Mechanical Valves

Most mechanical valves that are currently implanted are of the bileaflet type (e.g., St. Jude Medical, CarboMedics; Fig, 10-1A). Bileaflet valves have a low profile, provide relatively unobstructed flow, and have minimal areas of stagnation on the downstream side of the disks. Bileaflet valves have a characteristic appearance on echocardiography (Fig. 10-2).

Figure 10.1 Prosthetic valves in common usage. A, Bileaflet mechanical valve (St. Jude Medical); B, tilting-disk valve (Medtronic-Hall); C, ball-and-cage valve (Starr-Edwards aortic valve); D, stented tissue valve (Carpentier-Edwards Perimount); E, stentless tissue valve (Medtronic Freestyle).

(Reproduced, with permission, from Sidebotham D, Merry A, Legget M: Practical Perioperative Transoesophageal Echocardiography. Fig. 12.1, p. 186. Philadelphia, Butterworth Heinemann, 2003.)

Figure 10.2 TEE appearances of a bileaflet mechanical valve in the mitral position. In this systolic frame, the disks (arrows) are shown in the closed position. LA, left atrium; LV, left ventricle; TEE, transesophageal echocardiography.

(Reproduced, with permission, from Sidebotham D, Merry A, Legget M: Practical Perioperative Transoesophageal Echocardiography. Fig. 12.2, p. 187. Philadelphia, Butterworth Heinemann, 2003.)

Tilting-disk valves (e.g., Medtronic-Hall; see Fig. 10-1B; Fig. 10-3) have a single pivoting circular disk. Compared to bileaflet valves, tilting-disk valves cause greater impedance to forward flow and a larger area of stagnation on the downstream surface of the disk. The Medtronic-Hall valve has a characteristic central regurgitant jet (see Fig. 10-3).

Figure 10.3 TEE appearances of a tilting disk valve (Medtronic-Hall valve) in the mitral position. A, The valve is in diastole. The central strut and the tilting disk are labeled. B, The valve is in systole, with a characteristic central jet of regurgitation (arrow).

(Reproduced, with permission, from Sidebotham D, Merry A, Legget M: Practical Perioperative Transoesophageal Echocardiography. Fig. 12.4, p. 189. Philadelphia, Butterworth Heinemann, 2003.) TEE, transesophageal echocardiography.

The “ball-in-cage” valve, typified by the Starr-Edwards valve (see Fig. 10-1 C), is the oldest type of mechanical valve. The efficacy of the Starr-Edwards valve is well established; hundreds of thousands of implantations have been performed over 40 years. However, the valve is bulky, results in moderate valvular obstruction, may cause hemolysis, and carries a slightly higher risk for thromboembolism than other valve types. All three types of valves may be used in the mitral or aortic positions.

Bioprosthetic Valves

Bioprosthetic valves may be stented or unstented. Stented valves are made from porcine aortic valves (e.g., Mosaic) or from bovine pericardial tissue (e.g., Carpentier-Edwards Perimount; see Fig. 10-1 D). The stents facilitate implantation and help maintain the three-dimensional structure of the valve. Stented bioprosthetic valves may be used in the aortic or mitral position.

Stentless bioprosthetic valves are made from porcine aortic roots (e.g., Medtronic Freestyle; see Fig. 10-1 E) or cryopreserved human cadaveric aortic roots (homografts). Compared to stented valves, stentless valves provide less obstruction to flow, a reduced risk for endocarditis, and increased durability, but their implantation is more technically demanding, and they can be used only in the aortic and pulmonary positions. Stentless valves may be inserted using a modified subcoronary method as for a standard aortic valve replacement. In addition, some stentless valves, such as the homograft and Freestyle, may be implanted as a freestanding aortic root, in which the aortic valve and sinuses of Valsalva are replaced by the graft, and the coronary arteries are reimplanted as buttons onto fenestrations in the bioprosthesis. An aortic root replacement may be preferred to a subcoronary stentless aortic valve insertion because it can be easier to perform and it provides a larger aortic diameter.

An alternative to a stentless aortic root replacement is the Ross procedure, in which the patient’s own pulmonary valve is transplanted into the aortic position (autograft), and a pulmonary homograft is placed in the pulmonary position. Usually a patient undergoing a Ross procedure (particularly if for aortic incompetence) also requires an aortic root annuloplasty to reduce the annular diameter to between 26 and 28 mm. The pulmonary autograft is durable and may grow with the patient.⁴ Thus, the Ross procedure is popular for use in younger patients. However, the operation is a long, technically demanding procedure, and it has a mortality rate about twice that of a standard valve replacement. In the long term, autograft dilatation and homograft stenosis can occur.⁵

For a patient with aortic valve disease and dilatation of the ascending aorta, a Bentall procedure, in which the aortic valve and ascending aorta are replaced with a valved conduit (a bioprosthetic or mechanical valve attached to a Dacron tube graft), is indicated. If the aortic annulus is of a normal size and the leaflets are normal, resuspension of the native valve within a Dacron tube graft may also be possible (the David procedure).

