Cmc Closed Mitral Commissurotomy

• Ventricular septal defects with aortic cusp prolapse

left ventricular dilation to accommodate a larger volume without changing filling pressures and by ventricular hypertrophy, allowing ejection of a larger total stroke volume (31). The majority of such patients remain asymptomatic for prolonged periods of compensation, during which time they maintain forward stroke volume within the normal ranges. Once the left ventricle can no longer compensate, patients may present with symptoms of dyspnea and exertional angina, reflecting declining systolic function, elevated filling pressures, or diminished coronary flow reserve of the hypertrophied myocardium (32). Several natural history studies have identified age and left ventricular end-systolic pressure (or volume) as predictive factors associated with higher risk of mortality in this clinical population (Table 7) (7).

Table 7

Natural History of Aortic Regurgitation

Asymptomatic patients with normal left ventricular systolic function

Asymptomatic patients with left ventricular systolic dysfunction

Symptomatic patients

Progression to symptoms and/or left ventricular dysfunction Progression to asymptomatic left ventricular dysfunction Sudden death

Progression to cardiac symptoms

Mortality rate

• With heart failure

Although the progression of asymptomatic aortic regurgitation is slow, approximately one-fourth of patients will develop systolic dysfunction, or even die, before the onset of warning symptoms (7). Therefore, quantitative evaluation of left ventricular function with echocardiography is necessary because a serial history and physical exam alone are insufficient.

The clinical diagnosis of chronic severe aortic regurgitation by a trained physician can be made in the presence of a diastolic murmur (the third heart sound) or a rumble (Austin-Flint sign) on auscultation, combined with a displaced left ventricular impulse and wide pulse pressure (33,34). Similar to aortic stenosis, the chest x-ray and ECG will reflect left ventricular enlargement/hypertrophy and may elicit evidence of conduction disorders. Echocardiography is then indicated to: (1) confirm the diagnosis of aortic regurgitation; (2) assess valve morphology; (3) estimate the severity of regurgitation; (4) assess aortic root size; and (5) assess left ventricular dimension, mass, and systolic function. If the patient has severe aortic regurgitation and is sedentary or has equivocal symptoms, exercise testing is helpful to assess the following: functional capacity, symptomatic responses, and the hemodynamic effects of exercise.

In patients who are symptomatic on initial evaluation, cardiac catheterization and angiography are typically indicated if the echocardiogram is of insufficient quality to assess left ventricular function and to provide additional information as to the severity of aortic regurgitation or for the subsequent evaluation of coronary artery disease for possible revascularization therapy. The ultimate aim of any serial evaluation of the asymptomatic patient with chronic aortic regurgitation is to detect the onset of symptoms and objectively assess changes in left ventricular size and function that may occur in the absence of physical symptoms (Fig. 6). Medical therapy for aortic regurgitation is primarily based on the use of vasodilating agents, which are believed to improve forward stroke volume and reduce regurgitant volume; the use of such agents can often result in regression of left ventricular dilation and hypertrophy.

Initial left ventricular systolic dysfunction in chronic aortic regurgitation is associated with increased afterload pressure and is considered reversible with full recovery of left ventricular size and function following aortic valve replacement (7). However, as the ventricle becomes more hypertrophic and dilation progresses the chamber to a more spherical geometry, depressed myocardial contractility (rather than volume overload) is responsible for the systolic dysfunction. At this stage, neither return of normal left ventricular function nor improved long-term survival have been documented after aortic valve replacement (7). For patients with chronic aortic regurgitation, left ventricular systolic function and end-systolic size have been identified as the most important determinants of postoperative survival and normalization of left ventricular function with aortic valve replacement (7).

In addition, aortic valve replacement and aortic root construction are indicated in patients with proximal aortic disease and aortic regurgitation of any severity when the degree of aortic root dilation reaches or exceeds 50 mm (as commonly assessed by echocardiography) (35). Importantly, the surgical options for treating aortic regurgitation are expanding, with growing experience in aortic homografts, pulmonary auto-grafts, unstented tissue valves, and aortic valve repairs. It is conceivable that the thresholds for recommending operations may even be reduced, should these techniques ultimately demonstrate improved long-term survival or reduce postoperative valve complications.

3.1.2.2. Acute Aortic Regurgitation

When damage to the aortic valve is acute and severe, the subsequent and sudden large regurgitant volumes that return into the left ventricle will decrease the functional forward stroke volume dramatically. In contrast to chronic aortic regurgitation, in such acute cases there is no time for compensatory ventricular hypertrophy and dilation to develop. As a result, the considered typical exam findings of ventricular enlargement and diastolic murmur associated with chronic aortic regurgitation are absent. Instead, the patient with acute aortic regurgitation presents with pronounced tachycardia, pulmonary edema, or potentially life-threatening cardiogenic shock.

