Disclosure
Background: Heart valves permit forward flow of blood through the cardiac chambers when open and prevent backward leakage when closed. Mitral regurgitation is characterized by abnormal backflow of blood through the mitral valve during the systolic period of the cardiac cycle. The left ventricle (LV) must pump additional volume to compensate for the amount regurgitated. As mitral regurgitation becomes severe, the continued hemodynamic burden can lead to ventricular dysfunction, heart failure, and sudden death. Mitral regurgitation may be acute or chronic. Common causes of severe acute mitral regurgitation include ruptured chordae tendineae, ischemic papillary muscle dysfunction or rupture, and infective endocarditis. Chronic severe mitral regurgitation is commonly due to myxomatous degeneration of the valve, rheumatic heart disease, or mitral annular calcification. Echocardiography has emerged as the diagnostic imaging modality of choice that can provide vivid images of the LV and the mitral valve, and it may provide clues to the mitral-valve abnormalities responsible for the regurgitation. The Doppler echocardiographic technique is excellent for determining the severity of mitral regurgitation. Acute mitral regurgitation often requires prompt surgical correction. However, symptomatic patients with chronic mitral regurgitation may be initially treated with digitalis, afterload reduction, and diuretics. After the LV function begins to deteriorate, clinical and echocardiographic parameters can be used to determine the timing for surgical reconstruction or replacement of the mitral valve. Pathophysiology: The pathophysiology of mitral regurgitation can be divided into 3 phases: acute, subacute compensated, and chronic. Acute phase When mitral regurgitation is acute, the left atrium (LA) and the LV has not had an opportunity to gradually enlarge and compensate for the added volume overload. As mitral regurgitation becomes severe, the sudden backflow of blood into the LA wastes a part of the LV stroke volume as backward flow that should have gone forward. This added regurgitant volume creates volume overload on the LV, which begins to enlarge by stretching the myocardial sarcomeres. The use of the Frank-Starling mechanism is thus maximized, increasing the end-diastolic volume (EDV). However, the end-systolic volume (ESV) decreases because the regurgitation unloads the LV in systole by dumping blood into the relatively low-pressure chamber, the LA. Although the increased EDV and decreased ESV increase the total stroke volume, the forward cardiac output remains subnormal because more of the ejected blood is regurgitated into the LA than before. Therefore, LA pressure rises, and the patient develops heart failure with diminished cardiac output and pulmonary venous congestion, even in the presence of apparently normal LV function. Most patients with severe acute mitral regurgitation require emergency surgical intervention. Subacute compensated phase IF patients are adequately supported through the acute stage, they may then enter the subacute, somewhat compensated, phase. In this phase, the cardiac chambers have an opportunity to develop gradual compensation in the form of eccentric LV hypertrophy (LVH) and increased EDV. These changes, together with normal contractile function, allow for the ejection of a sufficiently large total stroke volume that makes the forward stroke volume return toward normal despite the fraction being regurgitated. The LA enlarges to accommodate the regurgitant volume and can maintain a lowered filling pressure. In this phase, the patient may be relatively symptom free. Chronic phase Volume overload of the left-sided cardiac chambers accompany chronic mitral regurgitation. The volume overload begets enlargement of both the LV and the LA. Although patients may tolerate severe chronic mitral regurgitation for many years, it eventually causes LV dysfunction because, after mitral regurgitation is established, it tends to hemodynamically worsen over time. After the ejection performance of the LV is impaired and it begins to dilate, ESV increases. This change, in turn, augments LV residual volume at end systole and increases EDV and, subsequently, end-diastolic pressure (EDP). The symptoms of pulmonary congestion then begin to appear. Acute and chronic rise in aortic blood pressure may also worsen the hemodynamic severity of mitral regurgitation by increasing the afterload, causing pulmonary edema. Additional LV dilatation may worsen the amount of regurgitation by causing further enlargement of the mitral annulus and malalignment of the mitral leaflets and support structures. In some cases, contractile dysfunction is reversible with timely mitral valve repair or mitral valve replacement (MVR). Frequency:
Mortality/Morbidity: Most cases of chronic mitral regurgitation follow a benign course, and patients remain symptom free for many years. Symptoms develop late, especially in the United States, in the fourth to sixth decades, and generally include dyspnea on exertion and palpitations.
