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.

Table 10-2 Grading of Aortic Stenosis Based on Transvalvular Pressure Gradient and Valve Area

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.

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