Pathophysiology

Aortic stenosis imposes a pressure load on the left ventricle that results in increased intraventricular pressure and systolic wall tension (Fig. 1-7). Over time, this pressure overload leads to concentric left ventricular hypertrophy, increased end-diastolic pressure and, not infrequently, clinically important diastolic dysfunction. Systolic function is usually preserved until late in the disease process.

Patients with aortic stenosis are at high risk for myocardial ischemia. Myocardial oxygen demands are increased due to the effects of increased pressure work, muscle mass, and wall tension, but coronary blood flow, particularly to the subendocardium, is reduced as a consequence of increased end-diastolic pressure. Also, more than 50% of patients with aortic stenosis have significant coronary artery disease.⁶ Patients with severe aortic stenosis have a relatively fixed stroke volume and may develop profound hypotension (and myocardial ischemia) in response to modest vasodilation or exercise.

Clinical Features and Investigations

Calcific aortic stenosis typically has a slowly progressive but occasionally unpredictable course. Symptoms appear late and are indicative of severe disease. The characteristic symptoms are angina, exertional syncope, and dyspnea. Examination findings include a small-volume, slow-rising pulse; reduced pulse pressure; sustained apical impulse; a soft first heart sound; a single or reverse split-second heart sound; a prominent fourth heart sound; and a long, late-peaking ejection systolic murmur. Clinical assessment of the severity of aortic stenosis is unreliable.

The ECG may demonstrate left ventricular hypertrophy and strain. Nonspecific ST segment changes occur in the majority of patients. Rarely, calcific aortic stenosis is associated with atrioventricular (AV) block. The chest radiograph is frequently normal, although calcification of the valve may be evident. Echocardiography is mandatory to confirm the diagnosis and to assess severity (Table 10-2). Also, it is essential to confirm that the stenosis is due to valvular obstruction and not subvalvular pathology. Significant valvular stenosis is unlikely in the absence of heavy calcification of the valve. Coronary angiography is required in patients over the age of 40 and in those with significant risk factors for coronary artery disease.

Assessment of the severity of aortic stenosis is difficult in patients with depressed left ventricular function. A low transvalvular pressure gradient may represent severe aortic stenosis with secondary low cardiac output or, alternatively, represent minor aortic valve stenosis in which cardiac output is low for some other reason (e.g., alcoholic or ischemic cardiomyopathy). Low-dose dobutamine-stress echocardiography is useful in this situation; an increase in the transvalvular pressure gradient and a failure to increase the measured valve area in response to dobutamine is suggestive of severe aortic stenosis as the cause of the low cardiac output.

Medical Treatment

Symptomatic aortic stenosis is a surgical condition, and medical therapy should not be used to delay surgery. β Blockers provide some relief from angina and may protect against tachyarrhythmias.

Acute Decompensation

Patients with aortic stenosis may present to the intensive care unit with myocardial ischemia, arrhythmias, or congestive cardiac failure. Initial treatment of myocardial ischemia includes oxygen, aspirin, analgesia and, in the absence of heart failure, β blockers. An intraaortic balloon pump (IABP) may be helpful to augment coronary perfusion pressure. In patients with acute coronary syndromes, urgent angiography and combined surgical revascularization and aortic valve replacement should be considered. Pulmonary edema should be treated with diuretics and respiratory support as appropriate. Tachyarrhythmias such as atrial fibrillation are poorly tolerated and must be treated promptly (see Chapter 21). Induction of general anesthesia (e.g., for cardioversion) can cause profound hypotension.

Despite the conventional wisdom that vasodilators are contraindicated in aortic stenosis, low-dose nitroprusside (in slow increments, up to 150 μg/min) has recently been shown to increase cardiac output in normotensive patients with congestive cardiac failure and severe aortic stenosis.⁷ The authors of this study argue that systemic vasoconstriction may contribute to congestive cardiac failure in patients with severe aortic stenosis. Although this study has received a lot of attention, it must be stressed that potent vasodilators can precipitate cardiovascular collapse in patients with severe aortic stenosis, and that this treatment is not routine.

Patients with shock are at very high risk for progressive cardiac decline or ischemia-induced malignant arrhythmias. Treatment includes fluids and inotropic support. However, β-adrenergic drugs such as epinephrine may provoke tachycardia and myocardial ischemia. An IABP may help to stabilize the patient prior to urgent aortic valve replacement. In the event of a cardiac arrest, external cardiac massage is likely to be ineffective; death is likely.