Race: No particular racial predilection appears to be present. Sex: The progression to severe mitral regurgitation varies with sex. In the case of MVP, this progression is twice as likely in men as in women. Age:
Anatomy: The mitral valve apparatus comprises the mitral annulus, the anterior and posterior cusps, the subvalvular supporting structures (eg, the chordae tendineae), and the 2 papillary muscles. Abnormalities of any of these structures may lead to mitral regurgitation. Causes Rheumatic disease remains the most common cause of chronic mitral regurgitation in much of the developing world. However, in the United States, the most frequent cause of mitral regurgitation is MVP, which is responsible for approximately two thirds of all cases. MVP is due to the myxomatous degeneration of the fibrous skeleton of the valve leaflets. Ischemic heart disease, leading to papillary muscle dysfunction or infarction, is the next most common cause and occurs in approximately one fourth of patients. Annular calcification, endocarditis, collagen vascular disease, and rheumatic heart disease are other causes. In recent years, the weight-loss agents dexfenfluramine, fenfluramine, and possibly phentermine, have been implicated in causing valvular damage. Cause of acute mitral regurgitation include the following:
Cause of chronic mitral regurgitation include the following:
Clinical Details: Most patients with chronic mitral regurgitation have a benign clinical course. SymptomsSlowly progressive shortness of breath on exertion is usually the main symptom. Patients who develop a massive LA dilatation may have fatigue, which indicates a low-output state. Palpitations are reported mostly with the onset of atrial fibrillation. Angina is uncommon in mitral regurgitation and may indicate concomitant ischemic heart disease. Hemoptysis is rare. Potential causes of mitral regurgitation should be sought by interviewing the patient for a history of a heart murmur or abnormal results during cardiac examination, rheumatic heart disease, endocarditis, myocardial infarction, or use of weight-reducing drugs. Physical examinationInspection In acute mitral regurgitation, a large V wave may produce rapid equilibration of LA and LV pressure, reducing the driving gradient and shortening the murmur. Palpation Due to LV enlargement, the apical impulse is usually displaced laterally and caudally into the sixth left intercostal space. A late systolic thrust (precordial lift) may be palpable. This is caused by massive systolic enlargement of the LA in severe mitral regurgitation. The arterial pulse has a brisk upstroke but small amplitude. Auscultation First heart sound (S1) is usually muffled, whereas second heart sound (S2) is usually physiologically split into aortic (A2) and pulmonary (P2) components. In severe mitral regurgitation, a mid-diastolic third heart sound (S3) may be audible. This does not necessarily indicate heart failure; rather, it may reflect rapid filling of the LV by a large volume of blood stored in the LA during systole. The characteristic murmur of mitral regurgitation is a holosystolic, blowing, high-pitched apical murmur that often radiates toward the axilla. The murmur starts immediately after a soft S1 and continues beyond A2 (aortic component of S2). The intensity of the murmur may represent the severity of the mitral regurgitation, but this relationship is weak. Unlike aortic stenosis, the murmur intensity usually does not vary with the R-R interval. Therefore, its intensity is constant even in the presence of atrial fibrillation. Pulmonary hypertension may develop in the late stages and produce a right ventricular (RV) lift, increased P2, and, if RV dysfunction has developed, signs of right-sided heart failure. MVP occurs when one or both of the mitral valve leaflets prolapses into the LA superior to the mitral valve annular plane during systole. In MVP, the regurgitant murmur is late systolic and crescendo toward A2. A situation that produces a small LV (eg, Valsalva maneuver) enhances the murmur. In this setting, reduced ventricular volume causes relative lengthening of the chordae tendineae and subsequent worsening of MVP. Nitrate use can mimic these findings. Handgrip can be used to enhance the murmur as well. It increases afterload, increases the V wave of the LA, and intensifies the hemodynamic severity of the murmur. Preferred Examination: Electrocardiography The electrocardiogram (ECG) may exhibit an LA abnormality, LVH, and, in some patients, atrial fibrillation. ECG evidence of LV enlargement occurs in about one third of patients with severe mitral regurgitation. Approximately 15% of patients have ECG evidence of RV hypertrophy. Chest radiography Although the heart may not be enlarged in acute mitral