Echocardiography, which is considered crucial in the initial workup of acute aortic regurgitation, will likely demonstrate a rapid equilibration of aortic and left ventricular diastolic pressure and may provide some insights regarding the etiology of aortic regurgitation. Echocardiography also allows a rapid assessment of the associated valve apparatus, the aorta, and the degree of pulmonary hypertension (if tricuspid regurgitation is present). Transesophageal echocardiography is indicated when aortic dissection is suspected (36-38). Importantly, acute aortic regurgitation resulting from aortic dissection is a known surgical emergency requiring prompt identification and management. Cardiac catheterization, aortography, and coronary

Acute Aortic Regurgitation

Fig. 8. Aortic aneurysm repair using a Teflon felt reinforcement technique preserving the aortic valve and coronary arteries. From Yun, K.L. and Miller, D.C. Technique of aortic valve preservation in acute Type A aortic dissection, in Operative Techniques in Cardiac and Thoracic Surgery, (Cox, J.L. and Sundt III, T.M., eds.), Saunders, Philadelphia, PA, pp. 68-81. © 2003, with permission from Elsevier.

Fig. 8. Aortic aneurysm repair using a Teflon felt reinforcement technique preserving the aortic valve and coronary arteries. From Yun, K.L. and Miller, D.C. Technique of aortic valve preservation in acute Type A aortic dissection, in Operative Techniques in Cardiac and Thoracic Surgery, (Cox, J.L. and Sundt III, T.M., eds.), Saunders, Philadelphia, PA, pp. 68-81. © 2003, with permission from Elsevier.

angiography are important components of such an evaluation of aortic dissection with acute aortic regurgitation and thus should be performed if these procedures do not unduly delay the required urgent surgery. Following trauma, computed tomo-graphic imaging is useful in obtaining the appropriate clinical status and underlying diagnosis.

Nevertheless, appropriate treatment of acute aortic regurgitation is dependent on the etiology and severity of the disease. For example, only antibiotic treatment may be required in a hemodynamically stable patient with mild acute aortic regurgitation resulting from infective endocarditis. Conversely, severe acute aortic regurgitation is a surgical emergency, particularly if hypotension, pulmonary edema, or evidence of low output are present. In such cases, temporary preoperative management may include the use of agents such as nitroprusside (to reduce afterload) and inotropic agents such as dopamine or dobutamine (to augment forward flow and reduce left ventricular end-dias-tolic pressure). Intraaortic balloon counterpulsation is contrain-dicated in such patients, and p-blockers should be used cautiously because of their potential to reduce output further by blocking the compensatory tachycardia. Mortality associated with acute aortic regurgitation is usually the result of pulmonary edema, ventricular arrhythmias, electromechanical dissociation, or circulatory collapse.

In general, aortic valve replacement is the treatment of choice in aortic regurgitation. In cases of aortic disease resulting in aortic regurgitation, aneurysm repairs (Fig. 8) or aortic root replacements (Figs. 9 and 10) are considered clinically effective. Aortic root replacement with a homograft or autograft should be offered to patients in whom anticoagulation is contraindicated (e.g., elderly with risk, women of child-bearing years) as the tissue valve graft does not require anticoagulation. In addition, patients with disease resulting from endocarditis benefit as a homograft appears to have more resistance to infection. Finally, although the use of mechanical valves is effective, the prosthesis may impose a clinically relevant degree of stenosis in certain patients because of unavoidable size mismatch. Homografts and autografts are superior as they can be tailored to provide a larger outflow tract (39). In certain situations, repair of the aorta may involve the use of an artificial conduit using materials such as Dacron (Fig. 10).

Careful postaortic valve replacement follow-up is necessary during the early and long-term postoperative course to evaluate both prosthetic valve and left ventricular function. An excellent predictor of long-term success of aortic valve replacement is a reduction in left ventricular end-diastolic volume within the first 14 days after the operation. It should be emphasized that as much as 80% of the overall reduction in end-diastolic volume that will occur does so in this time period. In addition, the degree of regression in left ventricular dilation correlates well with the magnitude of increase in ejection fraction (40). Nevertheless, long-term follow-up should include an exam at 6 months postaortic valve replacement and then yearly if the clinical course is uncomplicated. Note that serial postoperative

Valve Sparing Aortic Root Replacement

Fig. 9. David procedure for aortic root replacement. The dilated aorta is resected, sparing the aortic valve and coronary buttons. The repair is then completed with insertion of a graft with reimplantation of the coronary arteries. Adapted from Smedira, N. G., (2003) Mitral valve replacement with a calcified anulus, in Operative Techniques in Cardiac and Thoracic Surgery, (Cox, J.L. and Sundt III, T.M., eds.), Saunders, Philadelphia, PA, pp. 2-13. © 2003, with permission from Elsevier.

Fig. 9. David procedure for aortic root replacement. The dilated aorta is resected, sparing the aortic valve and coronary buttons. The repair is then completed with insertion of a graft with reimplantation of the coronary arteries. Adapted from Smedira, N. G., (2003) Mitral valve replacement with a calcified anulus, in Operative Techniques in Cardiac and Thoracic Surgery, (Cox, J.L. and Sundt III, T.M., eds.), Saunders, Philadelphia, PA, pp. 2-13. © 2003, with permission from Elsevier.

echocardiograms after the initial early postoperative study are usually not indicated. However, repeat echocardiography is warranted at any point when there is: (1) evidence of a new murmur, (2) questions of prosthetic valve integrity, or (3) concerns about adequate left ventricular function.

