Acute Ischemic Mitral Regurgitation
Clinically, acute IMR usually presents abruptly with chest pain and/or shortness of breath. The presentation is that of an acute myocardial infarction and occasionally may be silent. These patients are often hemodynamically unstable, in cardiogenic shock. They often present in extremis with symptoms of congestive heart failure, including pulmonary edema, systemic hypotension, oliguria, acidosis, and poor periperhal perfusion. On physical examination, in the setting of profound MR, most patients have a loud apical, holosystolic murmur that radiates to the left axilla; but with lesser degrees of MR, a murmur is inconsistently detected.
Nearly all electrocardiograms are abnormal,17,42,43 but only slightly more than half are diagnostic of AMI. Some of the nondiagnostic changes include right or left bundle branch block and nonspecific ST- and T-wave changes in the anteroseptal, lateral, or inferior leads.17,42,44 Most patients are in sinus rhythm. In autopsy series, the incidence of subendocardial infarctions is approximately equal to the incidence of transmural infarctions.17,43 Frequently patients with papillary muscle rupture have electrocardiographic evidence of an inferior MI. When the ECG is diagnostic, inferior wall infarctions are much more common than anterior and lateral wall infarctions. Conduction abnormalities are relatively uncommon and are more often found in patients with postinfarction ventricular septal defects. Chest x-rays nearly always show signs of pulmonary congestion, interstitial pulmonary edema, and pulmonary venous engorgement.42 Cardiomegaly is usually not present, and there is usually no sign of left atrial enlargement in acute MR.17
The differential diagnosis for acute IMR includes postinfarction ventricular septal defect, massive AMI without significant MR, and ruptured chordae tendineae without AMI. Right heart catheterization usually shows elevated pulmonary arterial pressures with prominent V waves reaching 40 mm Hg or higher.42,45 Mean pulmonary artery wedge pressures are greater than 20 mm Hg unless cardiac output is very low. Mixed venous oxygen saturations are often well below 50% and reflect low cardiac output with indices that range from 1.0 to 2.9 L/m2/min.45 In the presence of a loud systolic murmur, absence of an oxygen step-up in the pulmonary artery is strong evidence against the diagnosis of postinfarction ventricular septal defect. Electrocardiographic evidence of AMI distinguishes acute IMR from acute chordal rupture, but the lack of EKG changes does not differentiate the two diseases.42
Transthoracic echocardiography (TTE) assesses the degree of MR, confirms wall motion abnormalities, and may demonstrate flail mitral leaflets. However, transesophageal (TEE) echocardiography is the diagnostic imaging tool of choice. This modality definitively documents the degree and characteristics of the MR jet of IMR, associated wall motion abnormalities, and the status of the posterior papillary muscle. In the modern era, the information provided by TEE is vital in making an accurate decision to repair versus replace the mitral valve. Typically the left atrium is not enlarged, but the left ventricle shows signs of volume overload and segmental wall motion abnormalities. Color flow Doppler velocity mapping documents the presence of MR after myocardial infarction and semiquantitates its severity. Ejection fractions vary widely, but do not reflect the extent of the LV infarction.
Despite hemodynamic instability, most patients have a diagnostic cardiac catheterization primarily for definition of coronary arterial anatomy. However, the wisdom of prescribing cardiac catheterization for patients in cardiogenic shock is highly questionable in that revascularization of obstructed, remote coronary vessels is not likely to improve a patient's chances for immediate survival. Approximately half of catheterized patients have single-vessel disease, most often of the right coronary artery.42,45 Most of the remainder have three-vessel disease.17,42–44 Ventriculography shows increased LV volume at both end diastole and end systole, severe MR, segmental wall motion abnormalities, and a wide range of ejection fractions, which are generally over 40% and frequently over 60%.44,45 LV end-diastolic pressures are usually elevated, with prominent left atrial V waves and moderate pulmonary hypertension. Occasionally patients may have mild or moderate tricuspid regurgitation. Cardiac output is usually very low in this disease process.