regurgitation, severe pulmonary edema is frequently present as a result of left-sided cardiac failure. In chronic mitral regurgitation, the LA and the LV border appears enlarged, and it may be massive because of volume overload and increased pressure. When the LA is enlarged, it may extend toward the right side, and it may be observed as a double shadow along the right atrial border. Coexistent pulmonary arterial hypertension or tricuspid regurgitation may cause dilation of the right atrium and ventricle, as well as enlargement of the pulmonary arteries. Echocardiography Echocardiography is the preferred examination. It demonstrates the extent of LA and LV enlargement, as well as the presence and severity of mitral regurgitation. Two-dimensional (2D) echocardiography or transesophageal echocardiography (TEE) with Doppler echocardiography and color flow Doppler imaging enables detailed assessment of the structure and function of the mitral valve. Echocardiography resulted in overestimations of the prevalence of MVP in the past. Early studies suggested a prevalence of as high as 21% in healthy young women. Many persons who were thought to have an MVP in early studies simply had normal bowing of the mitral valve. Magnetic resonance imaging MRI can demonstrate the abnormality of the valve apparatus, and it may be useful in evaluating the amount of regurgitant flow with velocity encoding (VENC) and with model-independent measurements of stroke volumes of RV and LV. Cardiac catheterization Cardiac catheterization is often needed. This procedure should include coronary arteriography in patients older than 40 years or in those with symptoms suggestive of coronary disease. The main indications for catheterization include (1) evaluating a discrepancy between echocardiographic findings and the clinical presentation, (2) detecting and assessing the severity of any other associated valvular lesions, and (3) determining the presence and extent of coronary artery disease. Limitations of Techniques: The limitations are minimal. Color flow Doppler echocardiography of the valve helps in determining the severity of regurgitation, but because this technique measures flow velocity rather than actual flow, and it is subject to error in interpretation. The Doppler technique is good for excluding mitral regurgitation and for differentiating between mild and severe degrees of the condition. However, color flow Doppler examination may not be sufficient for more exact quantification of mitral regurgitation or for determining if the lesion is severe enough to cause LV dysfunction.
Mitral valve prolapse
Findings: Chest radiography is useful in evaluating mitral regurgitation in several ways, but it mostly reveals nonspecific findings. Cardiomegaly The chest radiograph usually shows an enlarged cardiac silhouette. The heart is increased in size secondary to enlargement of both the LA and the LV. The absence of cardiomegaly indicates that the mitral regurgitation is either mild or acute. The enlarged atrial appendage can be seen along the middle portion of the left cardiac border. Also, a double shadow may be present on the right cardiac border, indicating an increase in the size of the LA. In patients with combined mitral stenosis and mitral regurgitation, overall cardiac enlargement and particularly LA dilatation are prominent findings. Relatively mild cardiomegaly and clinically significant changes in the lung fields suggest predominant mitral stenosis. In comparison, predominant mitral regurgitation is most likely when the heart is greatly enlarged and when the changes in the lungs are relatively inconspicuous. Calcification Calcification of the mitral annulus, an important cause of mitral regurgitation in the elderly, is most prominent in the posterior third of the cardiac silhouette. The lesion is best visualized on chest radiographs in the lateral or right anterior oblique projections, on which it appears as a dense, coarse, C-shaped opacity. Pulmonary edema Pulmonary interstitial edema with Kerley B lines is usually seen in patients with progressive LV failure and chronic mitral regurgitation. In acute mitral regurgitation, the chest radiograph reveals pulmonary edema, moderate or no enlargement of the LA, and little if any cardiac enlargement. Degree of Confidence: Chest radiographic findings are nonspecific. False Positives/Negatives: False findings are rare. |
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Findings: CT can show the cardiac silhouette and chamber sizes with clarity. However, because of the widespread use of echocardiography, CT is rarely performed in the evaluation of mitral regurgitation. Degree of Confidence: The degree of confidence is moderate. False Positives/Negatives: False findings are rare.