Surgical Treatment

Sudden death as a result of aortic stenosis is rare in asymptomatic patients. Thus, the presence of symptoms is the primary indication for surgery, irrespective of the aortic valve area or gradient. Recently, levels of B-type natriuretic peptide (BNP; see Chapter 19) have been shown to reflect the onset of symptoms in aortic stenosis. In two studies, patients with symptomatic aortic stenosis had median (± interquartile range) levels of N-BNP (the aminoterminal portion of BNP): 112 pmol/l (70 to 193) and 131 pmol/l (50 to 202) compared to 33 pmol/l (16 to 58) and 31 pmol/l (19 to 56) in asymptomatic patients.^8,9 Thus, levels of these hormones may prove to be a useful complement to symptom onset in determining the timing of surgery.

Aortic valve surgery may also be offered to asymptomatic patients who require other surgery, for example, patients with moderate aortic stenosis undergoing coronary artery bypass graft surgery or patients with severe aortic stenosis who require pulmonary resection for lung cancer. In contrast to mitral valve disease, the long-term outcome after surgery for decompensated aortic stenosis is reasonably good, and only very rarely are patients considered too sick for surgery.

Valve replacement is virtually always required in aortic stenosis because calcified, immobile valve leaflets cannot be repaired. Aortic valve surgery is usually performed through a midline sternotomy. Minimally invasive incisions involving an upper sternotomy and a J incision into the third or fourth intercostal space are also used. The technique of cardiopulmonary bypass (CPB) is similar to that described in Chapter 9. Myocardial protection may be difficult in the setting of severe left ventricular hypertrophy, particularly if there is concomitant aortic regurgitation (see later discussion). Damage to the His bundle may occur during placement of sutures and may cause complete heart block. After CPB, myocardial ischemia may arise as a consequence of (1) a coronary embolus involving aortic or valvular debris; (2) the incorrect seating of a prosthetic valve, causing coronary ostial obstruction; (3) distortion of a coronary artery during reimplantation when performing aortic root replacement. Heavy calcification of the valve or proximal aorta also predisposes to systemic emboli. Percutaneous balloon valvuloplasty of the aortic valve is associated with a very high procedural complication rate; it confers minimal long-term benefit and is rarely performed.¹⁰

Postoperative Issues

The operative mortality rate in isolated, first-time aortic valve replacement is 3% to 4%,^11,12 but it increases substantially if additional cardiac surgery is required and if left ventricular function is impaired.¹¹ Unlike other valve lesions, the hemodynamic state is immediately improved by valve replacement, even in the presence of preexisting left ventricular dysfunction.

Many patients undergoing aortic valve replacement have preserved left ventricular systolic function but impaired diastolic function. Thus, cardiac output and blood pressure are critically dependent on adequate preload and on the maintenance of sinus rhythm. Postoperative hypotension is a common manifestation of hypovolemia, despite normal atrial pressures. In the absence of preexisting left ventricular dysfunction, inotropic agents are rarely needed. An exception to this is cases in which there have been difficulties with myocardial protection that have resulted in myocardial stunning. Postoperative myocardial ischemia may arise for the reasons outlined earlier. If ischemia is suspected, and urgent echocardiography is consistent with coronary ostial pathology, then revision surgery is indicated. Atrial fibrillation is usually poorly tolerated and should be treated aggressively. Rapid pacing, particularly ventricular pacing, may cause hypotension. Damage to the His bundle or bundle branches at the time of surgery can cause temporary or permanent bundle branch block or complete heart block.

Occasionally, patients with marked left ventricular hypertrophy (particularly involving the basal anterior septum) develop dynamic left ventricular outflow tract (LVOT) obstruction and systolic anterior motion (SAM) of the anterior mitral valve leaflet after aortic valve replacement. Severe SAM can cause hypotension, low cardiac output, and mitral regurgitation. The treatment of this condition is described in Chapter 20.

Aortic valve surgery involves aortic suture lines that are exposed to systemic arterial pressure. Marked hypertension must be avoided in the early postoperative period. However, hypertensive patients may require a high blood pressure to maintain renal perfusion. Patients undergoing surgery for aortic stenosis are usually elderly and commonly have extensive aortic atherosclerosis, which increases their risk for neurologic injury.

Pathophysiology

Because the regurgitant volume is returned to the left ventricle during each diastolic period, aortic regurgitation imposes a volume load on the left ventricle, which results in progressive left ventricular dilatation and eccentric left ventricular hypertrophy. Left ventricular compliance is increased, allowing large ventricular volumes to be accommodated with minimal increase in end-diastolic pressure (see Fig. 1-7). As the left ventricular diameter increases, wall tension and hence afterload are increased. There is compensatory systemic vasodilation. Arterial end-diastolic pressure is low because of diastolic run off into the left ventricle. Thus, the aortic valve opens at a low pressure but peak systolic aortic pressure is increased due to the high stroke volume. Arterial pulse pressure is increased. There may be baroreceptor-mediated tachycardia.

