression of tricuspid regurgitation, and 28% had complete resolution following mitral valve surgery without operation on the tricuspid valve.¹²

Excluding hospital mortality, about 40% of patients undergoing tricuspid valve surgery have premature death.⁸ It is also important to understand that mild-to-moderate (2+) regurgitation is a risk factor for late failure of tricuspid valve repair, and severe (4+) regurgitation preoperatively is a predictor of early residual regurgitation.¹⁷

	?? VALVE SELECTION FOR MULTIPLE VALVE REPLACEMENT

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For tricuspid valve replacement, alone or in conjunction with other valve procedures, use of a bioprosthesis may have advantages as regards minimizing risk of valve thrombosis.^20,21 Furthermore, there are few hemodynamic considerations in selecting a tricuspid prosthesis; the greater hemodynamic efficiency of mechanical valves compared to bioprostheses rarely is an issue in atrioventricular valve replacement, especially the tricuspid valve, in which the annulus diameter in adults is often 33 mm or more. In vitro studies demonstrate only minimal hemodynamic improvement with atrioventricular valves larger than 25 mm.²²

	?? SURGICAL METHODS

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CANNULATION

Arterial inflow is established by cannulation of the distal ascending aorta near the pericardial reflection just to the left of the origin of the innominate artery (Fig. 41-1A). Venous cannulation is simplified by using a two-stage cannula in the right atrium for venous return. Individual cannulation of the superior and inferior venae cavae is reserved for operations that require right atrial or ventricular incisions (Fig. 41-2A).

View larger version (56K): [in this window] [in a new window] ? FIGURE 41-1 Aortic and mitral valve replacements showing the sequence of cannulation (A) and exposure of valves (B). Aortic and mitral valve replacements showing the sequence of replacement of the mitral (C) and aortic valves (D).

View larger version (60K): [in this window] [in a new window] ? FIGURE 41-2 Combined mitral valve and tricuspid operation. The panels illustrate cannulation (A) and transseptal incision (B). Combined mitral valve and tricuspid operation: mitral replacement (C). (Superior vena cava snare not shown.

CARDIOPLEGIA

If the aortic valve is competent, myocardial protection during aortic cross-clamping is achieved by initial infusion of cold (4?C to 8?C) blood cardioplegia through a tack vent placed in the aorta proximal to the clamp. The volume of cardioplegia needed to achieve diastolic arrest and uniform hypothermia depends upon the heart size and the presence of aortic valve regurgitation. Generally, the initial volume of cardioplegia required for hearts with multiple valve disease is higher than that required for coronary revascularization because of myocardial hypertrophy. For patients without cardiac enlargement, we infuse approximately 10 mL per kg body weight, whereas 15 mL per kg body weight is used for patients with significant degrees of myocardial hypertrophy. Repeat infusions of 400 mL of cardioplegia are given directly into the coronary ostia at 20-minute intervals during aortic occlusion. We use custom-designed, soft-tipped coronary perfusion catheters to minimize the potential for trauma to the coronary ostia during intubation and infusion.²⁴

If aortic valve regurgitation is moderate or severe, cardioplegia is infused directly into the coronary ostia. Initial aortotomy is facilitated by emptying the heart, using suction on an aortic tack vent, and temporarily reducing cardiopulmonary bypass flow rate to maximize venous return. Some surgeons prefer retrograde infusion of cardioplegia,²⁵ and if this method is used, even larger volumes are necessary because of non-nutritive flow through the coronary venous system and variation in coronary venous anatomy.^26,27

PROCEDURE

After cardioplegia, the aortic valve is inspected through an oblique aortotomy extended into the noncoronary aortic sinus (Fig. 41-1B). Aortic valve regurgitation caused by cuspal perforation or prolapse of a congenitally bicuspid valve can often be repaired,²⁸ but the decision for or against aortic valve repair should take into consideration whether or not a mitral valve prosthesis will be needed. For example, even though aortic valve repair might seem technically possible, prosthetic replacement may be the best option for a patient who requires mitral valve replacement and will be maintained on warfarin for long-term anticoagulation.

Severe calcification of the valve, whether it is bicuspid or tricuspid, necessitates replacement,²⁹ and the cusps therefore are excised and annular calcium debrided carefully. The aortic annulus is then calibrated; experience has shown that subsequent replacement of the mitral valve usually reduces the aortic annular diameter by shortening the circumference that is in continuity with the attachment of the anterior mitral valve leaflet. Therefore, we routinely identify (but do not break the sterile packaging of) two aortic prostheses: one corresponds to the calibrated dimension, and the other is the next size smaller. Final selection of the aortic prosthesis is made after mitral valve replacement or repair.

Although first exposed, the aortic valve usually is replaced after mitral valve repair or insertion of the mitral valve prosthesis. Sutures placed in the portion of the aortic valve annulus that is continuous with the anterior leaflet of the mitral valve pull the anterior leaflet superiorly toward the left ventricular outflow area and thus hinder exposure of this area as viewed through the left atriotomy.

If the aortic annulus is small, it can be enlarged with a patch of pericardium.³⁰ This technique increases annular diameter by 2 to 4 mm or more, and only rarely are more radical techniques necessary.³¹³³ Another maneuver to accommodate as large a prosthesis as possible is to place the necessary sutures for the mitral valve repair or replacement but not secure the mitral prosthesis until the aortic valve is implanted. This eliminates downsizing of the aortic prosthesis but does not compromise insertion of sutures in the superior portion of the mitral valve annulus.

