Valvular Heart Disease

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Chapter 10 Valvular Heart Disease

Severe valvular heart disease imposes a volume or pressure load on the heart that if untreated can result in ventricular impairment and heart failure. Surgical correction prevents further ventricular dysfunction and improves the rate of survival. However, surgery is associated with appreciable morbidity and mortality rates. Therefore, appropriate timing of surgery is essential; excessive delay can lead to irreversible ventricular dysfunction, but if intervention is too early, the risks involved in surgery may outweigh the benefits.

Most of the problems encountered following heart valve surgery are the same as those following any cardiac surgery: bleeding, renal impairment, atrial fibrillation, and so forth. However, certain postoperative problems are characteristic of specific valve lesions. For instance, left ventricular systolic dysfunction is common following mitral valve replacement for mitral regurgitation, whereas left ventricular diastolic dysfunction is common following aortic valve replacement for aortic stenosis. Pulmonary hypertension often complicates mitral valve surgery but is uncommon following aortic valve surgery. Knowledge of these characteristics aids postoperative decision making in the intensive care unit.

In this chapter the causes, pathophysiology, treatments, and postoperative problems of valvular heart disease are reviewed. Many of the issues relating to comorbid conditions outlined in Chapter 9 apply equally to patients undergoing valve surgery.


Since the 1960s valve replacement surgery has formed the mainstay of surgical treatment for severe valvular heart disease, and for many lesions this remains the case today. However, valve replacement is associated with inherent problems, including (1) the need for anticoagulation and the risk of thromboembolic or bleeding complications; (2) the risk of endocarditis; (3) prosthetic valve degeneration; (4) the persisting ventricular dysfunction that is associated with surgery for certain valve lesions, notably mitral regurgitation. For these reasons, valve repair operations have become increasingly popular, particularly repair of the mitral and tricuspid valves but recently also of the aortic valve. However, valve repairs are technically demanding, have an appreciable incidence of early failure, and are not possible for all valve lesions.

Valves and Procedures

Prosthetic valves may be made of mechanical or bioprosthetic material. Mechanical valves are durable but require lifelong anticoagulation with warfarin. Bioprosthetic valves, at least in the aortic position, do not usually require lifelong warfarin, but are less durable and have a primary failure rate of about 30% at 10 to 15 years.13 Bioprosthetic valves are less durable in the mitral position than in the aortic position. In general, mechanical valves are preferred in younger patients, and bioprosthetic valves are preferred in older patients and in patients who may become pregnant. Smaller valves tend to be used in the aortic position (commonly 21 to 25 mm) and larger valves tend to be used in the mitral position (commonly 27 to 31 mm). Mechanical prostheses in each of the four heart valve positions on the frontal and lateral chest radiographs are shown in Fig. 6-6.

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 10.2 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).


Aortic Stenosis

The causes of aortic valve stenosis are listed in Table 10-1; of these, the most common is calcific degeneration. Calcific degeneration can affect a normal trileaflet valve (Fig. 10-4), a congenitally bicuspid valve, or a bioprosthetic valve. Calcific degeneration of a trileaflet valve typically occurs in patients more than 70 years of age, whereas degeneration of a bileaflet valve typically presents in young adulthood or middle age. Stenosis may also occur at the subvalvular level, either as dynamic left ventricular outflow tract (LVOT) obstruction or secondary to a subaortic membrane.

Table 10-1 Causes of Aortic Valve Stenosis

Causes Lesion
Calcific degeneration Predominantly stenosis
Degeneration of a bicuspid valve Stenosis, regurgitation, or mixed
Degeneration of a bioprosthetic valve Stenosis, regurgitation, or mixed
Rheumatic aortic valve disease Stenosis, regurgitation, or mixed
Thrombus or pannus formation on a mechanical valve Stenosis

Figure 10.4 TEE appearances of calcific aortic stenosis. The aortic valve is shown in short axis. The leaflets are heavily calcified, the valve orifice is small, and there are far field shadows (S).

(Reproduced, with permission, from Sidebotham D, Merry A, Legget M: Practical Perioperative Transoesophageal Echocardiography. Fig. 10.3, p. 158. Philadelphia, Butterworth Heinemann, 2003.) TEE, transesophageal echocardiography.

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.

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.

Aortic Regurgitation

Chronic aortic regurgitation results from aortic root dilatation (Fig. 10-5) or abnormalities of the aortic valve leaflets (Table 10-3). Acute aortic regurgitation results from dissection (see Fig. 11-7), endocarditis and, occasionally, trauma.


Figure 10.5 Appearances of aortic root dilatation on transesophageal echocardiography. There is loss of the normal sinotubular junction and marked dilatation of the ascending aorta.

(Reproduced, with permission, from Sidebotham D, Merry A, Legget M: Practical Perioperative Transoesophageal Echocardiography. Fig. 11.4, p. 176. Philadelphia, Butterworth Heinemann, 2003.) Ao, proximal ascending aorta; LA, left atrium; LVOT, left ventricular outflow tract.

Table 10-3 Common Causes of Aortic Regurgitation

Valvular Dysfunction
Rheumatic aortic disease
Degeneration of a bicuspid valve
Degeneration of a bioprosthetic valve
Endocarditis on a native or prosthetic (bioprosthetic or mechanical) valve
Leaflet prolapse due to trauma or myxomatous disease
Aortic Disease
Aortic root dilation
Aortic dissection


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.