Findings: Accurate measurement of the degree of mitral regurgitation is critical. Doppler echocardiography provides an estimate of the area and depth of the regurgitant jet, but the finding is only semiquantitative. A direct quantitative, noninvasive measurement of the mitral regurgitant volume can be precisely determined by using MRI. Spin-echo MRI Spin-echo (SE) images show structural consequences of mitral regurgitation, such as enlarged LV and LA. Cine gradient-echo MRI Cine gradient-echo (GRE) images can be used to assess the severity of mitral regurgitation by calculating the regurgitant fraction. The procedure involves mapping the area of the signal void starting from the mitral valve and extending into the LA. The signal void of mitral regurgitation is best seen on the 4-chamber and the coronal oblique views. Another way to calculate regurgitant fraction involves estimation of the ventricular volumes. This method is usable only if mitral valve is the sole regurgitant valve. VENC MRI VENC MRI is another method by which the severity of mitral regurgitation can be determined. In this method, the diastolic inflow across the mitral annulus is compared with systolic outflow across the ascending aorta. LV inflow is increased in mitral regurgitation. As an alternative, regurgitant volume can also be determined by measuring flows in the ascending aorta and pulmonary artery, instead. In fact, the best way to quantify the mitral regurgitant volume is to combine the ventricular volume calculations obtained by using cine GRE sequences with the estimated forward flow in aorta obtained with VENC MRI. Degree of Confidence: The degree of confidence is high. MRI is the most accurate technique for measuring regurgitant flow, and it provides measurements that are well correlated with those of quantitative Doppler imaging. MRI is also the most accurate noninvasive technique that enables the measurement of ventricular EDV, ESV, and mass. False Positives/Negatives: Errors can occur during application of cine GRE imaging to measure the area of the mitral annulus and the mitral flow velocity because of the constant motion of the atrioventricular valves during each cardiac cycle.
Findings: Two-dimensional echocardiography In patients with severe mitral regurgitation, 2D echocardiography shows enlargement of the LA and LV. The cause of mitral regurgitation can often be determined on the transthoracic echocardiogram and may include rupture of the chordae tendineae, MVP, a flail leaflet, vegetations, and LV dilatation. Calcification of the mitral annulus as a band of dense echoes can be seen between the mitral valve and the posterior wall of the heart. Three-dimensional echocardiography Three-dimensional (3D) transthoracic echocardiography (TTE) and 3D color Doppler imaging may be helpful in elucidating the mechanism of mitral regurgitation. The imaging of the mitral valve is excellent and offers clues to the mitral valve abnormalities responsible for the regurgitation. Color flow Doppler imaging Color flow Doppler imaging of the valve helps in semiquantitatively determining the severity of regurgitation. This technique measures flow velocity rather than actual flow; therefore, it is sometimes is subject to error. The severity of mitral regurgitation is directly proportional to the size of the regurgitant jet within the left atrium. The size of the jet is typically indexed to the size of the left atrium. Jets that are peripheral impinge on a wall, rather than the center, causing predictable problems with assessment of severity. Owing to the Coanda effect, a regurgitant jet impinging on a wall results in a color flow area smaller than an equivalent central regurgitant volume. A jet impinging on a wall underestimates the regurgitant volume by approximately 40%. In cases of moderate and severe mitral regurgitation, flow in the pulmonary veins may reverse direction in systole. A variation on this finding is attenuation of normal forward flow in the pulmonary vein during ventricular systole. Most recently, 3-dimensional reconstruction of mitral regurgitation jets has been shown to be feasible. The incremental value of this method has not yet been shown. Doppler echocardiography Doppler echocardiography in mitral regurgitation characteristically reveals a high-velocity jet in the LA during systole. The severity of the regurgitation is a function of the distance from the valve at which the jet can be detected and the size of the LA. In estimating the severity of mitral regurgitation, both color flow Doppler and pulsed Doppler results are used. Color Doppler imaging involves measurement of the area of the mitral jet. If the area of the jet is greater than 8 cm2, the mitral regurgitation is considered severe. Findings that indicate that mitral regurgitation is severe include reversal of flow in the pulmonary veins during systole and a high peak mitral inflow velocity. Transesophageal echocardiography TEE is better than TTE in imaging the regurgitant mitral valve. Angiographic assessments of mitral regurgitation are well correlated with the color flow mapping obtained by using TEE rather than TTE. Mitral valve prolapse Echocardiography is useful in diagnosing MVP, in determining the severity of associated mitral regurgitation, and in showing the pathologic anatomy of the mitral valve. An extreme form of MVP involves myxomatous degeneration of the valves with leaflet thickening (>3-5 mm), marked symmetrical bowing of the valve behind the annular plane, and/or highly asymmetrical buckling of 1 or both leaflets into the LA associated with mitral regurgitation. Because of the eccentric leaflet buckling, the mitral regurgitation jet can be eccentric rather than central. Acute mitral regurgitation after acute myocardial infarction Two complications of myocardial infarction that produce confusing clinical signs are mitral insufficiency caused by rupture of an infarcted papillary muscle and a ventricular septal defect that occurs after infarction and necrosis of the septum. These are easily identified by noting the intracardiac flow patterns seen on cine GRE images. Degree of Confidence: The degree of confidence is high. False Positives/Negatives: False findings are rare. Color flow Doppler examination may not be sufficient for exactly quantifying mitral regurgitation or for determining if the severity of the lesion is sufficient to cause eventual LV dysfunction.