After removal of the aortic valve, the right atrial cannula is repositioned, and the mitral valve is exposed through an incision posterior to the interatrial groove (see Fig. 41-1B). The presence or absence of thrombi in the left atrium is noted, and the mitral valve is inspected. When there is rheumatic disease of the aortic valve, the mitral valve almost always will be involved to some extent. If aortic valve replacement is necessary, the surgeon should have a low threshold for replacing a diseased mitral valve because scarring and fibrosis of the rheumatic process is progressive, and mitral valve repair (commissurotomy for stenosis or leaflet repair and annuloplasty for regurgitation) is less durable than repair for degenerative disease.³⁴³⁶ In contrast, when aortic valve replacement is necessary because of calcification of a bicuspid valve or because of senescent calcification, repair of mitral valve regurgitation owing to degenerative causes can be expected to give predictably good long-term results. Repair of the mitral valve is described in Chapter 37.

In preparation for replacement, the anterior leaflet of the mitral valve is excised, and, when possible, a portion of the posterior leaflet with its chordal attachments is preserved to maintain left ventricular papillary muscleannular continuity.³⁷³⁹ Some surgeons make special effort to preserve the anterior leaflet and its chordal attachments, believing this has a further beneficial effect on ventricular performance.⁴⁰ The mitral prosthesis is implanted using interrupted mattress sutures of 2-0 braided polyester reinforced with felt pledgets, which can be situated on the atrial or ventricular side of the valve annulus (Fig. 41-1C). The leaflets of mechanical valves should be tested for free mobility following valve seating.

When atrial fibrillation is present preoperatively, we obliterate the left atrial appendage by oversewing its orifice from within the left atrium or by ligating it externally. The left atriotomy is closed from each end with running polypropylene sutures. Vent tubing is inserted through the partially closed left atriotomy and left in place while the aortic valve is being replaced (Fig. 41-1D).

After appropriate exposure, the aortic prosthesis is sewn in place with interrupted 2-0 polyester mattress sutures backed with felt pledgets, and the aortotomy is closed, usually with two layers of 4-0 polypropylene. Any remaining air is evacuated from the heart with the usual maneuvers, and a tack vent in the ascending aorta is placed on suction as the aortic clamp is removed. The vent is removed from the left atrium and closure of the left atriotomy is secured.

In patients with annuloaortic ectasia, the mitral valve sometimes can be visualized and replaced through the enlarged aortic annulus.⁴¹

Aortic Valve Replacement and Mitral Valve Repair

Intraoperative transesophageal echocardiography is useful in assessing the degree of mitral regurgitation and, importantly, in identifying the cause of valve leakage. When mitral valve regurgitation is only moderate and leaflet morphology normal, we expect mitral valve function to improve following relief of severe aortic stenosis. In all other instances, the valve should be inspected directly to determine need for repair or replacement.

Sternotomy, cannulation, and assessment of the aortic valve proceed as previously described. When there is no indication of tricuspid valve disease and no other right atrial procedures are planned, venous return is obtained through a single two-staged cannula (Fig. 41-3A). Specific techniques of mitral valve repair depend on operative findings.⁴² Localized prolapse of a portion of the posterior leaflet with or without ruptured chordae usually is managed by triangular excision of that segment and repair with continuous 4-0 polypropylene suture. Ruptured chordae to the anterior leaflet are replaced with 4-0 or 5-0 PTFE sutures inserted into papillary muscle and through the free edge of the prolapsing leaflet.⁴³

View larger version (30K): [in this window] [in a new window] ? FIGURE 41-3 Mitral valve repair (A) and tricuspid valve repair (B) using a partial ring annuloplasty. (Superior and inferior vena cava snares not shown.)

Mitral Valve Replacement and Tricuspid Valve Replacement or Repair

In most instances, tricuspid valve regurgitation is caused by annular dilatation.⁴⁵ The severity of tricuspid valve leakage can be determined by transesophageal echocardiography prior to bypass and by digital exploration of the right atrium just prior to venous cannulation. Under general anesthesia, changes in blood volume and cardiac output can cause significant changes in the amount of regurgitation, and most often the severity of tricuspid valve leakage is lessened in the immediate prebypass period.

The patient's clinical condition must be correlated with echocardiographic findings and intraoperative assessment of the tricuspid valve. Patients with enlarged, pulsatile liver, peripheral edema, and jugular venous distention are likely to require tricuspid valvuloplasty following mitral valve replacement or repair. Those patients without the stigmata of right heart failure usually have less severe valve leakage, and tricuspid valve function may improve without direct repair or replacement after left-sided valvular lesions are corrected.

The decision for repair or replacement of functional tricuspid valve regurgitation at the time of mitral valve replacement is important because risk of subsequent reoperation is high. In our earlier experience, operative mortality was 25% in patients who required later reoperation for tricuspid valve regurgitation. Further, tricuspid regurgitation progresses in 10% to 15% of patients after replacement of rheumatic mitral valves.⁴⁶ Therefore, we maintain a liberal policy for annuloplasty or prosthetic replacement at initial operation.⁴⁷

PROCEDURE

For operations on the tricuspid valve, insertion of a Swan-Ganz catheter is optional; if it is used, the catheter is withdrawn from the right heart chambers during inspection and assessment of the tricuspid valve. We prefer direct cannulation of the inferior and superior venae cavae.⁴⁸ After commencement of cardiopulmonary bypass and cardioplegia, the cavae are snared around the venous cannulae, and the interatrial septum and tricuspid valve are exposed through a right atriotomy (Fig. 41-2A). A decision for repair or replacement of the tricuspid valve is made and the necessary prosthesis identified.

Usually we expose the mitral valve through an incision in the interatrial septum, which crosses the fossa ovalis and can be extended superiorly (Fig. 41-2B). Care should be taken during retraction to avoid tearing the septum inferiorly toward the coronary sinus and triangle of Koch. Alternatively, the mitral valve can be exposed through a standard left atriotomy posterior to the interatrial groove.