Immediate surgery is the best chance for survival for most patients with acute, severe postinfarction MR. The goal of medical therapy is to stabilize the patient and optimize hemodynamcs in preparation for surgical intervention. A few, highly selected patients without papillary muscle rupture early in their presentation have been treated by emergency PCI and/or thrombolytic therapy in an attempt to reduce the size of the infarct and thereby reduce mitral regurgitation.46–49 PCI or thrombolysis carried out within 4 hours of the onset of AMI may on occasion produce spectacular reversal of both the infarction and mitral regurgitation.47–49 However, less rapid PCI may not succeed in preempting the infarct and aborting mitral regurgitation.49 PCI and thrombolysis in catheterized patients are potentially worth trying if patients reach medical attention soon after the onset of symptoms, are sufficiently stable, and can be followed by echocardiography. However, in many patients PCI and thrombolysis do not provide a favorable outcome.46 In one study, 17% of patients with acute IMR and successful thrombolysis died in the hospital; in those with successful PCI, 50% died shortly afterward, and 77% were dead in 1 year.46 Of the survivors, the majority continue to have 3+ or 4+ MR.46
For patients who have acute postinfarction angina with 1+ or 2+ MR, urgent myocardial revascularization is indicated to relieve angina and prevent extension of the infarction. It is important to prevent progression of MR and the development of congestive heart failure or cardiogenic shock. This is usually accomplished by thrombolysis or PCI. If these measures are unsuccessful, operation is rarely completed in time to reverse the infarction, but early operation may reduce the size of the ultimate infarct.50–52 The presence of mild to moderate IMR does not increase operative mortality, but the presence of congestive heart failure is a risk factor.53 In these patients, the mitral valve is generally not addressed unless intraoperative transesophageal echocardiography indicates 3+ or 4+ MR.
Indications for emergency surgery for acute, severe postinfarction MR vary among institutions and probably explain wide discrepancies in reports of hospital mortality.54,55 In this group of patients, medical therapy does not produce survivors and patients denied operation are not reported.42,44 Aged patients are less likely to survive operation, and there are only anecdotal reports of successful operation in octogenarians.47,54,56 Other risk factors for hospital death are severe congestive heart failure, the number and severity of comorbid diseases such as renal or pulmonary problems, presence of an intra-aortic balloon pump, reduced ejection fraction, and greater number of diseased coronary arteries.57
Surgical intervention for acute, severe postinfarction MR consists of mitral valve repair or replacement with or without myocardial revascularization. Nearly all surgeons recommend revascularization of all significantly obstructed coronary vessels away from the site of the infarction.55 Improved methods of cardioplegia support this recommendation even in patients with preoperative cardiogenic shock who have had cardiac catheterization. The wisdom of blind revascularization of remote coronary vessels in patients who have not had preoperative cardiac catheterization and revascularization of the infarct artery more than 4 to 6 hours after onset of pain is less clear.58 On a statistical basis, only half of patients with acute IMR have multivessel coronary artery disease.17,42,45 Revascularization of completed infarctions favorably influences subsequent ventricular remodeling.51,52,59
With echocardiographic findings amenable to repair, a simple, central regurgitant jet, minimally tethered leaflets, and no papillary muscle pathlogy such as rupture, a simple repair with an annuloplasty ring can be enterained. However, replacement of the diseased valve should be considered if the effectiveness and durability of the repair are at all in question. These patients are often critically ill, and will not tolerate the increased cardiopulmonary bypass time associated with mitral valve replacement after failed mitral repair. When performing mitral valve replacement, it is important to preserve the chordal attachments to the annulus to limit adverse ventricular remodeling (Fig. 29-4). Bioprosthestic valves are a reasonable choice since anticoagulation is not benign and durability is a relatively minor concern in these patients with poor long-term prognosis.60,61
Okita's method for retaining chordal attachment to the mitral annulus during replacement of the mitral valve. (A) Diagram showing the mitral valve from the left atrium. The center of the anterior leaflet is excised (shaded area) and the leaflet is divided retaining the chordae from each papillary muscle attached to the residual anterior leaflet tissue. The posterior leaflet may be divided at its midpoint if necessary. (B) Remnants of the anterior leaflets are sutured to the annulus using a single stitch as shown. This tissue is later included in sutures used in sewing the valve to the annulus. (Modified slightly with permission from Okita Y, Miki S, Kusuhara K, et al: Analysis of left ventricular motion after mitral valve replacement with a technique of preservation of all chordae tendineae. J Thorac Cardiovasc Surg 1992; 104:786.)