Findings: Radionuclide angiography may be useful in assessing mitral regurgitation.
Degree of Confidence: Radionuclide angiography is good for assessing LV function. False Positives/Negatives: False findings are unusual.
Findings: LV angiography may be performed to evaluate mitral regurgitation. The immediate appearance of contrast material in the LA after its injection into the LV indicates mitral regurgitation. The regurgitant volume can be determined from the difference between the total LV stroke volume, which is estimated by using angiocardiography, and the simultaneous measurement of the effective forward stroke volume, which is determined by using the Fick method. In patients with severe mitral regurgitation, the regurgitant volume may approach the effective forward stroke volume; in rare instances, it may even exceed this volume. Qualitative but clinically useful estimates of the severity of mitral regurgitation may be made by means of cineangiographic observation of the degree of opacification of the LA and the pulmonary veins after the injection of contrast material into the LV. The cause of the regurgitation (eg, MVP) and a flail leaflet can often be distinguished by using angiography. Mitral regurgitation secondary to rheumatic heart disease is angiographically characterized by a central regurgitant jet and by thickened leaflets that have reduced motion. In regurgitation due to other causes, particularly dilatation or calcification of the mitral annulus or ruptured chordae tendineae and papillary muscles, the systolic jet may be eccentric, and the valves consist of thin filaments that display excessive motion. Degree of Confidence: The degree of confidence is excellent. False Positives/Negatives: False findings are rare.
Intervention: In almost every instance, the definitive treatment for severe mitral regurgitation is mechanical restoration of the valve function. Newer surgical procedures, such as mitral valve repair (vs MVR) are being performed with increasing frequency. In moderately severe mitral regurgitation, ascertaining when valve replacement or repair should be performed is important. Several clinical and echocardiographic indices are used to decide the optimal timing of such surgery. Medical therapyIn patients with poor LV function and dilatation of the mitral annulus, mitral regurgitation can intensify the severity of LV failure. In such patients, the risk of surgery is high and the benefits not obvious, and a trial of intensive medical therapy, including offload reduction to reduce LV volume and the diameter of the annulus, may be worthwhile. General acute mitral regurgitation Afterload reduction is the key in the management of both the acute and chronic forms of mitral regurgitation. This intervention reduces the volume of blood regurgitating into the LA. Decreasing LV volume also narrows the regurgitant valvular orifice. Mean LA pressure and the elevated V wave both decline. In patients with acute mitral regurgitation due to papillary muscle rupture during an acute myocardial infarction, afterload reduction with intravenous nitroprusside may be lifesaving. It may help stabilize the patient's condition and permit coronary arteriography and surgery. In patients with acute mitral regurgitation and hypotension, an inotropic agent such as dobutamine may be infused along with the nitroprusside. Intra-aortic balloon counterpulsation may be necessary to stabilize the patient's condition before surgery. Severe acute mitral regurgitation In severe acute mitral regurgitation, the patient is usually symptomatic, with heart failure or even shock. The goal of medical therapy is to increase forward cardiac output while reducing regurgitant volume. Arterial vasodilators reduce systemic resistance to flow and thereby preferentially increase aortic outflow. They simultaneously decrease the amount of mitral regurgitation and LA hypertension. If hypotension is already present, vasodilators, such as nitroprusside, lower blood pressure further, and they cannot be used. In such cases, intra-aortic balloon counterpulsation is preferred if the aortic valve is competent. Counterpulsation increases forward cardiac output by lowering the ventricular afterload while augmenting the systemic diastolic pressure. In patients with developing severe mitral regurgitation, the therapy is the same as that for other causes of mitral regurgitation. Chronic asymptomatic mitral regurgitation Vasodilator therapy is clearly effective in the treatment of acute mitral regurgitation and chronic aortic regurgitation. However, perhaps because afterload is usually not increased in chronic asymptomatic mitral regurgitation, vasodilators have had little effect in reducing the LV volume or in improving the