Patients with severe aortic regurgitation are at risk of myocardial ischemia, even in the absence of coronary artery disease. Myocardial oxygen delivery is impaired because of reduced diastolic blood pressure and reduced diastolic time (secondary to tachycardia), but oxygen demand is increased because of greater myocardial work and tachycardia. With chronic severe aortic regurgitation, the left ventricle progressively fails, the ejection fraction falls, the end-diastolic pressure rises, and congestive cardiac failure develops.

Left ventricular dilatation may be profound and can cause functional mitral regurgitation. Severe aortic regurgitation can impair the diastolic opening of the mitral valve, causing functional mitral stenosis. Acute severe aortic regurgitation results in acute volume overload of the left ventricle and a sharp increase in end-diastolic pressure. Pulmonary edema and shock develop rapidly.

Clinical Features and Investigations

Symptoms occur late in chronic severe aortic regurgitation, by which time important left ventricular dysfunction may have developed. Symptoms, when they do occur, are of congestive cardiac failure: exertional dyspnea and orthopnea. Physical findings include a collapsing pulse, a wide pulse pressure, and diastolic hypotension. The apex beat is displaced laterally and is hyperdynamic. The aortic component of the second heart sound may be soft and there is often a third heart sound. The murmur of aortic regurgitation occurs in early diastole, is high in pitch, and is best heard at the left sternal edge with the patient sitting up and holding his or her breath at expiration.

The ECG may demonstrate tachycardia, left axis deviation, and left ventricular hypertrophy with strain. On the chest radiograph, an increased cardiothoracic ratio is usually evident, and there may be signs of pulmonary venous hypertension and interstitial edema. If the cause of the aortic regurgitation is an aortic aneurysm, it too may be evident on the chest radiograph. Echocardiography is essential for determining the cause and severity of the aortic regurgitation and to assess left ventricular dimensions and function. Coronary angiography is indicated in patients older than 40 and in patients at risk for coronary artery disease.

Medical Treatment

Afterload reduction helps to maintain cardiac output, reduce left ventricular wall stress, and reduce the regurgitant fraction. Drugs such as angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, nitrates, hydralazine, and α-receptor blockers provide symptomatic relief and help prevent ventricular dilatation. Pulmonary congestion is treated with diuretics.

Acute Decompensation

Acute decompensation may occur in the settings of aortic dissection, aortic valve endocarditis, or acute prosthetic valve dysfunction. Hemodynamic instability may result from causes other than the valve lesion; for example, from tamponade (aortic dissection) or sepsis (endocarditis).

In the absence of hypotension, cardiac output is best maintained with inodilating drugs such as milrinone or dobutamine. Inoconstricting drugs such as norepinephrine increase the regurgitant fraction but may be necessary in the presence of septic shock. In patients with aortic dissection, acute control of blood pressure with β blockers and vasodilators is appropriate, even in the presence of severe aortic regurgitation. An IABP is contraindicated in moderate or severe aortic regurgitation. Acute severe aortic regurgitation is an unstable and unpredictable condition that is best managed surgically; cardiac arrest and sudden death can occur.

Surgical Treatment

To prevent irreversible ventricular damage, surgery for chronic severe aortic regurgitation is indicated in patients who are symptomatic or who have evidence of ventricular dysfunction or dilatation (ejection fraction <50% or end-systolic dimension >5.5 cm).¹³ Severely depressed left ventricular dysfunction (e.g., ejection fraction <20%) imposes a very high perioperative risk and may be considered a contraindication to surgery.

The appropriate operation is determined by the cause of aortic regurgitation. For patients with aortic dissection or ascending aortic aneurysm, as long as the aortic annulus is of a normal size and the leaflets are intact, valve resuspension within a Dacron tube graft may be possible. If the valve cannot be resuspended, aortic root replacement is necessary. If aortic regurgitation is due to a torn or prolapsed cusp, valve repair may be possible. However, in the presence of valve destruction due to endocarditis, rheumatic disease, or calcification, valve replacement is required.