Published results of mitral valve replacement for acute IMR are poor. Hospital mortality ranges from 31 to 69% and probably reflects the selection process more than quality of care. Variables that increase early mortality include patient age, cardiogenic shock, comorbid conditions, the amount of infarcted myocardium, and delay in operation.42,44,45,54 More recent experience may be better because of prompt diagnosis, early surgery, complete revascularization, and application of chordal preservation techniques that better preserve left ventricular function.60–67 Several techniques are available for preserving chordae (see Fig. 29-4).62,68,69
Controversy exists over whether the mitral valve should be repaired or replaced in the setting of acute IMR. Repair of the valve in acute IMR potentially enhances the complexity of the operation as well as the cardiopulmonary bypass time as compared with mitral valve replacement. As demonstrated, the anatomical derangements in the acute IMR setting may be very subtle, resulting in annular dilatation and malcoaptation of the leaflets, in which case an undersized ring annuloplasty is a reasonable option. Long-term (5-year) survival in patients who survive the perioperative period is poor and even in modern reports hovers around 50%.60,61 Even with poor prognosis, we believe mitral valve annuloplasty ring is a reasonable option for pathology amenable to repair.
Papillary muscle rupture is less common as the etiology for acute ischemic mitral regurgitation, and this subset of patients is usually much less ill. A recent retrospective analysis of post-MI papillary muscle rupture patients noted a marked improvement in postoperative survival when either valve repair (reimplantation of the papillary muscle and annuloplasty) or replacement was performed in combination with concomitant revascularization. It is encouraging that the authors noted normalization in 5-year survival (79%) and freedom from congestive heart failure to that of matched MI controls without papillary mucle rupture (28 ± 8% versus 36 ± 6%) was noted, predicting an optimistic outcome for this patient population in the modern surgical era.70
Chronic Ischemic Mitral Regurgitation
Chronic IMR represents the majority of patients with IMR. Between 10.9 and 19.0% of patients with symptomatic coronary artery disease who have cardiac catheterization3,4 and 3.5 to 7.0% of patients who have myocardial revascularization have IMR.71–74 The majority of these patients have 1+ to 2+ mitral regurgitation, without evidence of heart failure.3,4,71–73 In patients with chronic IMR, three major variables interrelate to produce the clinical spectrum of patients with varying combinations of symptomatic ischemia and heart failure. As with acute IMR, the three major variables are: (1) the presence and severity of ischemia, (2) the severity of mitral regurgitation, and (3) the magnitude of left ventricular dysfunction. First, patients with obstructive coronary artery disease may be asymptomatic or have stable, progressive, unstable, or postinfarction angina or its equivalent. Because of disabling symptoms, threat to left ventricular mass or statistically shortened survival, ischemia is a compelling problem that must be addressed therapeutically. The approach and methods do not differ from similar patients who do not have IMR.
The second variable is the severity of mitral regurgitation. At present, 1+ or 2+ mitral regurgitation in patients without symptoms of heart failure does not compel invasive therapy for mitral regurgitation. Severe mitral regurgitation and/or symptoms of heart failure require evaluation for possible operation irrespective of the therapy needed for ischemia. The third variable is the degree of left ventricular dysfunction. LV dysfunction is the most difficult to assess in the presence of mitral regurgitation. Symptoms of heart failure may be caused by left ventricular dysfunction secondary to ischemia, mitral regurgitation, or both.