After repair or replacement of the mitral valve (Fig. 41-2C), the septal or left atrial incision is closed, and the tricuspid valve is repaired or replaced. For tricuspid valve repair, we use either the deVega method or ring annuloplasty.^11,16,49,50 Both techniques are based on the observation that the anterior and posterior valve portions of the tricuspid valve annulus are more prone to dilation than the septal leaflet portion of the annulus as previously described. When ring annuloplasty is indicated, we prefer a flexible device such as the Cosgrove-Edwards prosthesis⁵¹ or a partial Duran ring (Fig. 41-3B). The use of a partial ring avoids placement of sutures in the annulus near the penetrating bundle of His and reduces risk of injury to conduction tissue.

Tricuspid Valve Replacement and Pulmonary Valve Replacement for Carcinoid Heart Disease

If there is no involvement of the mitral and aortic valves,⁵² tricuspid and pulmonary valve replacement can usually be performed without the need for aortic occlusion and cardioplegic arrest. It is important to exclude the presence of a patent foramen ovale to eliminate risk of air entering the left atrium, and if a defect in the atrial septum is identified, it is closed using a brief period of aortic occlusion. In the past, our strategy for patients with carcinoid heart disease was to replace the tricuspid valve and excise the diseased pulmonary valve. Subsequent experience suggests that right ventricular function is better preserved with a functioning pulmonary valve, so we now favor pulmonary valve replacement rather than valvectomy.⁵³ Tricuspid valve replacement always is indicated, and it is usually necessary only to remove the anterior leaflet. Carcinoid disease produces fibrosis and retraction of the leaflets, so that anchoring sutures (interrupted mattress of 2-0 braided polyester backed with felt pledgets) can be inserted into the remaining septal and posterior leaflets. We prefer to position the pledgets on the ventricular side of the valve annulus. If exposure is difficult, a brief period of aortic clamping and cardioplegic arrest is utilized during placement of sutures in the posterior and septal leaflets; the aortic cross-clamp is removed, and the heart is allowed to beat rhythmically. The remaining sutures are placed, and all sutures are secured with observation of the electrocardiogram. If atrioventricular block develops, the sutures in the area of the penetrating bundle of His are removed and reinserted in a more superficial location.

Pulmonary valve replacement is performed through a longitudinal incision across the valve annulus on to the outflow portion of the right ventricle. We prefer to insert the prosthetic valve using continuous 3-0 polypropylene suture, anchoring the sewing ring to the native valve annulus for approximately two thirds of the valve annulus and then anteriorly to a pericardial patch that is used routinely to augment the valve annulus and to facilitate closure of the pulmonary artery and right ventricle.

Triple Valve Replacement

Operative preparation is similar to that previously described. Usually left-sided valvular lesions are corrected prior to tricuspid valve procedures. Again, if there is aortic valve regurgitation, the aortotomy is performed first, and cardioplegia is administered; simultaneously, we snare the cavae and open the right atrium. After excision of the aortic valve and calibration of the annulus, the interatrial septum is incised, and the mitral valve is repaired or replaced. Next, the aortic valve is implanted, and after closure of the aortotomy and septotomy, the tricuspid valvuloplasty or prosthetic replacement can be performed without aortic cross-clamping.⁵⁴

	?? RHEUMATIC HEART DISEASE AFFECTING MULTIPLE VALVES

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Long-term follow-up of children with rheumatic heart disease suggests that approximately 50% of patients have multivalvular involvement.^56,57 In a study of patients undergoing mitral valvotomy for rheumatic mitral stenosis (Table 41-5), 13% had clinical evidence of other rheumatic valve stenosis or regurgitation. Most of these patients had associated rheumatic aortic disease.⁵⁸

Approximately 10% of patients with rheumatic mitral valve stenosis also have rheumatic aortic regurgitation.⁵⁹ Clinical and laboratory characteristics of patients with mitral stenosis and aortic regurgitation are summarized in Table 41-7.

Physical findings An early blowing diastolic murmur is present along the left sternal border in about 75% of patients with rheumatic mitral stenosis.^60,61 This murmur can mimic a Graham Steell murmur of pulmonary valve regurgitation; however, this diastolic murmur usually originates from the aortic valve and represents mild aortic regurgitation.⁶² In patients with aortic regurgitation, a late diastolic murmur can either be the murmur of mitral stenosis or the Austin Flint murmur caused by a regurgitant jet directed toward the anterior mitral leaflet.⁶³ Exercise or amyl nitrite inhalation intensifies the murmur of organic mitral stenosis while diminishing the murmur of aortic regurgitation and the Austin Flint murmur.⁶¹ Doppler echocardiography differentiates mild aortic regurgitation and pulmonic regurgitation.⁶⁴ Occasionally the murmur and peripheral signs of aortic regurgitation are absent because of mitral stenosis.^60,65

Electrocardiography Electrocardiographic and roentgenographic evidence of eccentric left ventricular hypertrophy in patients with mitral stenosis is an important clue to associated aortic valve regurgitation. Also, atrial fibrillation early in the course of aortic regurgitation is a clue to associated mitral stenosis.^61,66

Echocardiography Left ventricular hypertrophy and volume overload detected by echocardiography suggest severe aortic valve regurgitation because these findings are not normally associated with mitral stenosis.⁶¹ Diastolic fluttering of the anterior leaflet of the mitral valve and the ventricular septum is an additional finding suggesting aortic valve regurgitation in patients with mitral stenosis.^61,67 In the presence of aortic valve regurgitation, the Doppler determination of mitral valve area is overestimated when pressure half-time measurements are used.⁶⁸