Aortic regurgitation creates specific difficulties for the conduct of CPB. Following institution of CPB, loss of cardiac ejection (due to ventricular fibrillation, heart block, or asystole) before placement of the aortic cross-clamp can cause gross left ventricular distension and myocardial damage. Thus, a left ventricular vent is placed shortly after commencement of CPB, usually via the left superior pulmonary vein through the mitral valve. If loss of ejection occurs before placement of the vent, manual cardiac decompression is needed. Once the aortic cross-clamp is in place, aortic regurgitation makes the usual delivery method of antegrade cardioplegia impracticable because cardioplegia administered into the aortic root will pass primarily to the left ventricle (causing distension) rather than down the coronary arteries (causing arrest in diastole). Thus, the initial dose of cardioplegia is usually administered retrograde into the coronary sinus. The aortic root may then be opened and cardioplegia delivered selectively into the coronary ostia. Other intraoperative problems are as described for aortic stenosis.

Postoperative Problems

Left ventricular systolic dysfunction is common postoperatively and is treated with optimization of preload, maintenance of a high normal heart rate (e.g., with pacing at 90/min), and inotropic support (see Chapter 21). Echocardiography and a pulmonary artery catheter are helpful to guide therapy. Severe pulmonary hypertension and right ventricular dysfunction are uncommon. The issues of systemic hypertension and damage to the His bundle are the same as those following surgery for aortic stenosis. Following complex aortic root replacement procedures, myocardial stunning, coagulopathy, bleeding, and a marked systemic inflammatory response syndrome are not uncommon.

Surgery for aortic regurgitation commonly involves younger patients who have been chronically treated with ACE inhibitors; they usually tolerate a lower blood pressure than patients with aortic stenosis, who are usually elderly and have hypertension.

Pathophysiology

As with aortic regurgitation, chronic mitral regurgitation results in left ventricular volume overload with ventricular dilatation and eccentric hypertrophy. Unlike aortic regurgitation, left ventricular afterload is reduced with mitral regurgitation due to systolic ejection into the low-impedance left atrium. (Although this is partially offset by left ventricular dilatation, which increases wall stress and therefore afterload). The combination of high preload and low afterload preserves ejection fraction despite potentially important systolic dysfunction. Over time, chronic severe mitral regurgitation causes left atrial dilatation, pulmonary hypertension, and right ventricular dysfunction. Atrial fibrillation is common once the left atrial diameter exceeds 4.5 cm.¹⁵ Atrial fibrillation is generally better tolerated in the context of mitral regurgitation than in cases of aortic or mitral stenosis.

The regurgitant volume is dependent on the relative resistances across the mitral and aortic valves. Thus, mitral regurgitation is made worse by increased systemic vascular resistance, aortic stenosis, and left ventricular dilatation, the last because it increases the area of the regurgitant orifice. Progressive ventricular dilatation exacerbates mitral regurgitation, resulting in a self-reinforcing cycle of worsening mitral regurgitation and declining ventricular function.

Acute mitral regurgitation results in sudden volume overloading of the left ventricle. Left ventricular dilatation has not had time to develop, which causes abrupt rises in left ventricular end-diastolic and left atrial pressures. Pulmonary edema, pulmonary hypertension, acute right ventricular dysfunction, and shock can develop rapidly.

Clinical Features and Investigations

Patients with chronic mitral regurgitation present with the gradual onset of congestive cardiac failure. Symptoms include dyspnea and orthopnea. Physical findings include tachycardia, a displaced apical impulse, a quiet first heart sound, a widely split second heart sound, and a third heart sound. The murmur of mitral regurgitation is pansystolic, high pitched, varies little with respiration, is of greatest intensity at the apex, and radiates to the axilla. The intensity of the murmur bears little relationship to the severity of the valve lesion. Signs of left ventricular failure or pulmonary hypertension may also be present.

The ECG may show tachycardia and either atrial fibrillation or evidence of left atrial enlargement with P-mitrale. The chest radiograph typically demonstrates an increased cardiothoracic ratio. There may be radiographic evidence of pulmonary venous hypertension and interstitial edema. Echocardiography, often with both transthoracic and transesophageal imaging, is required to determine the severity and mechanism of the mitral regurgitation, to assess left and right ventricular function, and to determine the presence of pulmonary hypertension. Because mitral regurgitation flatters ventricular function, it is usual to assess systolic function as being one grade lower than it appears on the echocardiogram. Coronary angiography is indicated in patients above 40 years of age or with risk factors for coronary artery disease.

Medical Treatment

Chronic medical treatment is similar to that for aortic regurgitation, namely, afterload reduction with ACE inhibitors and diuretics to correct pulmonary congestion. Atrial fibrillation may require pharmacologic rate control and anticoagulation with warfarin.

Acute Decompensation

Acute severe mitral regurgitation typically develops as a consequence of the dehiscence of a mitral prosthesis or valve repair, a torn chorda, endocarditis, or myocardial infarction. Patients present with shock and acute pulmonary edema. The definitive treatment is surgery, but it is usually appropriate to try to stabilize the patient prior to surgery. The principles of treatment are similar to those for acute severe aortic regurgitation: an IABP and inodilating drugs to promote forward flow and diuretics and ventilatory support for pulmonary edema. Treatment of the underlying condition (e.g., myocardial ischemia, endocarditis) may also be appropriate.