3.2. Diseases of the Mitral Valve

Diseases of the mitral valve can be subdivided in a similar fashion as those affecting the aortic valve: stenosis and regurgitation. The normal anatomy of the mitral valve consists of a pair of leaflets attached to the left ventricle by chordae tendineae. Normal mitral valve area ranges between 4.0 and 5.0 cm2. However, in the case of mitral stenosis, symptoms do not typically develop until the functional valve area is reduced to less than 2.5 cm2 (41). For more details on valve anatomy, refer to Chapter 3 and the Visible Heart® CD.

3.2.1. Mitral Stenosis

Stenosis of the mitral valve orifice typically produces a funnel-shaped mitral apparatus described to resemble a "fish mouth," which then hinders normal diastolic filling of the left ventricle. Roughly 60% of all patients with mitral stenosis present with a history of rheumatic fever (42,43). Three typical pathological processes are observed in such patients: (1) leaflet thickening and calcification; (2) commissural and chordal fusions; or (3) a combination of these processes (44,45). Yet, congenital malformations of the mitral valve are usually responsible for mitral stenosis observed in infants and

Valve Dacron

Fig. 10. Aortic root replacement using Dacron graft as the technique used for correct sizing is demonstrated for suturing in place to yield the final graft implantation along with coronary reimplantation. Adapted from M. Yacoub, Valve-conserving operation for aortic root aneurysm or dissection, in Operative Techniques in Cardiac and Thoracic Surgery, Vol. 1, No. 1 (Cox, J.L. and Sundt III, T.M., eds.), Saunders, Philadelphia, PA, pp. 57-67. © 2003, with permission from Elsevier.

Fig. 10. Aortic root replacement using Dacron graft as the technique used for correct sizing is demonstrated for suturing in place to yield the final graft implantation along with coronary reimplantation. Adapted from M. Yacoub, Valve-conserving operation for aortic root aneurysm or dissection, in Operative Techniques in Cardiac and Thoracic Surgery, Vol. 1, No. 1 (Cox, J.L. and Sundt III, T.M., eds.), Saunders, Philadelphia, PA, pp. 57-67. © 2003, with permission from Elsevier.

children (45). Overall, women (at a rate of 2:1) account for the majority of mitral stenosis cases (42,43,46). Other entities can also simulate the clinical features of rheumatic mitral stenosis, such as left atrial myxoma, infective endocarditis, and mitral annulus calcification in the elderly.

Mitral stenosis is a slowly progressive disease with a typical mean age of presentation of symptoms in the fifth to sixth decade of life (47,48). Diagnosis of mitral stenosis may be made solely on the presence of abnormal physical exam findings or may be suggested by symptoms of fatigue, dyspnea, frank pulmonary edema, atrial fibrillation, or embolus (43). In the asymptomatic patient, survival is 80% at 10 years, with 60% of these patients eliciting no progression of symptoms (7). However, once symptoms related to pulmonary hypertension develop, to date there is a dismal 0-15% 10-year survival rate (7). Common causes of death in the untreated patients with mitral stenosis are caused by: (1) progressive heart failure (6070%); (2) systemic embolism (20-30%); (3) pulmonary embolism (10%); or (4) infection (1-5%) (45,46).

Shortness of breath (dyspnea), precipitated by exercise, emotional stress, infection, pregnancy, or atrial fibrillation, is typically the first symptom to present in patients with mild mitral stenosis (49). Yet, as the obstructions across the mitral valve increase, there will typically be progressive symptoms of dyspnea as the left atrial and pulmonary venous pressures increase (50). Increased pulmonary artery pressures and distension of the pulmonary capillaries can lead to pulmonary edema, which occurs as pulmonary venous pressure exceeds that of plasma

Closed Mitral Commissurotomy
Fig. 11. Treatment of mitral stenosis using the finger fracture closed mitral commissurotomy technique. Adapted from Braunwald (1992), Heart Disease (Zipes, D. P., ed.), Saunders, Philadelphia, PA, p. 1016. © 1992, with permission from Elsevier.

oncotic pressure. Subsequently, the pulmonary arterioles will elicit vasoconstriction, intimal hyperplasia, and medial hypertrophy, which then further exacerbates pulmonary arterial hypertension.

Commonly, the diagnosis of mitral stenosis can be made based on patient history, physical examination, chest x-ray, and ECG. For example, at the initial examination, a patient may be asymptomatic although abnormal physical findings, including a diastolic murmur, may be present (47,48). At this point, the diagnostic imaging tool of choice is 2D and Doppler tran-sthoracic echocardiography. Transesophageal echocardiography or cardiac catheterization are not required unless questions concerning diagnosis remain (7). Yet, heart catheterization is indicated to: (1) assess the potential for coronary artery disease or aortic valve disease; (2) assess pulmonary artery pressure; (3) perform balloon valvotomy; or (4) evaluate the situation when the clinical status of a symptomatic patient is not consistent with the echocardiography findings.