The primary purpose of diagnostic studies is to determine the severity of coronary artery disease and its anatomy, the severity and mechanism of mitral regurgitation, and the degree of left ventricular dysfunction. In chronic IMR, the ventricular geometry and function reflect remodeling owing to both the mitral regurgitation and infarction; therefore, these patients may require diagnostic studies and perhaps operative procedures that are different from patients with CAD associated with mitral regurgitation. It is also important to define comorbidity of other organ systems by appropriate diagnostic studies dictated by the patient's history, physical examination, and screening laboratory findings.
In patients with IMR, the ECG usually shows evidence of a prior myocardial infarction. The incidence of arrhythmias varies but atrial fibrillation as noted earlier is quite common. In patients without failure and mild mitral regurgitation, heart size by chest x-ray is normal or slightly enlarged; the left atrium is seldom enlarged. In those with moderate or severe mitral regurgitation and/or severe left ventricular dysfunction, the heart is enlarged and usually the left atrium is also enlarged.
Transthoracic echocardiography and TEE are useful in determining the etiology of mitral regurgitation. Two-dimensional echocardiography reliably detects ruptured chordae, annular calcification, and myxomatous degeneration, which are not features of chronic IMR, and differentiates rheumatic valve disease, endocarditis, and degenerative valve disease. Echocardiography also effectively assesses regional wall motion abnormalities and global left ventricular function. The degree of mitral regurgitation is also well quantified by color flow Doppler measurements. Characteristics of the mitral regurgitation demonstrated by TEE will also aid in the decision to repair or replace the mitral valve. Extremely dilated annulus with severe bileaflet tethering (Carpentier Type IIIB) and eccentric or complex regurgitation jet are echocardiographic findings that repair may not be effective or durable.
Cardiac catheterization provides information regarding the coronary arterial anatomy and pathology. Ventriculograms add little to the data provided by TTE or TEE and should be avoided, especially in patients with impaired renal function. Measurements of chamber pressures and estimates of cardiac output contribute to the overall evaluation of left ventricular function. Pulmonary hypertension, when present, is typically moderate and correlates with the degree of left ventricular dysfunction and/or severity of mitral regurgitation.
The decision to intervene surgically in IMR can be a challenging process. Chronic IMR represents a set of patients with symptoms of insidious onset and often of chronic duration. Patients may primarily present with symptoms of ischemic coronary artery disease, and on preoperative workup are found to have significant concomitant mitral regurgitation. Although this group of patients may have preserved left ventricular function, compromised ventricular function is not uncommon. The surgical indication in this group of patients is coronary artery disease requiring CABG with coexistent significant mitral regurgitation. Important factors to consider in the decision to intervene on mitral regurgitation include the following: the impact of coronary artery bypass grafting (CABG) alone on the progression of IMR; the impact of CABG with or without MVR on survival; the additional risk of MVR at the time of CABG; and the choice of valve repair and replacement.
Other patients may primarily present with symptoms of congestive heart failure and signs of significant mitral regurgitation. Preoperative catheterization subsequently may reveal significant CAD. These patients tend to have more compromised left ventricular function compared with the first group. The indication for surgery is congestive heart failure. In reality, most patients present in a clinical spectrum somewhere along the two clinical scenerios. In this section, however, the indications for surgery of each scenerio are discussed separately.
Ischemic Mitral Regurgitation and Coronary Artery Disease
The optimal management of concomitant IMR at the time of CABG remains to be determined. Most surgeons agree that concomitant severe (4+) mitral regurgitation should be addressed at the time of CABG and that revascularization alone will not ameliorate severe mitral regurgitation. Similarly, most surgeons agree that trace to mild (1+) mitral regurgitation should be left alone because it will not adversly affect long-term symptomatology or prognosis. Yet, the optimal management of mild to moderate (2+) mitral regurgitation remains controversial.