Indications for Surgery

Surgery is indicated for patients with severe mitral regurgitation who are symptomatic or who are asymptomatic and have evidence of mild to moderate left ventricular dysfunction (ejection fraction 30-60%, left ventricular end-systolic dimension >4.0 cm).¹³ Thus, even mild ventricular dysfunction is an indication for surgery because the low afterload state masks significant ventricular impairment. Surgery may also be offered to symptomatic patients with severe (ejection fraction <30%) left ventricular dysfunction, particularly if valve repair is thought to be feasible.

The risks involved in mitral valve surgery are particularly high in patients who have severely impaired left ventricular function (ejection fraction <30%) or who are elderly (>75 years). Successful surgery has been described in these patient groups, but in many circumstances the risks related to surgery outweigh the benefits.

Surgical Treatment

The mortality rates seen in isolated mitral valve replacement are higher than those in aortic valve replacement; they are about 6%.¹¹ Mortality rates increase to above 10% when multiple valves are replaced or when left ventricular function is severely impaired; it is approximately 15% when mitral valve replacement is combined with coronary revascularization.¹¹ Mitral valve repair is associated with lower mortality rates than is valve replacement,^16,17 mainly because of improved ventricular function and reduced risk for thromboembolism. Certain valve pathologies, notably myxomatous degeneration that is limited to the posterior leaflet and ischemic mitral regurgitation, have a high chance of successful repair. Valve replacement is usually required for rheumatic heart disease, endocarditis, or myxomatous degeneration with extensive anterior or bileaflet involvement.

If valve replacement is required, postoperative ventricular function is better maintained if the subvalvular apparatus (chordae and papillary muscles) is preserved at the time of surgery.¹⁸ Bioprosthetic valves deteriorate relatively rapidly in the mitral position, and their use tends to be limited to individuals who are unsuitable for warfarin, such as those who wish to become pregnant. Patients with pulmonary hypertension or rheumatic heart disease may have coexisting tricuspid valve disease, necessitating concomitant repair (see later material). Patients with atrial fibrillation may be suitable for a maze type-procedure (see later material).

Mitral valve surgery is usually performed through a midline sternotomy. Minimally invasive approaches involving a right parasternal or right anterolateral thoracotomy incision may also be used. Access to the mitral valve is usually via the left atrium. In certain circumstances, notably when the left atrium is very small or when tricuspid valve surgery is also required, access to the mitral valve may be obtained via the right atrium and interatrial septum. For mitral surgery, most surgeons use selective cannulation of the vena cavae to improve surgical access. Selective cannulation is mandatory for a right atrial approach.

A number of complications can arise during mitral valve surgery. Damage to the AV node, which lies adjacent to the mitral annulus, can cause complete heart block. A misplaced suture may catch either the noncoronary cusp of the aortic valve, causing aortic regurgitation, or the circumflex coronary artery, causing ischemia. During mitral valve replacement with sparing of the subvalvular apparatus, it is possible for the chordae to become entangled in the leaflets of a mechanical prosthesis, causing incomplete opening or closing of the valve. The most feared complication of mitral valve replacement is cardiac rupture. Cardiac rupture usually occurs along the posterior AV groove and is more likely when the mitral annulus is heavily calcified. This complication is very rare, but it is associated with catastrophic bleeding and a high mortality rate.

Postoperative Problems

Postoperatively, left ventricular systolic dysfunction is common due to the combined effects of preexisting dysfunction and acute increase in left ventricular afterload secondary to the newly competent mitral valve. Even with chordal-sparing procedures, mitral valve replacement reduces the hemodynamic efficiency of left ventricular contraction. Additionally, mitral valve surgery is often combined with surgery on other valves or with a maze procedure, resulting in long CPB times and increasing the likelihood of postoperative myocardial stunning. A period of hemodynamic support by means of pacing, inotropic agents, and an IABP is often required.

New or recurrent atrial fibrillation is common after mitral valve surgery. Large V waves suggestive of mitral regurgitation are occasionally seen on the pulmonary artery wedge trace despite a normally functioning prosthesis, particularly when the left atrium is small. Right ventricular dysfunction may occur as a consequence of preexisting pulmonary hypertension and the acute increases in pulmonary vascular resistance associated with CPB. The implications and treatment of pulmonary hypertension are outlined in Chapter 24.