Typically, echocardiography is capable of providing an assessment of: (1) the morphological appearance of the mitral valve apparatus; (2) ventricular chamber size/function; (3) the mean transmitral gradient (51,52); (4) the relative mitral valve area; and (5) the pulmonary artery pressures (53). If necessary, noninvasive dobutamine or exercise stress testing can be completed with either the patient supine (using a bicycle) or upright (on a treadmill) to assess changes in heart rate and blood pressure in response to their overall exercise tolerance. Patients who are symptomatic with a significant elevation of pulmonary artery pressure (>60 mmHg), mean transmitral gradient (>15 mmHg), or pulmonary artery wedge pressure (>25 mmHg) on exertion have, by definition, a hemodynamically significant mitral stenosis that likely requires further intervention (7).

In mitral stenosis, medical treatment is typically indicated for the prevention of emboli (10-20%), which is primarily associated with the onset of atrial fibrillation (42,43,54-56). Atrial fibrillation ultimately develops in 30-40% of patients with symptomatic mitral stenosis, and importantly, about 65% of all embolic events occur within the first year of the onset of atrial fibrillation (42,43). The etiology behind atrial fibrilla tion is thought to be disruption of the normal conduction pathways caused by structural changes in the myocardium resulting from a pressure/volume overloaded atrium or, in fewer cases, rheumatic fibrosis of the atrium (48). Development of atrial fibrillation in mitral stenosis occurs more commonly in older patients and has been associated with a decreased 10-year survival rate (25 vs 46%) (43,46).

In addition to the thromboembolic potential, acute onset of atrial fibrillation can herald sudden deterioration in patients with mitral stenosis. This is considered secondary to an acute reduction in left ventricular ejection fraction and elevated pulmonary artery pressures, which thus result from loss of the atrial contribution to left ventricular filling. Urgent treatment of an acute episode of atrial fibrillation with a rapid rate consists of: (1) anticoagulation with heparin; (2) heart rate control (digoxin, calcium channel blockers, p-blockers, or amiodarone); or (3) electrical cardioversion. It should be noted that, in patients with atrial fibrillation for more than 24 to 48 h without anticoagulation, cardioversion is associated with an increased risk of embolism.

In chronic or recurrent atrial fibrillation resistant to prevention or cardioversion, heart rate control (digoxin, calcium channel blockers, p-blockers, or amiodarone) and long-term anticoagulation are considered the mainstays of therapy today (56,57). Yet, use of anticoagulation for patients with mitral stenosis who have not had atrial fibrillation or embolic events is not indicated secondary to the risk of bleeding complications.

The principle for treating symptomatic mitral stenosis rests on the alleviation of the fixed left ventricular inflow obstruction, thereby reducing the transvalvular gradient. Methods of disrupting the fused valve apparatus (open or closed mitral commissurotomy or percutaneous mitral balloon valvotomy) or mitral valve replacement have demonstrated significant postprocedural improvements in both reducing symptoms and increasing survival. The timing of intervention is related to the severity of disease; the method of intervention chosen is based on: (1) morphology of the mitral valve apparatus, (2) presence of other comorbid diseases, and (3) expertise at each specific center. Significant calcification, fibrosis, and subvalvular fusion of the valve apparatus can make either commissurotomy or percutaneous balloon valvotomy less likely to be successful. It should also be noted that the presence of mitral regurgitation is a contraindication for valvotomy/commissurotomy and is considered best treated with mitral valve replacement.

Closed commissurotomy is a surgical technique that uses finger fracture of the calcified valve (Fig. 11). This procedure has the advantage of not requiring cardiopulmonary bypass; however, the operator is not afforded direct visual examination of the valve apparatus. In contrast, open commissurotomy, which uses cardiopulmonary bypass, has gained favor in the United States because it allows inspection of the mitral valve apparatus under direct vision. During this procedure, division of the commissures, splitting of fused chordae tendineae/pap-illary muscles, debridement of calcium deposits (7), or mitral valve replacement can be completed to attain optimal results. The 5-year reoperation rate following open commissurotomy has been reported to be between 4 and 7%, and the 5-year complication-free survival rate ranges from 80% to 90%.

Catheter Balloon Visual Inspection

Fig. 12. Treatment of mitral stenosis using balloon valvotomy. Sequence of percutaneous mitral valvotomy: (A) Floating balloon catheter in position across the atrial septum through the mitral and aortic valves. The tip is in the ascending aorta. (B) An 8-mm dilating balloon catheter enlarging the atrial septal puncture site. (C) Two 20-mm dilating balloon catheters advanced into position across the stenotic mitral valve over two separate 0.038-in transfer guidewires. (D) Partially inflated dilating balloon catheters across the mitral valve. Note the "waist" produced by the stenotic valve (arrows). (E) Fully inflated dilating balloon catheters in position across the mitral valve. (F) Illustration of balloon commissurotomy technique. Adapted from Braunwald (1992), Heart Disease (Zipes, D.P., ed.) Saunders, Philadelphia, PA. © 2003, with permission from Elsevier.