Multiple factors must be addressed in deciding on the management of IMR at the time of CABG. First, IMR has been demonstrated to have a negative impact on long-term survival. Numerous studies have documented the negative impact of IMR on long-term survival after an acute MI.75–78 Similarly, in patients undergoing PCI for acute coronary syndromes, IMR has been demonstrated to have a negative impact on survival. Three-year survival in this group ranges from 46 to 76%, based on the severity of mitral regurgitation.79 Moreover, in the setting of CABG, myocardial revascularization alone in patients with chronic IMR has a higher hospital mortality than in patients without IMR.74 Mild (1+) IMR increases operative mortality from 3.4 to 4.5%72–74,80 and moderate (2+) IMR raises operative mortality from 6 to 11%.72–74,81 Two-year survival for revascularization alone in patients with 1+ and 2+ mitral regurgitation is 78 and 88%, respectively.82 Five-year survival rates for patients with mild mitral regurgitation range between 70 and 80%.3,72,83,84 For moderate mitral regurgitation, 5-year survival ranges between 60 and 70%.85,86 Many surgeons argue that these data suggest that concomitant IMR should be addressed during CABG to affect survival.
Those who advocate the conservative approach of revascularization alone, without treatment of the IMR, argue that revascularization will improve regional wall motion abnormalities, papillary muscle function, and potentially correct IMR.71,87,88 Moreover, there are data that suggest that survival and long-term functional status are not improved with concomitant MVR,89,90 thus bringing into question the benefit of the higher operative risk associated with simultaneous MVR. Surgeons who advocate mitral valve repair/replacement for moderate IMR during CABG cite studies that suggest revascularization does not correct IMR,91 and that uncorrected IMR may result in late symptoms and decreased long-term survival.76,82 Furthermore, mitral valve repair with annuloplasty ring is nearly always technically feasible, obviating the need for valve replacement and the associated anticoagulation of mechanical valves or subsequent valve replacement required of bioprosthetic valves. Operative risk with combined CABG/MV repair today is much better than the older series, with operative mortality in the 3 to 4% range.92–94 Kron and collegues have concluded that the addition of MVR does not increase the operative risk of CABG in ischemic cardiomyopathy.95 Considering the increased complexity associated with redo sternotomy with patent grafts for MVR for recurrent or progressive IMR, some feel aggressive management of IMR is justified on initial sternotomy and revascularization, given simplicity of repair when compared with subsequent redo-operation.
The impact of isolated CABG without MVR on the progression of moderate IMR has been examined. Previous studies suggest that CABG alone improves IMR grade and functional status.71,87,88 However, in contrast recent reports have suggested that CABG alone is not the optimal therapy for moderate IMR.91,96,97 A study from the Cleveland Clinic Foundation reported that moderate (2+) IMR does not resolve with CABG alone, and furthermore, is associated with reduced survival.98 Between 1980 to 2000, 467 patients with moderate IMR underwent CABG alone. Longitudinal analysis of 267 follow-up echocardiograms from 156 patients demonstrated that early postoperative improvements in IMR did not persist. IMR of moderate or greater severity was present in 60% of patients by postoperative week 6. Interestingly, postoperative IMR severity was not predicted by cardiac function or extent of CAD. Furthermore, early survival of patients with unrepaired moderate IMR was reduced compared with similar patients without IMR. Based on their results, the authors concluded that a mitral valve procedure is warranted for such patients at the time of CABG. A retrospective registry review of the progression of mitral regurgitation following isolated coronary artery bypass surgery, examined 438 patients with preoperative mitral regurgitation of less than or equal to 2+ requiring CABG.99 New 3+ to 4+ mitral regurgitation developed in 10% of patients with no prior mitral regurgitation, 12% with pre-CABG 1+ mitral regurgitation, and 25% with pre-CABG 2+ mitral regurgitation, thereby implying significant progression of IMR without treatment. Preoperative left ventricular dysfunction and large left ventricular size were identified as predictors of mitral regurgitation progression post-CABG. Although no correlation was identified between the extent of CAD or the number of grafts performed, incomplete revascularization in the PDA territory was identified as a significant predictor of mitral regurgitation progression, suggesting a role for incomplete revascularization and left ventricular remodeling in the progression of IMR.