Catheterization data With current echocardiographic methods, cardiac catheterization to determine severity of valvular heart disease is rarely indicated; however, hemodynamic profiles of such patients have been studied thoroughly. Characteristically, the left ventricular diastolic pressure is elevated in about 35% of patients with mitral stenosis and aortic regurgitation. This can cause the transmitral gradient at rest to be small even when significant stenosis of the mitral valve is present.^41,69 In patients with isolated aortic valve regurgitation, the left ventricular diastolic pressure is elevated more frequently than in patients with concomitant mitral stenosis and aortic regurgitation.⁴⁵ Aortography may underestimate the severity of aortic regurgitation in patients with associated mitral stenosis because low cardiac output and low stroke volume produce a concomitant reduction in regurgitant volume.³⁸

PATHOPHYSIOLOGY

In patients with mitral valve stenosis and aortic valve regurgitation, decreased cardiac output minimizes the classic signs of aortic regurgitation (waterhammer pulse, head bobbing, or visibly pulsating capillaries). Also, concomitant mitral stenosis reduces left ventricular volume overload that is a characteristic of isolated aortic regurgitation.⁶⁹ The underfilling of the left ventricle characteristic of mitral stenosis is offset by overfilling secondary to aortic valve regurgitation. Pulmonary artery hypertension characteristic of mitral stenosis usually is present.

OPERATIVE DECISION MAKING

Patients with rheumatic mitral stenosis and rheumatic aortic regurgitation of more than a mild degree usually require replacement of both valves. Aortic valve repair is possible using techniques such as cuspal extension with glutaraldehyde-treated bovine or autologous pericardium.⁷⁰ Although early results with cuspal extension have been good, inexorable progression of valve fibrosis will necessitate later prosthetic replacement for many patients.⁷¹

Preoperative transthoracic and intraoperative transesophageal echocardiography aids in assessing function of the aortic valve in patients requiring surgery for mitral stenosis. At operation, the degree of ventricular fullness and amount of aortic root distention with infusion of cardioplegia are clues to important aortic valve regurgitation. As stated previously, if mitral valve replacement is necessary, strong consideration should be given to replacement of the aortic valve when there is moderate or worse leakage owing to rheumatic valvulitis.

Great care should be exercised to avoid ventricular distention if ventricular fibrillation occurs prior to aortic clamping. If ventricular fibrillation develops, distention of the heart can be prevented by inserting a left ventricular vent and by manually compressing the heart. Also, even mild or moderate degrees of aortic regurgitation can complicate cardioplegia delivery through the proximal aorta.

Rheumatic Mitral Stenosis with Rheumatic Aortic Stenosis

DIAGNOSIS, SIGNS, AND SYMPTOMS

Physical findings When rheumatic valve disease produces the combination of mitral valve stenosis and aortic stenosis, the signs and symptoms of both lesions can be present; however, those of mitral stenosis (dyspnea) tend to predominate, and the signs and symptoms of aortic stenosis (syncope, angina) occur less frequently. Table 41-8 outlines the clinical characteristics of patients in four studies of combined mitral and aortic stenosis. Dyspnea, the most frequently observed symptom, was present in 95% of patients, and angina and syncope were observed in 29% and 25% of patients, respectively. Mitral valve stenosis may even mask the signs and symptoms of aortic stenosis, making the clinical recognition of aortic stenosis difficult in patients with combined disease.⁷²

PATHOPHYSIOLOGY

In contrast to isolated mitral stenosis in which ventricular function frequently is preserved, the combination of mitral and aortic stenosis is associated with ventricular hypertrophy and diastolic dysfunction. The pressure load from the aortic stenosis causes a concentric hypertrophy with a small, noncompliant ventricular cavity.⁶⁶ Mitral stenosis compromises the ventricle's ability to maintain cardiac output (in contrast to isolated aortic stenosis in which cardiac output is maintained).^74,76 The decrease in cardiac output minimizes the signs and symptoms of aortic stenosis and may make the diagnosis of aortic stenosis difficult.⁷⁷ Other hemodynamic parameters are similar to isolated mitral stenosis, e.g., elevation of left atrial and pulmonary arterial pressures.^76,78

OPERATIVE DECISION MAKING

Although mitral valve stenosis sometimes can be treated effectively with valvuloplasty, commissurotomy for rheumatic aortic stenosis is rarely indicated. Thus, for patients with both aortic and mitral valve stenoses caused by rheumatic heart disease, we favor prosthetic replacement with mechanical prostheses if patients can manage long-term anticoagulation. If aortic valve stenosis is only mild in severity and the decision is made not to replace the aortic valve at the time of mitral valve replacement, then the patient should be followed carefully because over 50% will develop moderate to severe disease by 15 years postoperatively.⁷⁹ The combination of aortic stenosis and mitral stenosis may present unique problems for the surgeon. First, concentric hypertrophy of the left ventricle may displace the mitral valve orifice anteriorly, producing poor exposure through a standard atriotomy; several maneuvers and alternative incisions are described for patients in whom mitral valve exposure is difficult.^77,8084 Also, the small left ventricular cavity may impinge upon struts of caged-ball or stent-mounted bioprostheses. There is the potential for left ventricular outflow obstruction from high-profile prostheses in the mitral position in patients with aortic and mitral valve stenoses and small left ventricular cavity size.

Rheumatic Mitral Regurgitation with Rheumatic Aortic Regurgitation

DIAGNOSIS, SIGNS, AND SYMPTOMS

Physical findings When mitral regurgitation and aortic regurgitation are both present, the cardinal signs of either lesion may be masked by the other,⁶⁶ and when the clinical features of aortic regurgitation predominate, it may be difficult to determine whether coexisting mitral regurgitation requires surgical treatment.⁶⁶ The clinical characteristics of patients with combined mitral and aortic regurgitation are summarized in Table 41-13. Dyspnea and congestive heart failure are most common, whereas angina, syncope, and evidence of emboli occur less frequently.