Fig. 12. Treatment of mitral stenosis using balloon valvotomy. Sequence of percutaneous mitral valvotomy: (A) Floating balloon catheter in position across the atrial septum through the mitral and aortic valves. The tip is in the ascending aorta. (B) An 8-mm dilating balloon catheter enlarging the atrial septal puncture site. (C) Two 20-mm dilating balloon catheters advanced into position across the stenotic mitral valve over two separate 0.038-in transfer guidewires. (D) Partially inflated dilating balloon catheters across the mitral valve. Note the "waist" produced by the stenotic valve (arrows). (E) Fully inflated dilating balloon catheters in position across the mitral valve. (F) Illustration of balloon commissurotomy technique. Adapted from Braunwald (1992), Heart Disease (Zipes, D.P., ed.) Saunders, Philadelphia, PA. © 2003, with permission from Elsevier.

In centers with highly skilled operators, percutaneous balloon valvotomy is the initial procedure of choice for the symptomatic patient with moderate-to-severe mitral stenosis, those with favorable valve morphology and no significant mitral regurgitation or left atrial thrombus (Fig. 12). Immediate reduction in the transvalvular gradient (50-60%) is associated with gradual regression of pulmonary hypertension over several months (7). If selected appropriately, 80 to 95% of patients undergoing the procedure will achieve a functional mitral valve area larger than 1.5 cm2 and a resultant decrease in left atrial pressure without complication.

Yet, potential acute complications include mitral regurgitation (10%), an atrial septal defect (5%), left ventricle perforations (0.5-4.0%), emboli formation (0.5-3%), myocardial infarctions (0.3-0.5%), and increased mortality (<1%) (58). Patients with valvular calcification, thickened fibrotic leaflets with decreased mobility, and subvalvular fusions have a higher incidence of acute complications following balloon valvotomy

Table 8

Mitral Valve Replacement for Mitral Stenosis

Moderate-to-severe mitral stenosis (mitral valve area <1.5 cm2)

• With New York Heart Association functional class III-IV symptoms.

• Who are not considered candidates for percutaneous balloon valvotomy or mitral valve repair. Patients with severe mitral stenosis (mitral valve area <1 cm2)

• With severe pulmonary hypertension (pulmonary artery systolic pressure >60 to 80 mmHg).

• With New York Heart Association functional class I-II symptoms who are not considered candidates for percutaneous balloon valvotomy or mitral valve repair.

Source: From ref. 7.

Pulmonary Artery Plication

Fig. 13. Placement of circumferential sutures and plication of the anterior leaflet of the mitral valve. Adapted from Smedira, N. G., (2003) Mitral valve replacement with a calcified anulus, in Operative Techniques in Cardiac and Thoracic Surgery, Vol. 8, No. 1 (Cox, J.L., ed.), Saunders, Philadelphia, PA, pp. 2-13. © 2003, with permission from Elsevier.

Fig. 13. Placement of circumferential sutures and plication of the anterior leaflet of the mitral valve. Adapted from Smedira, N. G., (2003) Mitral valve replacement with a calcified anulus, in Operative Techniques in Cardiac and Thoracic Surgery, Vol. 8, No. 1 (Cox, J.L., ed.), Saunders, Philadelphia, PA, pp. 2-13. © 2003, with permission from Elsevier.

and a higher rate of recurrent stenosis on follow-up. Presence of left atrial thrombus, typically detected by transesophageal echocardiography, is a relative contraindication and, at a minimum, warrants 3 months of oral warfarin anticoagulation in an attempt to resolve the thrombus prior to the procedure. A postprocedure echocardiogram 72 h after the procedure is useful to assess postoperative hemodynamics and exclude significant complications such as mitral regurgitation, left ventricular dysfunction, or an atrial septal defect. However, recurrent symptoms have been reported to occur in as many as 60% of patients 9 years postprocedure (53,59,60); it should be noted that recurrent stenosis accounts for symptoms in less than 20% of such patients (59). In patients with an adequate initial result, progressive mitral regurgitation and development of other valvular or coronary problems are more frequently responsible for recurrent symptoms (59). Thus, in patients presenting with symptoms late after commissuro-tomy, a comprehensive evaluation is required to look for other causes.

Mitral valve replacement is an accepted surgical procedure for patients with severe mitral stenosis who are not candidates for surgical commissurotomy or percutaneous mitral valvotomy (Table 8, Figs. 13 and 14). In addition, patients with recurrent severe symptoms, severe deformity of the mitral apparatus, severe mitral regurgitation, or a large atrial septal defect should be offered mitral valve replacement.

The risk of mitral valve replacement is also highly dependent on age, left ventricular functional status, cardiac outputs, presence of comorbid medical problems, and concomitant coronary artery disease. More specifically, morbidity and mortality associated with mitral valve replacement are directly correlated with age, with risk in a young healthy person of less than 5%, increasing to as high as 10-20% in the older patient with concomitant medical problems or pulmonary hypertension. Mitral valve replacement is further complicated by: (1) the potential for embolic events, (2) the need for (and risk of) long-term anticoagulation therapy, and/or (3) the potential for valve thrombosis, dehiscence, infection, or malfunction.