To directly address the impact of MVR for moderate IMR, studies have compared the results of CABG alone versus CABG with concomitant MVR in the setting of IMR.100–105 The results do suggest that post-operative mitral regurgitation is improved with CABG with concomitant MVR. However, whether there exists an improvement in long-term survival remains unclear. Several studies suggest no improvement in survival following CABG with concomitant MVR.102,104–107 In contrast, two studies100,101 comparing CABG versus CABG/MVR in patients with CAD and IMR have found a significant improvement in survival. Both studies involved patients with 2+ to 3+ IMR with depressed LVEF. A recent study103 examining 111 patients with moderate to severe IMR and multivessel CAD undergoing either medical therapy, isolated CABG, or CABG/MVR found a greater than 50% reduction in mortality in the CABG and CABG/MVR groups when compared with medical therapy. However, only CABG/MVR independently predicted survival. Moreover, a history of CHF was an independent predictor of cardiac death. Five-year survival has been found to be influenced by the severity of left ventricular dysfunction at the time of operation, age, and comorbid disease.57 Collectively, these studies suggested that concomitant MVR with CABG may improve late survival, especially in the setting of LV dysfunction and CHF, but the definitive answer remains elusive. To clarify the appropriate management of moderate IMR during CABG, a multi-institutional randomized, prospective NIH NHLBI–sponsored clinical trial has begun. In this study, patients with moderate IMR at the time of CABG are randomized to either repair of the MR or isolated CABG alone.
The final factor to address when dealing with IMR is the decision to repair or replace the valve. Gillinov demonstrated the short-term efficacy of mitral valve repair in 97% of patients undergoing elective surgery for 3+ to 4+ chronic IMR.60 Ring annuloplasty was employed in 98% of these repairs and was the sole surgical maneuver on the valve in greater than 80%. There was a distinct inclination in this study to undersize the annuloplasty ring; 79% of the rings were 30 mm or less. Iatrogenic mitral stenosis was not seen even in patients who received 26-mm annuloplasty devices. However, there was no benefit to repair versus replacement in high-risk patients, including older age, higher NYHA functional class, significant wall motion abnormalities, and renal dysfunction. In contrast, Calafiore and colleagues have found no difference in either short- or long-term mortality between MV repair and replacement for patients with 2+ to 4+ IMR.92 Similarly, a recent study found no difference in either operative or 6-year mortality following MV repair as compared with replacement. A prospective, randomized multi-institutional NIH NHLBI–sponsored study is presently underway to definitively determine if there is a difference between MV repair and replacement in the setting of severe ischemic mitral regurgitation.
In summary, patients with CAD with concomitant moderate to severe (3+ to 4+) IMR should undergo CABG/MVR. In patients with moderate (2+) IMR, recent studies may suggest that CABG/MVR may be justified, given the lower rate of morbidity and mortality in the modern surgical era, but this remains to be determined. Left ventricular dysfunction and increased left ventricular dimension along with incomplete revascularization may predict a higher rate of progression of IMR, suggesting CABG/MVR should be performed in this particular group of patients. Patients with symptoms of CHF appear to benefit most from CABG/MVR. Mild (1+) IMR should be left alone, unless: (1) preoperative signs and symptoms are suggestive of periods of more severe mitral regurgitation; and (2) intraoperative TEE demonstrate anatomical findings requiring MVR (ie, significant annular dilatation, leaflet tenting). Most patients with IMR benefit from mitral valve repair. In the most complex, high-risk settings, replacement may be preferable, with no demonstrable difference in survival between repair and replacement.
Ischemic Mitral Regurgitation and Congestive Heart Failure
The ischemic cardiomyopathy patient subset is a complex population to manage. In the current era of aggressive medical management and revascularization, there has been a dramatic decrease in the incidence of acute myocardial infarction and death. However, there is a significant increase in the number of patients suffering from ischemic cardiomyopathy. This disease is often coincident with ischemic mitral regurgitation. As described in previous sections, postinfarction LV remodeling is characterized by progressive LV dilatation with a change to a spherical shape with resultant functional MR secondary to annular dilatation, papillary muscle displacement, and chordal tethering. With functional MR there is increased ventricular volume overload (preload), myocardial wall tension, and LV workload; all of which further contribute to a deleterious cycle of progressive heart failure.