Combined aortic and mitral regurgitation also results in significant left ventricular enlargement,⁸⁶ which is evident on both electrocardiogram^66,85 and chest x-ray.^66,85,87,88 Characteristic electrocardiographic findings are summarized in Table 41-14. On chest x-ray, nearly all patients have cardiomegaly and left atrial enlargement.^66,85 Calcification of the mitral or aortic valve is relatively uncommon.⁶⁶

Catheterization data Most patients have elevated right atrial and pulmonary arterial capillary wedge pressure. There is usually a prominent wave in pulmonary capillary wedge tracing. Approximately 75% of patients have an elevated left ventricular end-diastolic pressure.^59,66

PATHOPHYSIOLOGY

The combination of mitral and aortic valve regurgitation produces severe volume overload of the left ventricle. The reduction of impedance to ejection allows the ventricle to empty further, reducing ventricular wall tension with a resultant increase in the velocity of shortening.⁸⁹ Chronic volume overload increases stroke volume and distention of the left ventricle so that a larger stroke volume can be achieved with less myocardial fiber shortening compared to normal hearts.⁶⁶ Patients who respond to increased volume load by left ventricular dilation appear to tolerate surgical correction better than patients with left ventricular hypertrophy owing to an increased pressure load.⁶⁶

Patients with aortic valve regurgitation have augmented stroke volume to maintain an adequate cardiac output, but when mitral regurgitation coexists, part of the augmented stroke regurgitates into the left atrium and pulmonary veins. For this reason, when aortic regurgitation is severe, concomitant mitral regurgitation greatly reduces systemic cardiac output and can produce severe pulmonary congestion.⁹⁰

OPERATIVE DECISION MAKING

As stated previously, aortic valves involved with rheumatic disease usually require replacement. When the mitral valve also has rheumatic involvement, we replace the mitral valve at the time of aortic valve operation. After the aortic valve is excised, the mitral valve is visually inspected if it is suspected of being diseased or if the degree of regurgitation is severe.

	?? MYXOMATOUS AND PROLAPSING VALVE DISEASE AFFECTING MULTIPLE VALVES

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Aortic valve regurgitation in patients with Marfan syndrome is caused by progressive enlargement of the sinus portion of the aorta and the aortic valve annulus, i.e., annuloaortic ectasia.^94,95 The principal causes of mitral regurgitation in patients with Marfan syndrome are mitral annular dilation, floppy or prolapsing leaflets, and mitral annular calcification.⁹⁵ The pathological lesion in Marfan syndrome is cystic medial necrosis, which is characterized by degeneration of elastic fibers and infrequent cysts.⁹⁵ Alterations in the synthesis and cellular secretion of fibrillin are responsible for the phenotypic characteristics of many patients with Marfan syndrome.⁹⁶ Some patients have myxomatous cardiovascular lesions and annuloaortic ectasia without the other clinical characteristics of Marfan syndrome.

Two-dimensional echocardiographic studies show that the frequency of aortic valve prolapse in patients with mitral valve prolapse varies between 3% and 24% (Table 41-15).^97,98 In one necropsy study, the frequency of mitral regurgitation in Marfan patients with aortic aneurysms (most with aortic regurgitation) was 54% (7 of 13).⁹⁵ About 17% of patients who undergo surgery for myxomatous aortic valve require surgical correction of mitral regurgitation (Table 41-16).

Diagnosis, Signs, and Symptoms

Signs and symptoms of aortic and mitral valve regurgitation are reviewed in the section on rheumatic valvular disease. In addition to complete evaluation of the aortic and mitral valves and proximal aorta, patients with Marfan syndrome should have assessment of the descending aorta for aneurysm or chronic dissection.

Operative Decision Making

If annuloaortic ectasia is not present, patients with mitral and aortic valve regurgitation caused by myxomatous degeneration are candidates for repair of both valves. The aortic valve is inspected initially, and the decision for repair or prosthetic replacement is made depending on cuspal morphology. If tissue is sturdy and there is little prolapse or prolapse is limited to one cusp, repair can be undertaken with commissural narrowing and cusp resuspension. Often, aortic valve regurgitation is central, and simply narrowing the annulus by commissural plication restores valvular competence. Outcome of repair of both mitral and aortic valves has been good as regards patient survival and freedom from valve-related complications, but reoperation is necessary in 35% of patients 10 years after the initial procedure; patients with most severe aortic valve regurgitation have increased risk of late reoperation.¹⁰² If tissue is attenuated or if multiple cusps have severe prolapse, the valve is replaced.

In most instances, patients with Marfan syndrome and aortic regurgitation require composite replacement of the aortic valve and ascending aorta.¹⁰³ Occasionally, moderate aortic regurgitation can be repaired at the time of aortic replacement by suspending the aortic valve inside a tube graft or remodeling the sinus portion of the aorta.¹⁰⁴ Even if the aortic valve is replaced with a composite graft and mechanical valve, the surgeon should favor repair of associated mitral regurgitation. Gillinov et al report that valvuloplasty is possible in approximately 80% of patients with mitral regurgitation and Marfan syndrome, and that 5 years postoperatively, 88% of patients are free of significant mitral valve insufficiency.¹⁰⁵

Myxomatous Mitral Regurgitation with Tricuspid Regurgitation

Myxomatous degeneration may also involve the tricuspid valve, and presentation of mitral and tricuspid valve regurgitation owing to degenerative disease is not uncommon. In one study, 54% of patients with mitral valve prolapse also had tricuspid prolapse; however, most of these patients did not have significant regurgitation.⁹⁰ As with tricuspid regurgitation associated with rheumatic mitral disease, preoperative and intraoperative echocardiography is important in evaluating tricuspid disease in patients with myxomatous mitral regurgitation. In contrast to rheumatic disease, myxomatous mitral and tricuspid regurgitation almost always lends itself to valve repair.