3.2.2. Mitral Regurgitation

The common etiologies for mitral regurgitation include mitral valve prolapse secondary to myxomatous degeneration, rheumatic heart disease, coronary artery disease, infective endocarditis, and collagen vascular disease. As with aortic regurgitation, mitral regurgitation has both acute and chronic presentations. In some cases, mitral regurgitation caused by ruptured chordae tendineae or infective endocarditis may present as both acute and severe. Alternatively, mitral regurgitation may worsen gradually over a prolonged period of time. Yet, these very different presentations of mitral regurgitation are both treated with surgical intervention as dictated by the character of the symptoms presented.

3.2.2.1. Acute Severe Mitral Regurgitation

In acute severe mitral regurgitation, a sudden volume overload is imposed on the left ventricle without time for typical compensatory left ventricular hypertrophy. Thus, a sudden drop in forward stroke volume and cardiac output occurs (cardiogenic shock), with simultaneous pulmonary congestion. In severe mitral regurgitation, the hemodynamic overload often cannot be tolerated, and mitral valve repair or replacement must be performed urgently.

The acute nature of this form of mitral regurgitation results in patients who almost always present with symptoms; in a physical exam, it may only be positive for a holosystolic murmur and a third heart sound. Transthoracic echocardiography is typically used to confirm the diagnosis and to assess the general degree of disruption of the mitral valve apparatus. Furthermore, the use of transesophageal echocardiography is the procedure of choice for evaluation of the mitral valve and is warranted if mitral valve morphology and regurgitation are still not clearly elucidated following transthoracic echocardiography. Note that it is the high level of detail provided by transesophageal echocar-diography that is also helpful in demonstrating the anatomical cause of mitral regurgitation and, subsequently, directing successful surgical repair. Coronary arteriography is necessary before surgery in all patients older than 40 years. If necessary, myocardial revascularization should be performed during mitral valve surgery in those patients with concomitant coronary artery disease (61,62).

If the patient is not a candidate for surgery or if preoperative stabilization is required, medical therapy can help to diminish the amount of mitral regurgitation, thus increasing forward output and reducing pulmonary congestion; it should be initiated promptly. In normotensive patients, nitroprusside has been used to increase the forward output not only by preferentially increasing aortic flow, but also by partially restoring mitral valve competence as the left ventricular size diminishes (63,64). In hypotensive patients with severe reduction in forward output, aortic balloon counterpulsation can be employed to increase forward outputs and mean arterial pressures while diminishing mitral valve regurgitant volumes and left ventricular filling pressures. If infective endocarditis is the cause of acute mitral regurgitation, identification and treatment of the infectious organism is essential.

3.2.2.2. Chronic Asymptomatic Mitral Regurgitation

As with chronic aortic regurgitation, time for hypertrophy and chamber dilation is typically present in the patient present-

Chronic Aortic Regurgitation

Fig. 14. Mitral valve positioning into the mitral oriface. Adapted from Smedira, N. G., (2003) Mitral valve replacement with a calcified anulus, in Operative Techniques in Cardiac and Thoracic Surgery, Vol. 8 No. 1 (Cox, J.L., ed.), Saunders, Philadelphia, PA, pp. 2-13. © 2003, with permission from Elsevier.

Fig. 14. Mitral valve positioning into the mitral oriface. Adapted from Smedira, N. G., (2003) Mitral valve replacement with a calcified anulus, in Operative Techniques in Cardiac and Thoracic Surgery, Vol. 8 No. 1 (Cox, J.L., ed.), Saunders, Philadelphia, PA, pp. 2-13. © 2003, with permission from Elsevier.

ing with chronic severe mitral regurgitation (31,65). The dilation, or increase in left ventricular end-diastolic volume, is a compensatory mechanism that permits an increase in total stroke volume and allows for restoration of forward cardiac output (66). At the same time, an increase in left ventricle and left atrial size accommodates the regurgitant volume with a lower filling pressure; consequentially, symptoms of pulmonary congestion abate. Thus, such patients may remain asymptomatic for variable, but significant, time periods; however, the prolonged burden of volume overload may eventually result in left ventricular dysfunction. At this time, contractile dysfunctions impair myocardial ejections, and end-systolic volume increases; there may also be further left ventricular dilations and increased left ventricular filling pressures. Therefore, correction of mitral regurgitation should occur at the diagnosis of severe mitral regurgitation irrespective of the presence or absence of symptoms.

Initial diagnosis of chronic mitral regurgitation is commonly accomplished by physical exam, which may demonstrate findings of left ventricular apical impulse displacement, indicating that mitral regurgitation is severe and chronic and has likely caused cardiac enlargement. Typically, ECG and chest x-ray can be useful to evaluate rhythm changes and heart sizes, respectively. Nevertheless, an initial echocardiogram, including Doppler interrogation of the mitral valve, is considered indispensable in the management of the patient with mitral regurgitation. Such an echocardiogram typically provides a baseline estimation of left ventricle and left atrial volume, an estimation of left ventricular ejection fraction, and an approximation of the severity of regurgitation. Note that any presence of pulmonary hypertension is worrisome because it likely indicates advanced disease with a worsened prognosis (67).