In the past, operative repair of mitral regurgitation was associated with a prohibitively high perioperative mortality, making surgeons cautious about MVR and MVR/CABG in the setting of left ventricular dysfunction. The traditional teaching incorporated the "popoff" valve hypothesis, which believed that the mitral valve functioned as a low-pressure runoff to decompress the failing ventricle. It was believed that surgical correction of mitral regurgitation in the failing ventricle would further contribute to ventricular overload and further contribute to myocardial failure.
However, this hypothesis has been challenged and disproved by Bolling who believes that there is an "annular solution for the ventricular problem."108–111 It is believed that correction of mitral regurgitation alleviates excessive ventricular workload, improves ventricular geometry, and enhances ventricular function; a process referred to as reverse remodeling. The Stanford group has reported in an ovine model of ischemic mitral regurgitation, that reduction of the annulus by an undersized ring reduces the radius of curvature of the left ventricle at the base, equiatorial, and apical levels.112 This decrease in the radius of curvature supports the concept that a small ring can restore a more elliptical shape. Reduction of left ventricular dimensions to a more elliptical shape, reverse remodeling, after annuloplasty have also been demonstrated by clinical studies.113–115
The previously published high operative mortality associated with mitral valve replacement was most likely the result of loss of the subvalvular apparatus, thus indicating the importance of maintaining the integrity of the annular and subvalvular continuity during mitral valve surgery. More recent series have indeed demonstrated much lower perioperative morbidity and mortality (1.6 to 5%), demonstrating safety in carefully selected patients.60,61,116,117
Data from most recently published series have demonstrated improvements in left ventricular ejection fraction, mitral regurgitation, clinical symptoms (NYHA classification), and left ventricular reverse remodeling with surgical intervention.89,100,107–109,118–121 However, questions remain regarding improvements in long-term survival and its overall effect on the natural history of IMR. Some have recently raised questions, despite previous data, about the potential improvement in long-term survival in patients with IMR in the setting of depressed LVEF. In perhaps the largest experience of MVR in patients with severe left ventricular dysfunction, Wu and coworkers examined the impact of mitral valve annuloplasty on mortality risk in patients with mitral regurgitation and left ventricular dysfunction.122 Reviewing their echocardiographic database (n = 682), the authors identified 419 patients who met the criteria for surgical intervention. One hundred twenty-six patients underwent MVR, whereas 263 continued conservative medical therapy. It should be noted that the etiology of mitral regurgitation included both ischemic and nonischemic subtypes. Their analysis demonstrated no improvements in long-term survival in the MVR group versus medical therapy. Talkwalkar and coworkers89 reported a series of 338 patients who underwent MVR. Compared with the control group, patients with depressed left ventricular ejection fraction were more likely to be associated with IMR, concomitant CABG, and NYHA class IV symptoms. Five-year survival was 54%, and when associated with prior CABG, prior myocardial infarction, or concomitant CABG, it was 0, 37, and 63%, respectively.
In agreement with previous reports, these recent studies confirmed the poor prognosis associated with IMR in the presence of LV dysfunction. In Wu's series,122 5-year survival in the setting of IMR and left ventricular dysfunction is less than 50%, regardless of surgical versus medical therapy. A randomized study comparing surgical versus medical therapy for IMR is needed to clarify the benefit of mitral valve surgery in this population of patients.
Patients who present primarily with symptoms of congestive heart failure and IMR provide surgeons with a fairly straightforward indication for intervention. Although it remains unclear if there is a survival benefit with repair, it is clear that there are improvements in symptoms, exercise tolerance, and ventricular remodeling. Given the low operative mortality associated with modern surgical techniques it is reasonable to correct severe IMR in the setting of heart failure. The operative indications for this group of patients are similar to mitral regurgitation of nonischemic origin. Symptoms of CHF and depressed left ventricular function are indications for surgical mitral repair or replacement. The current ACC/AHA valve disease guidelines include a cautious recommendation for consideration of MV surgery in patients with advanced heart failure, but only if MV repair or replacement with chordal sparing are options. Most surgeons agree that concomitant CABG is indicated in the presence of significant CAD.