SENILE CALCIFIC AORTIC VALVE DISEASE WITH MULTIPLE VALVE INVOLVEMENT

Unlike aortic stenosis caused by rheumatic disease in which associated mitral valve disease is common, senile calcific aortic stenosis usually presents as an isolated lesion. Although the combination of mitral valve disease and senile calcific aortic stenosis is uncommon, senile aortic calcification is a frequent cause of aortic valve stenosis.⁹² The incidence of senile calcific aortic disease has steadily increased in the last 20 years. Therefore, although mitral valve disease associated with calcific aortic stenosis is less common than that seen with rheumatic disease of the aortic valve, as the incidence of calcific aortic stenosis increases, so does the likelihood of encountering patients with disease of both valves.

Patterns of Multiple Valve Involvement with Calcific Aortic Stenosis

CALCIFIC AORTIC STENOSIS WITH INFECTIVE ENDOCARDITIS OF THE MITRAL VALVE

Stenotic aortic valves are frequently sites of infective endocarditis. As discussed in the section on endocarditis, the mitral valve may become involved with infective endocarditis by common abscess, by verrucous extension, or from a jet lesion, and infection may cause mitral valve aneurysm, perforation, and chordae disruption.¹⁰⁶ Management of these patients usually requires aortic valve replacement and assessment of the mitral valve at the time of operation. Vegetations of the mitral valve can sometimes be removed and perforations patched if the remaining tissue is sturdy and appears healthy.

CALCIFIC AORTIC STENOSIS WITH FUNCTIONAL MITRAL VALVE DISEASE

Senile calcification of the aortic valve may lead to mixed stenosis and regurgitation,⁹² and the volume load from regurgitation may lead to left ventricular dilatation and secondary mitral regurgitation of an otherwise normal mitral valve.⁹² Mitral regurgitation secondary to aortic valvular disease is discussed in the section on pathophysiology of multiple valve disease.

CALCIFIC AORTIC STENOSIS WITH CALCIFICATION OF THE MITRAL VALVE

Degenerative calcification is an age-related process usually affecting the aortic and mitral valves. In a study of patients over 75 years of age, one third had degenerative aortic or mitral calcification.⁹⁰ About 25% to 50% of patients with calcific aortic stenosis have calcification of the mitral valve annulus. Generally, patients with associated mitral annular calcification are older, have more severe aortic stenosis, and are more often female when compared with patients with aortic stenosis without mitral annular calcification.⁹⁸ Mills reported 17 patients undergoing mitral valve replacement for valvular disease related to severe annular calcification. Four of these patients also had concomitant aortic valve replacement.¹⁰⁷ Patients with mitral annular calcification have increased incidence of conduction defects¹⁰⁸ and aortic outflow murmurs, and annular calcification may exist in combination with rheumatic or myxomatous disease.¹⁰⁹

Diagnosis, Signs, and Symptoms

PHYSICAL FINDINGS

Auscultatory findings in aortic stenosis and mitral regurgitation consist of two systolic murmurs that can be distinguished by location of maximum intensity and radiation. Characteristically, aortic stenosis produces a crescendo-decrescendo murmur at the base, and mitral regurgitation produces a holosystolic murmur at the apex. Occasionally, a prolonged ejection murmur of aortic stenosis may simulate a holosystolic murmur at the apex, and the murmur of severe mitral regurgitation may radiate toward the base and may take on a crescendo-decrescendo pattern simulating an ejection murmur.^61,64

ELECTROCARDIOGRAPHY

Atrial fibrillation is uncommon in isolated aortic stenosis, and its presence is a clue to associated mitral valve disease.⁶¹ Both aortic stenosis and mitral regurgitation produce left ventricular hypertrophy and left atrial enlargement.

ECHOCARDIOGRAPHY

Echocardiography is necessary to delineate mitral valve morphology and presence of flail segments, and to assess the severity of aortic valve stenosis. Transesophageal echocardiography, either preoperatively or intraoperatively, may be required to fully evaluate the mitral valve.

	?? INFECTIVE ENDOCARDITIS AFFECTING MULTIPLE VALVES

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Aortic Regurgitant Jet Lesion of the Mitral Valve

Perforation of the anterior leaflet of the mitral valve may occur from the regurgitant jet of aortic valve endocarditis, and the diagnosis can be made from transesophageal echocardiography.¹¹⁸ Often, the perforation in the mitral valve can be debrided and repaired with a patch of pericardium or prosthetic material.

Prosthetic Valve Endocarditis

Risk of prosthetic valve endocarditis is greatest approximately 4 to 6 weeks postoperatively and decreases to a stable rate by about one year after operation.^119,120 Staphylococcus epidermidis and Staphylococcus aureus account for 20% to 30% of cases, respectively.¹²¹ Transesophageal echocardiography can identify vegetations caused by infection as well as prosthetic valve dysfunction and associated abscess cavities.¹²¹ In general, management of patients with endocarditis affecting multiple valves is similar to management of patients with infection of one valve. There are, however, some special considerations. When aortic valve endocarditis is complicated by abscess formation, infections may extend into the mitral annulus and necessitate concomitant mitral valve replacement; this occurs in approximately 12% of patients with aortic root abscess¹²² and is especially prevalent when there is involvement of the aorticomitral junction or subannular interventricular septum.^113,122

Tricuspid Valve with Left-Sided Valve Replacement

When the tricuspid valve is excised at the time of left-sided valve replacement, there remains a question of whether the tricuspid valve needs to be replaced. Simple excision of the tricuspid valve seems appropriate only in the absence of pulmonary hypertension and left-sided failure. A prosthetic left-sided valve is intrinsically stenotic, and many patients with tricuspid valve endocarditis can have pulmonary hypertension secondary to septic pulmonary emboli. Silverman found that patients who had tricuspid excision alone with left-sided valve replacement required perioperative inotropic support, and management of their postoperative congestive heart failure was more difficult than that of the patients who had tricuspid replacement.¹¹³

Results

Early mortality following surgery for multiple valve endocarditis is in the range of 20% to 30%, and Table 41-19 compares NYHA-class matched groups that had multiple valve procedures for infective endocarditis and for other reasons.