Serial follow-ups are used to assess changes in symptomatic status, left ventricular functions, and exercise tolerances. Annual echocardiography becomes necessary once patients demonstrate moderate mitral regurgitation. Left ventricular end-systolic dimensions (or volumes) can typically aid in the timing of mitral valve surgery. For example, an end-systolic dimension, which may be less load dependent than ejection fraction, should be less than 45 mm preoperatively to ensure normal postoperative left ventricular function (66,68). In general, if patients become symptomatic, they should undergo mitral valve surgery even if left ventricular function is considered normal. Similar to acute mitral regurgitation, cardiac catheterization is also indicated if: (1) there is discrepancy between clinical and noninvasive findings; (2) there is a need for preoperative coronary assessment for potential revascu-larization at the time of mitral valve replacement; or (3) an absence of chamber enlargement raises the question of the accuracy of the diagnosis, which should then be assessed with ventriculography at cardiac catheterization.

To date, there is no generally accepted therapy for asymptomatic patients with chronic mitral regurgitation. In such patients who develop symptoms but have preserved left ventricular function, surgery is considered the most appropriate therapy. Atrial fibrillation is commonly associated with mitral regurgitation, and preoperative atrial fibrillation can be an independent predictor of reduced long-term survival after mitral valve surgery for chronic mitral regurgitation (69). Atrial fibrillation should be treated with heart rate control (digitalis, calcium channel blockers, p-blockers, or amiodarone) and anticoagulation to avoid embolism (70,71). Common predictors for the persistence of atrial fibrillation after successful valve surgery include the presence of atrial fibrillation for longer than 1 year or a left atrial size larger than 50 mm (72). Although patients who develop atrial fibrillation also usually manifest other symptomatic or functional changes that would warrant mitral valve repair or replacement, today many clinicians would also consider the onset of episodic or chronic atrial fibrillation an indication, in and of itself, for surgery (73,74).

Three categories of surgical procedures are now in vogue for correction of mitral regurgitation: (1) mitral valve repair, (2) mitral valve replacement with preservation of part or all of the mitral apparatus, and (3) mitral valve replacement with removal of the mitral apparatus. Each procedure has its advantages and disadvantages, as well as separate indications. In general, with the appropriate valve morphology and sufficient surgical expertise, mitral valve repair is the operation of choice. Yet, mitral valve repair may require longer extracor-poreal circulation time and may occasionally fail, thus requiring mitral valve replacement. Valve calcification, rheumatic involvement, and anterior leaflet involvement all decrease the likelihood of repair, whereas uncalcified posterior leaflet disease is almost always repairable.

The primary advantage of repair is the avoidance of anticoagulation and prosthetic valve failure. In addition, postoperative left ventricular function and survival are improved with preservation of the mitral apparatus because the mitral apparatus is considered essential for maintenance of normal shape, volume, and function of the left ventricle (7).

Similar advantages are gleaned with the use of mitral valve replacement with preservation of the mitral chordal apparatus, except that it adds both the risks of deterioration inherent in tissue valves and the need for anticoagulation with mechanical valves. Mitral valve replacement, in which the mitral valve apparatus is excised, should be performed only when the native valve and apparatus are so distorted by the preoperative pathology (rheumatic disease, for example), such that the mitral apparatus cannot be spared.

In an asymptomatic patient with normal left ventricular function, repair of a severely regurgitant valve may be offered as a means to: (1) preserve left ventricular size and function and (2) prevent the sequelae of chronic mitral regurgitation (Fig. 15). Similarly, this approach has proven successful in the hemodynamically stable patient with newly acquired severe mitral regurgitation as the result of a ruptured chordae or recent onset of atrial fibrillation. The timing of surgery in asymptomatic patients is indicated by the appearance of echocardiography indicators of left ventricular dysfunction (i.e., left ventricular ejection fraction less than 60% or left ventricular end-systolic dimension above 45 mm). Mitral valve repair or replacement at this stage will likely prevent further deterioration in left ventricular function and improve survival (69).

Patients with symptoms of congestive heart failure, despite normal left ventricular function as determined by echocardio-graphy (ejection fraction greater than 60%, end-systolic dimension less than 45 mm), will likely require surgery. In both situations, mitral repair is preferred when possible. Mitral valve surgery is recommended for severe symptomatic mitral regurgitation with evidence of left ventricular systolic dysfunction; it is likely both to improve symptoms and to prevent further deterioration of left ventricular function (75).