After mitral valve replacement, unexpected hemodynamic instability or pulmonary edema may indicate a problem with the prosthesis. A disk that is stuck in a partially open or closed position can cause severe valvular regurgitation. The diagnosis is readily apparent by means of transesophageal echocardiographic (TEE) examination. The disk may spontaneously start functioning normally within a few hours of surgery. Failing this, or if the patient is hemodynamically unstable, urgent surgical revision is indicated. In patients with mitral annular calcification, difficulty placing annular sutures may result in paravalvular regurgitation. Again, the diagnosis is confirmed with TEE.

After mitral valve repair, problems involving dehiscence of the repair, mitral stenosis, or SAM (see also Aortic Stenosis, in earlier material) can develop. Dehiscence of the repair causes severe mitral regurgitation. SAM involves prolapse of the anterior mitral leaflet into the LVOT during systole, causing outflow tract obstruction and mitral regurgitation. The echocardiographic appearances are characteristic (see Fig. 7-12). Risk factors for SAM in this situation include a small nondilated left ventricle, the use of an undersized annuloplasty ring, and excessive posterior leaflet tissue causing anterior displacement (i.e., toward the LVOT) of the mitral coaptation line. The treatment of this condition is described in Chapter 20. Mitral stenosis is uncommon after mitral valve repair, but it can occur. The diagnosis is usually confirmed by the intraoperative TEE examination. For the reasons outlined, it is essential that any patient who becomes hemodynamically unstable or develops pulmonary edema following mitral valve surgery should undergo urgent TEE examination.

Pathophysiology

Mitral stenosis causes obstruction of left ventricular filling. The left atrium becomes pressure- and volume-loaded, and the left ventricle is underfilled. Increased left atrial pressure results in pulmonary congestion and left atrial dilatation. Once the left atrial dimension exceeds 4.5 cm, atrial fibrillation is likely. Pulmonary venous hypertension initially results in passive pulmonary arterial hypertension, but over time, changes within the pulmonary arterioles lead to reactive arterial pulmonary hypertension (see Chapter 24). Severe pulmonary arterial hypertension can cause pressure and volume overload of the right ventricle, which results in functional tricuspid regurgitation and, eventually, right ventricular failure. Shunts from the pulmonary vein to the bronchial veins may develop, and they can rupture, causing hemoptysis. The combination of mitral stenosis and atrial fibrillation is a potent stimulus for the formation of left atrial thrombus, which can embolize systemically.

Despite being distal to the obstruction, left ventricular systolic function is commonly impaired. Chronic underfilling of the left ventricle can lead to its becoming atrophied, resulting in wall thinning and reduced systolic function. Heavy calcification of the mitral apparatus (annulus, chordae, and papillary muscles) can restrict longitudinal shortening of the left ventricle, impairing systolic function.

Clinical Features and Investigations

The symptoms of mitral stenosis are those of pulmonary congestion (dyspnea, orthopnea, coughing, and wheezing) and hemoptysis. Physical findings include mitral facies, small volume, irregularly irregular pulse, a loud first heart sound, and an opening snap best heard at the apex. The murmur of mitral stenosis is a low-pitched diastolic rumble, best heard at the apex with the bell of the stethoscope. Placing the patient in the left lateral position and having the patient hold his or her breath in expiration augments the murmur. Signs of pulmonary hypertension and right ventricular failure may be present.

The ECG may show atrial fibrillation or, if the patient is in sinus rhythm, P-mitrale. Right ventricular hypertrophy may be present and is a marker of severity. The chest radiograph may demonstrate characteristic features of left atrial enlargement (see Fig. 6-3). In severe mitral stenosis, there may be evidence of enlargement of the pulmonary artery, the right ventricle, and the right atrium. Radiographic signs of pulmonary venous hypertension and pulmonary edema may be present.

Echocardiography is essential for determining the severity of the mitral stenosis (Table 10-5). Additionally, the presence of other valve pathology (particularly mitral and tricuspid regurgitation), left atrial thrombus, right ventricular dysfunction, and pulmonary hypertension can be evaluated. TEE may be required to rule out left atrial thrombus. In the presence of overt right ventricular failure, a right heart catheter study should be considered to assess pulmonary artery pressures and resistance. Coronary angiography should be performed in patients above 40 years of age and those with risk factors for coronary artery disease.

Table 10-5 Severity of Mitral Stenosis Based on Valve Area and Pressure Gradients

Medical Treatment

There is no effective medical treatment for severe mitral stenosis. Symptomatic relief of pulmonary congestion may be achieved by means of diuretics and pharmacologic control of atrial fibrillation. In the absence of contraindications, patients with atrial fibrillation should undergo anticoagulation with warfarin.