	?? CARCINOID HEART DISEASE AFFECTING MULTIPLE VALVES

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Signs and Symptoms/Diagnosis

Jugular venous distention with waves (from tricuspid regurgitation) and waves (from tricuspid stenosis) can be evident. Right ventricular enlargement can produce a pericardial lift. Most patients have murmurs from the tricuspid and pulmonary valves.¹²³ Patients often demonstrate ascites and liver enlargement as a result of either right-sided heart failure or hepatic metastases, or both. Therefore, these findings are not necessarily indicative of severe tricuspid valve regurgitation.

The electrocardiogram of patients with carcinoid heart disease often shows low voltage (85%), right bundle branch block (42%), and evidence of right atrial enlargement (35%).^2,123 The chest x-ray characteristically shows cardiomegaly (69%), pleural effusions (58%), and pleural thickening (35%).¹²³

Echocardiography

Echocardiographic findings of carcinoid heart disease include thickening and reduced motion of the tricuspid valve leaflets; the pulmonic valve cusps may be thickened and retracted. Fusion of the pulmonary valve commissures results in a stiff fibrotic ring that may cause a stricture in the entire pulmonary orifice. Pulmonary regurgitation and stenosis may both be present.¹²⁴

Invasive Studies

Cardiac catheterization is not necessary unless ischemic symptoms or a history of myocardial infarction suggest coronary artery disease.

Pathophysiology

Carcinoid heart disease results from deposition of plaques on the endocardium of the valves and atria; this usually occurs on the right side of the heart. However, plaques can develop on the mitral and aortic valves when there is carcinoid tumor in the lungs, or in the presence of intracardiac shunting that bypasses the lungs. Valves are damaged by exposure to circulating substances released from carcinoid tumors such as serotonin and bradykinin. Both of these components are inactivated by the lungs and the liver; the relationship between tumor location and the location of cardiac lesions is summarized in Table 41-20.¹²⁵

The dominant functional lesion of carcinoid heart disease is tricuspid valve regurgitation; the valve is fixed in a semi-open position, so that some degree of stenosis is present. Fibrosis and plaque deposition also affect the pulmonary valve, causing mixed stenosis and regurgitation, which increases the degree of tricuspid regurgitation.²

Operative Decision Making

TIMING OF OPERATION

The primary indications for surgery are increasing symptoms of congestive failure with objective evidence of valvular disease.¹²⁶ Again it should be noted that some of the signs of right heart failure, such as peripheral edema, ascites, and hepatomegaly, can be caused by the primary disease. Another indication for operation may be progressive right ventricular enlargement in the absence of symptoms. In a small series of carcinoid patients, right ventricular size and function did not correlate with operative or late mortality.¹²³ Currently we employ exercise testing to provide an objective assessment of the functional status and a guideline to the timing of cardiac surgery. If the primary cause for debilitation is right heart failure, it is reasonable to offer valve replacement even though the prognosis may be guarded.¹²⁶

TRICUSPID VALVE OPERATION

The tricuspid valve always requires replacement, and in our earlier experience we used mechanical prostheses because of the possibility of carcinoid plaque formation on a bioprosthesis. However, review of our patients and those reported previously shows little difference in patient survival with mechanical or tissue valves. Bioprostheses are selected for patients who have liver dysfunction that would complicate anticoagulation with Coumadin and for patients who will undergo subsequent hepatic resection or hepatic artery embolization.

PULMONARY VALVE OPTIONS

As stated previously, we now advise valve replacement rather than excision when the pulmonary valve is involved.

Management of the carcinoid syndrome during and early after operation is critically important, and this has been simplified greatly by treatment with long-acting octreotide; this is supplemented intraoperatively with intravenous administration of short-acting octreotide when there is evidence of flushing and vasodilation.¹²⁷ Preoperative steroids and antihistamines can also be used to prevent adverse effects from tumor-released mediators.^127,128 We usually give octreotide, 500 ?g intravenously, prior to induction of anesthesia with additional intravenous doses as needed at the onset and termination of cardiopulmonary bypass. Postoperatively, octreotide is continued and the dose is adjusted according to the severity of the flushing and vasodilation. Aprotinin, a kallikrein inhibitor, may mitigate the effects of substances released by carcinoid tumors during anesthesia and reduce intraoperative and postoperative bleeding.¹²⁷

	?? RARE CAUSES OF MULTIPLE VALVE DISEASE

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	?? RESULTS OF MULTIPLE VALVE SURGERY

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Survival following multiple valve surgery has improved along with refinements in myocardial protection; for example, mortality for multiple valve operations performed using normothermic ischemic arrest was approximately 40%¹²⁹; the use of cardioplegic arrest reduced operative risk by three-quarters.^66,129,130 In recent reports, operative mortality (30-day mortality or hospital mortality) ranges from about 6% to 17% (Table 41-22, part A). The 5-year actuarial survival is 60% to 88% (Table 41-22, part B), and the 10-year actuarial survival is 43% to 81% (Table 41-22, part C). Risk factors identified for morbidity and mortality following multiple valve surgery include advanced NYHA class,¹³¹¹³³ advanced age,¹³¹¹³⁵ current or prior myocardial revascularization,¹³⁴ ejection fraction l1% to 35%,¹³¹ presence of coronary artery disease,^131,132 aortic stenosis,¹³⁶ elevated pulmonary artery pressure,¹³⁴ tricuspid regurgitation,¹³⁶ and diabetes mellitus.¹³⁴