An undersized annuloplasty ring is effective in the acute correction or reduction of IMR in the majority of patients. However, recurrent mitral regurgitation after annuloplasty has been reported to be present in 30 to 40% of patients. Although these studies are criticized for not addressing the appropriate annuloplasty ring selection and adequately downsizing the ring, both of which have been demonstrated to be vital in adequate long-term correction of IMR. These studies have often used flexible bands or partial rings, which fail to address the dilatation that occurs along the anterior annulus and fail to adequately fix the septal-lateral dimension of the valve.
The Cleveland Clinic reported its series of 585 patients who underwent annuloplasty alone for IMR between 1985 and 2002 in which 678 postoperative echocardiograms were evaulated in 422 patients. The majority of recurrent IMR occurred within the first 6 months. Overall, 28% of patients 6 months after surgery demonstrated 3+ to 4+ mitral regurgitation.123 These results stand in contrast to the findings by Spoor and Bolling, in which minimal recurrent MR was seen up to 4 years after mitral repair with rigid annuloplasty using a ring that was downsized by two sizes.121 It has been found that there is an almost fourfold increase in recurrence rate of IMR with the use of a flexible ring as compared with a nonflexible ring in patients with a preoperative ejection fraction less than 30%.124
Evidence of left ventricular reverse remodeling after annuloplasty ring has been demonstrated in small clinical studies, with excellent results and freedom from recurrent IMR for up to 2 years.113–115 Braun and coworkers reported a series of 87 patients with IMR and depressed left ventricular function (mean LVEF 32%) who underwent undersized mitral annuloplasty and coronary revascularization. Mitral regurgitation grade decreased significantly from a mean of 3.1 to 0.6 at 18 months. Both left ventricular end-systolic and end-diastolic dimensions decreased significantly when compared with preoperative echocardiograms. Interestingly, the left ventricular end-diastolic dimension was found to be the best predictor of reverse remodeling. Left ventricular end-diastolic dimension exceeding 65 mm was associated with a lower probability of reverse remodeling, suggesting a relationship between recurrent IMR and ventricular geometric dimension. Further studies would be useful to identify preoperative echocardiographic parameters predictive of durable mitral valve repair.
Operative results for mitral valve surgery with or without concomitant CABG have improved, with recent series reporting operative mortality of 3-4%.60,61,116,117 However, 5-year survival remains very low, with reported values as low as 30 to 40%, depending on the series (Fig. 29-5).3,72,73,83,125 More recently, Gillinov and coworkers reported 5-year survival in the propensity-matched best risk group of 58% for valve repair and 36% for replacement. This group had significantly fewer NYHA class IV patients and less severe mitral regurgitation preoperatively. In the propensity-matched poorer risk groups (more severe CHF, mitral regurgitation, and emergency surgery) and for the group as a whole, there was no difference between repair and replacement and 5-year survival was uniformly less than 50%.60
Survival after mitral valve surgery for all patients with ischemic mitral regurgitation. Each symbol represents a death according to Kaplan-Meier estimator. Vertical bars enclose asymmetric 68% confidence limits. Solid lines represent parametric survival estimates; these are enclosed between dashed 68% confidence limits. Numbers in parentheses are numbers of patients traced beyond that point. (Reproduced with permission from Gillinov AM, Wierup PN, Blackstone EH, et al: Is repair preferable to replacement for ischemic mitral regurgitation? J Thorac Cardiovasc Surg 2001; 122:1125-1141.)
There has been no randomized study demonstrating a survival benefit with mitral valve repair/replacement in IMR. In a restrospective analysis of cardiomyopathy including both ischemic and nonischemic etiology, Wu and coworkers reported in their series 5-year survival of less than 50%, regardless of surgical versus medical therapy in patients with mitral regurgitation and left ventricular dysfunction.122 Other series have also demonstrated no survival benefit with mitral valve surgery in patients with IMR.104–106 The similarity of results between surgical and medical therapy points out a need for better understanding of the pathophysiology of IMR and left ventricular remodeling. A randomized study examining the clinical outcome and survival benefit of mitral valve surgery for IMR is warranted.