Acute Decompensation

Acute decompensation is usually associated with a precipitating event such as pregnancy, sepsis, or the onset of atrial fibrillation. Patients present with acute pulmonary edema. The initial treatment includes diuretics, respiratory support, and control of atrial fibrillation. Hypotension should be treated with inotropic agents and an IABP. Norepinephrine may increase left atrial pressure and potent β-adrenergic agents may worsen tachycardia. Acute right ventricular failure may respond to inhaled pulmonary vasodilators such as nitric oxide (see Chapter 24). Urgent intervention, with either percutaneous valvuloplasty or surgery, is indicated.

Percutaneous Valvuloplasty and Surgery

Patients with moderate to severe mitral stenosis who are symptomatic or who have evidence of left atrial or pulmonary hypertension should be considered for either percutaneous valvuloplasty or surgery.

Most cases of rheumatic mitral stenosis can be treated successfully with percutaneous mitral balloon valvuloplasty. In this procedure, a balloon catheter is passed via the femoral vein through the interatrial septum and inflated across the mitral valve. Contraindications to the procedure include moderate or severe mitral regurgitation, left atrial thrombus, and heavy valvular calcification. The procedure carries low risk and the outcome is generally good. The requirement for subsequent intervention—usually surgery—is approximately 10% at 3 years and 40% at 7 years.^10,19 Percutaneous valvuloplasty is particularly useful in patients who become symptomatic during pregnancy.

Surgery is indicated for patients with severe mitral stenosis who are unsuitable for percutaneous valvuloplasty or who require additional cardiac procedures. Surgical options are (1) closed mitral valvotomy (now rarely performed); (2) open valve repair with commissurotomy, papillary muscle splitting, leaflet shaving, and chord débridement; or (3) valve replacement. For patients with heavy leaflet calcification, extensive subvalvular involvement, and mitral regurgitation that is more than mild, valve replacement is required. Tricuspid valve repair and a maze procedure (see subsequent material) are often performed at the same time as mitral valve replacement. Intraoperative issues are as described for mitral regurgitation.

Postoperative Problems

Patients with uncomplicated mitral stenosis who are treated with percutaneous valvuloplasty do not require routine postprocedure care in the ICU. Following surgery for mitral stenosis, the hemodynamic state is immediately improved; left atrial and pulmonary artery pressures are reduced, and right ventricular function is improved. However, patients with severe pulmonary hypertension are at risk for right ventricular dysfunction. Systolic left ventricular dysfunction can also arise for the reasons outlined earlier. New or recurrent atrial fibrillation is common.

Pathophysiology and Clinical Features

Structural tricuspid regurgitation causes right ventricular volume overload. This is initially well tolerated; forward stroke volume is maintained by compensatory right ventricular dilatation. However, over time, progressive right ventricular dilatation exacerbates tricuspid regurgitation and leads to right ventricular systolic failure. Pulmonary arterial hypertension is not a feature of structural tricuspid regurgitation. In contrast, functional tricuspid regurgitation commonly arises as a consequence of pulmonary arterial hypertension. In this situation, patients develop right ventricular volume and pressure overload (see Chapter 20).

Clinical signs of tricuspid regurgitation include evidence of raised systemic venous pressure (raised central venous or jugular venous pressure, pulsatile liver) or frank right ventricular failure (fatigue, ascites, systemic edema, weight gain). There may be features suggestive of pulmonary hypertension or signs of the underlying condition (e.g., emphysema, mitral stenosis, tricuspid valve endocarditis).

Echocardiography is important for assessing the severity and mechanism of the tricuspid valve pathology. Right ventricular function and pulmonary arterial pressure can also be evaluated. Normal pulmonary artery pressures are suggestive of structural tricuspid valve disease or primary right ventricular dysfunction. High pulmonary artery pressures are suggestive of left heart or pulmonary disease. Marked right ventricular volume overload can cause compression of the left ventricle.

Surgical Treatment and Postoperative Care

For patients with moderate or severe functional tricuspid regurgitation secondary to mitral valve disease, tricuspid valve repair with an annuloplasty ring is usually undertaken at the time of mitral valve surgery. Mild functional tricuspid regurgitation is likely to improve after correction of mitral valve disease and does not require specific intervention.

Patients with severe tricuspid regurgitation due to structural tricuspid valve disease may be considered for isolated tricuspid surgery. Ideally, valve repair is performed, but often valve replacement is the only option. The major postoperative problem is right ventricular failure. Gross dilatation of the right ventricle also causes impaired filling of the left ventricle. Patients develop high systemic venous pressure and low cardiac output. Damage to the atrioventricular node at the time of surgery can cause complete heart block. The treatment of right ventricular failure is described in Chapter 20. The mortality for tricuspid valve replacement is high: about 20%.^20–22

Percutaneous balloon valvuloplasty is a potential option for symptomatic tricuspid stenosis. Tricuspid regurgitation often coexists with stenosis; valvotomy may worsen the regurgitation and has a high failure rate.