Ischemic mitral regurgitation is usually caused by left ventricular myocardial infarction, resulting in an associated papillary muscle dysfunction. The prognosis for such a patient with ischemic mitral regurgitation is substantially worse when compared with other etiologies (62,76). Following an acute infarction with the development of severe mitral regurgitation, hypotension and pulmonary edema often occur. Hemodynamic stabilization, usually with insertion of an intraaortic balloon pump, is completed preoperatively, followed by coronary revascularization, which only rarely improves mitral valve function. Unlike the case with nonischemic mitral regurgitation, it is more difficult to demonstrate a benefit of repair over

Mitral Regurgitation Hemodynamics

Fig. 15. Operative repair of the mitral valve using a technique developed by Carpentier. (A) Triangular resection of anterior leaflet; (B) anterior leaflet repair; (C) sizing of annulus; (D) annuloplasty ring suture technique; and (E) completed repair. Adapted from J.W. Kirklin (2003), Cardiac Surgery, 3rd Ed., Churchill Livingstone, New York, NY, pp. 673-675.

Fig. 15. Operative repair of the mitral valve using a technique developed by Carpentier. (A) Triangular resection of anterior leaflet; (B) anterior leaflet repair; (C) sizing of annulus; (D) annuloplasty ring suture technique; and (E) completed repair. Adapted from J.W. Kirklin (2003), Cardiac Surgery, 3rd Ed., Churchill Livingstone, New York, NY, pp. 673-675.

replacement with ischemic mitral regurgitation. In general, operative mortality increases, and survival is reduced in such patients older than 75 years with coronary artery disease, especially if mitral valve replacement must be performed (77). In these patients, the goal of therapy is typically to first improve the quality of life rather than prolong it, and medical therapy may be utilized to a greater extent to control cardiac symptoms.

3.3. Tricuspid Valve Disease

Tricuspid valve disease can be subclassified as regurgitation, stenosis, or a combination of both; it is most commonly the result of rheumatic fever, with rare cases attributed to infective endocarditis, congenital anomalies, carcinoid causes, Fabry's disease, Whipple's disease, or methysergide therapy (7). Rheumatic tricuspid disease commonly presents as a combination of tricuspid stenosis and tricuspid regurgitation. Furthermore, tri-cuspid disease commonly presents with concomitant mitral or aortic valve defects, because acute rheumatic fever is also a common etiology for these. It should be noted that right atrial myxomas or any type of large vegetations that produce an outflow tract obstruction will mimic stenosis; however, regurgitation may also result as it often causes associated damage to the leaflet apparatus.

Pure tricuspid regurgitation may result from rheumatic fever, infective endocarditis, carcinoid causes, rheumatoid arthritis, radiation therapy, anorectic drugs, trauma, Marfan's syndrome, tricuspid valve prolapse, papillary muscle dysfunction, or congenital disorders (7). In addition, pressure/volume overload conditions that do not cause direct damage to the leaflets themselves, such as those associated with mitral stenosis and mitral regurgitation, typically cause ventricular enlargement, resultant tricuspid annular dilation, and thus pure tricuspid regurgitation (7).

The clinical features of tricuspid stenosis include auscultation of a tricuspid opening snap and a characteristic murmur. Auscultation may reveal a holosystolic murmur in the lower left parasternal region that may increase on inspiration (Carvallo's sign). In rare instances, severe tricuspid regurgitation may produce systolic propulsion of the eyeballs, pulsatile varicose veins, or a venous systolic thrill and detectable murmur in the neck. Echocardiography is commonly used to: (1) assess tricus-pid valve structure and function, (2) measure annular size, (3) evaluate right pressures, and (4) rule out other abnormalities influencing tricuspid valve function. Systolic pulmonary artery pressure estimations, combined with information about annular

Tricuspid Valve Leaflet Failure

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Fig. 16. Tricuspid annuloplasty procedure. AV, atrioventricular.

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Fig. 16. Tricuspid annuloplasty procedure. AV, atrioventricular.

circumference, further improve the accuracy of clinical assessment (7).

The etiology of tricuspid valve disease and the overall condition of the patient ultimately dictate the therapeutic approach. Tricuspid balloon valvotomy can be used to treat tricuspid stenosis; however, there is the potential for inducing severe tricuspid regurgitation. It has been documented that poor long-term outcome is associated with right ventricular dysfunction or systemic venous congestion associated with severe tricuspid regurgitation (7).

When pulmonary hypertension is the underlying cause of tricuspid annular dilation, medical management alone may result in substantial improvement of tricuspid regurgitation and thus minimize the need for surgical intervention. Surgical options for treating tricuspid regurgitation include annuloplasty or valve replacement (Fig. 16). Tricuspid regurgitation annuloplasty is effective and can be optimized using intraoperative transesophageal echocardiography. Valve replacement with a low-profile mechanical valve or bioprosthesis is often necessary when the valve leaflets themselves are diseased, abnormal, or destroyed (78). In both procedures, care must be taken to avoid causing damage to the conduction system. In such cases, use of biological prostheses is preferred to avoid the high rate of thromboembolic complications known to occur with mechanical prostheses placed in the tricuspid position. Combined tricuspid and mitral valve procedures are often completed in the same interventions, as in the setting of rheumatic disease; however, no long-term data regarding the value of such an approach exists. In patients with associated conduction defects, insertion of a permanent epicardial pacing electrode at the time of valve replacement is also suggested.

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