normal exercise tolerance of patients with mitral regurgitation. Chronic symptomatic mitral regurgitation In patients with symptomatic mitral regurgitation, angiotensin-converting enzyme (ACE) inhibitors can reduce LV volumes and improve symptoms. However, mitral valve surgery is usually preferred to medical therapy in most symptomatic patients with mitral regurgitation. Also, in chronic mitral regurgitation, when surgery is contraindicated, afterload reduction with an ACE inhibitor or hydralazine may be effective. Diuretics and digoxin are also indicated in patients with severe mitral regurgitation and heart failure, particularly in patients with atrial fibrillation who should also receive anticoagulation. When atrial fibrillation is present, chronic anticoagulation should achieve the same international normalized ratio (INR) goal as for mitral stenosis. Mitral valve prolapse Because most patients with MVP are asymptomatic, therapy is unnecessary. However, patients with MVP and its characteristic murmur should be given the standard prophylaxis for endocarditis. Some patients who present with chest pain and palpitations may benefit from beta-blockers or anxiolytics. Prophylaxis Patients with mitral regurgitation require appropriate prophylaxis to prevent bacterial endocarditis. In MVP, prophylaxis is indicated if mitral leaflets are thickened or if coexistent mitral regurgitation is noted. Surgical therapyThe timing of mitral valve surgery is based on the risks of the operation and of use of a prosthesis weighed against the risk of irreversible LV dysfunction if surgery is delayed. For most other valve diseases, surgical therapy usually involves the placement of a prosthetic valve. However, in mitral regurgitation, the native valve can often be repaired, obviating use of a prosthesis with its attendant risks. Indications Surgical treatment should be offered to patients who remain symptomatic despite optimal medical management, including those with only mild symptoms, but with progressively deteriorating LV function, as documented by noninvasive studies. Without surgical treatment, the prognosis for patients with mitral regurgitation and heart failure is poor. Acute mitral regurgitation Emergency surgical treatment may be required for patients with acute LV failure caused by trauma to the mitral valve or infective endocarditis or for patients with myocardial infarction and rupture of a papillary muscle. If mitral regurgitation secondary to acute myocardial infarction can be stabilized with medical treatment, deferring the operation until 4-6 weeks after the infarction is preferred. Vasodilator treatment may be useful during this period. However, medical management should not be prolonged if multisystem (renal and/or pulmonary) failure develops. Intra-aortic balloon counterpulsation may be required to preoperatively stabilize the patient's condition. In case of fungal endocarditis that responds poorly to medical management, the current practice is to recommend valve replacement in these patients before the onset of heart failure or embolization. Changing threshold The threshold for surgical treatment of mitral regurgitation has been lowered in recent years. Reasons include reductions in surgical mortality rates, improvements in both mitral valve reconstructive procedures, use of procedures involving prosthetic valves, and recognition that the long-term results are poor in many patients whose mitral regurgitation is corrected late after impaired LV function, atrial fibrillation, or pulmonary hypertension develops. Chronic mitral regurgitation In asymptomatic patients with a New York Heart Association (NYHA) class I condition, mitral valve reconstruction should be considered only if they have LV dysfunction (ejection fraction of 60% and/or LV end-systolic diameter of 45 mm). Patients with class I disease and a normal LV function should be followed up clinically and echocardiographically every 6-12 months. In rare patients, surgery may be considered if they have atrial fibrillation or pulmonary hypertension. At times, careful history taking and exercise testing often reveal that these patients are not truly asymptomatic. A complex and frequent problem involves the indications for mitral valve surgery in patients undergoing coronary bypass surgery with moderate mitral regurgitation. Intraoperative TEE is invaluable in assessing the severity of regurgitation, the reparability of the valve, and the integrity of the repair after cardiopulmonary bypass is discontinued. Patients with severe mitral regurgitation who are asymptomatic, who perform well on exercise testing, and who have excellent ventricular function (ejection fraction >70%, end-systolic diameter <40 mm, and ESV <40 mL/m2) can