Comparisons of late survival between patients having multiple valve versus single valve replacement are inconsistent. Some studies show poorer survival¹³² after multiple valve replacement, and others report no significant difference in survival.^{21,130,132,139144} The discrepancy in these results may be because the majority of deaths in many reports are secondary to progression of coronary artery disease and noncardiac causes rather than valve-related deaths.^130,132 The presence of coronary artery disease and concomitant coronary artery surgery increases mortality following multiple valve surgery.^134,145,146

Some causes of early death following multiple valve surgery are perhaps less common today owing to changes in practice. In a necropsy study from 1963 to 1985 of patients who died early following double valve replacement, prosthetic valve dysfunction secondary to mechanical interference was evident in almost 50%, and ventricular rupture had occurred in 15% of cases.⁹⁵ Most of these patients received Starr-Edwards caged-ball prosthetic valves. Mechanical failure of low-profile tilting-disc prostheses that are in current use is rare, and early valve-related death with this type of prosthesis is very unusual.^{21,132,133,147} The current practice of preserving the posterior leaflet and chordal attachments of the mitral valve during prosthetic replacement may decrease the chance of ventricular disruption.¹⁴⁸

Thromboembolism

Thromboembolic rates following multiple valve replacement are shown in Table 41-22, part D, and range from 1% to 7% per patient-year for double valve replacement. Ten years postoperatively, freedom from thromboembolic events ranges from 77% to 89% (Table 41-22, part E). Although the data presented in Table 41-22, part D, along with other sources,¹⁴⁹ do not indicate significant differences between single and multiple valve replacement, some reports suggest that both mechanical¹⁵⁰ and bioprosthetic¹⁵¹ valves have an increased risk of thromboembolism in the mitral position. This risk is present early (90 days after operation) in patients undergoing multiple valve replacement that includes a bioprosthetic mitral valve.¹⁵¹

Anticoagulation-Related Hemorrhage

Rates of anticoagulant-related hemorrhage following multiple valve replacement, as with single valve surgery, are dependent on target INR.¹⁵² Risks of hemorrhage are reported to be 0.1% to 4.5% per patient-year following multiple valve surgery (Table 41-22, part F). Alvarez reported a significantly higher rate of anticoagulant-related hemorrhage following multiple valve replacement compared to single valve replacement.¹⁴⁰

Prosthetic Valve Infective Endocarditis

Rates of infective endocarditis following multiple valve surgery range from 0.2% to 2.5% per patient-year as shown in Table 41-22, part G. In comparison to isolated valve surgery, Alvarez reports prosthesis infection is more frequent following double valve replacement when compared to either isolated aortic (p .05) or mitral replacement (p ¹⁴⁰

Valve Performance

Rates of bioprosthetic structural deterioration relate to valve position; tissue valves appear to fail earlier in the mitral position than in the aortic position. When multiple valve replacements include the mitral valve, the rates of deterioration are similar¹⁵³ or even worse than¹⁴⁹ isolated mitral valve replacement (Table 41-22, part H).

COMPARISON OF BIOPROSTHETIC VALVES TO MECHANICAL VALVES

Comparisons of outcomes of patients with two or more mechanical prostheses to patients with two or more bioprostheses show similar rates of thromboembolism,^18,154 but freedom from operation favors those with multiple mechanical valves.^18,154 As might be expected, anticoagulation-related hemorrhage is less in patients with two bioprosthetic valves,^154,155 but there is no clear advantage of one prosthesis over the other as regards early and late mortality.^18,154,155

Results of Tricuspid Valve Procedures with Other Valve Procedures

RESULTS OF MITRAL AND TRICUSPID SURGERY

Reported operative mortality following mitral valve replacement and tricuspid valve repair or replacement is approximately 12% to 15%,¹⁵⁶ and 65% to 75% of patients are alive 5 years postoperatively.^134,156 Outlook for patients with lesser degrees of tricuspid regurgitation at the time of mitral valve replacement is good; 5-year actuarial survival for patients with tricuspid regurgitation who do not have tricuspid repair or replacement is 80% to 84%, and 10-year survival is 62% to 77%.¹⁵⁷

TRIPLE VALVE REPLACEMENT

The operative mortality following triple valve replacement is higher than that for double valve replacement and ranges from 5% to 25%.^20,134 As with double valve replacement, advanced age and higher NYHA class are associated with a risk factor for early mortality.^20,158 Causes of perioperative death are similar to those following double valve replacement and include low cardiac output, multiorgan failure, hemorrhage, and dysrhythmia.²⁰

Five-year actuarial survival after triple valve replacement is 53% to 78%, and 10- and 15-year survival are 40% and 25%, respectively (Table 41-23).

DOUBLE VALVE REPLACEMENT AND TRICUSPID ANNULOPLASTY

Operative mortality for patients undergoing double valve replacement with tricuspid valve repair is about 25%,⁴⁸ and the 10- and 15-year survival rates are 35% and 27%, generally comparable to those of patients having triple valve replacement.⁴⁸ Rates of thromboembolism in this group are reported to be 5% per patient-year.⁴⁸

Other Results

The operative mortality for double re-replacement is about 10% to 20%.^132,160 Incidence of postoperative ventricular arrhythmias is higher in patients having combined valve surgery compared to single valve surgery.¹⁶¹ Hemolysis may be more common with multiple valve disease or following multiple valve replacement.^162,163

The incidence of perivalvular leak following multiple valve surgery is about 4% per patient-year and may be more frequent following multiple valve surgery compared to single valve surgery.^138,140

When multiple valve surgery is combined with myocardial revascularization, the morbidity and mortality are 12% to 24%.^145,164 Early death in this group of patients is associated with prolonged perfusion time, the need for postoperative inotropic support, and high blood loss.¹⁶⁴

	?? SUMMARY

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