be followed up with echocardiography every 6-12 months. However, surgery may be considered, even in asymptomatic patients, if they are younger than 70 years, if they are likely to be candidates for mitral valve repair, and if ventricular function (as reflected by the end-systolic diameter and ejection fraction) progressively deteriorates. Most patients with symptoms of dyspnea, orthopnea, or fatigue should undergo surgery because they already have lifestyle limitations due to their disease. Symptoms worsen their prognosis despite their relatively well-preserved LV function. Surgical risks The surgical mortality risk depends on the patient's clinical and hemodynamic status (particularly the function of the LV); on the presence of comorbid conditions, such as renal, hepatic, or pulmonary disease; and on the skill and experience of the surgical team. Valve replacement versus repair The decision to replace or to reconstruct the valve is of critical importance. Detailed echocardiographic examination should be performed to determine if mitral valve repair, rather than MVR, is possible. Replacement involves the risk of surgery; the risk of thromboembolism and anticoagulation (in patients receiving a mechanical prosthesis); the risk of late valve deterioration in patients receiving bioprostheses; and the risk of late mortality, especially in patients with associated coronary artery disease who require coronary artery bypass grafting. Surgical mortality does not substantially depend on the tissue or mechanical valve prosthesis selected. The reconstructive procedure consists of annuloplasty, often with the use of a rigid (Carpentier) or a flexible prosthetic (Duran) ring or with reconstruction of the valve. Prolapsed valves causing severe mitral regurgitation are usually treated with resection of the prolapsing segment and plication of the annulus. Replacing, reimplanting, elongating, or shortening of the chordae tendineae; splitting the papillary muscles; and repairing the subvalvular apparatus have been successful in selected patients with pure or predominant mitral regurgitation. Reconstruction of the mitral valve is most often successful in the following patients: (1) children and adolescents with pliable valves; (2) adults with mitral regurgitation secondary to MVP; (3) patients with annular dilatation; (4) those with papillary muscle involvement secondary to ischemia, dysfunction, or rupture; and (5) patients with chordal rupture and perforation of a mitral leaflet due to infective endocarditis. The procedure is least likely to be successful in older patients with the rigid, calcified, deformed valves of rheumatic heart disease or in those with severe subvalvular chordal thickening and major loss of leaflet substance. Many of the last group of patients require MVR, which is also usually the procedure of choice for patients with badly scarred mitral valves who previously underwent MVR. Young patients in developing countries who have severe rheumatic mitral regurgitation in the absence of active carditis may undergo successful repair. Ischemic mitral regurgitation after acute myocardial infarction may be managed by reattaching the papillary muscle to adjacent myocardium or by valve replacement. Ischemic mitral regurgitation secondary to severe annular dilatation may be treated with direct or ring annuloplasty. Outcome The cause of mitral regurgitation is predictive of the outcome after surgery. In patients with mitral regurgitation due to ischemic heart disease, the 5-year survival rate is 40%, whereas the rate in patients with rheumatic mitral regurgitation is 75%. Obstruction of the LV outflow tract due to systolic anterior motion of the mitral valve occurs in 5-10% of patients after mitral valve repair. The causes are not clear; but they may include excess valvular tissue with severe leaflet redundancy and/or an interventricular septum bulging into a small LV. Surgical mortality rates Mortality rates of 3-9% are encountered for patients with pure or predominant mitral regurgitation (NYHA class II or III) who undergo elective isolated MVR. The Society of Thoracic Surgeons National Database Committee reported overall surgical mortality rates of 6.4% in 13,936 patients undergoing isolated MVR and 3% in 4167 patients undergoing isolated mitral valve repair. The combination of MVR and repair and coronary artery bypass grafting has a mortality rate of 8%. The mortality rate is about 25% in older patients with severe LV dysfunction, especially when mitral regurgitations is secondary to myocardial ischemia, when pulmonary or renal function is impaired, or when an emergency operation is performed. Medical/Legal Pitfalls:
Special Concerns:
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