Disclosure
Background: Heart valves permit unobstructed forward blood flow through the cardiac chambers while preventing backward flow. Aortic stenosis represents obstruction to left ventricular (LV) outflow that is localized most commonly at the aortic valve. However, obstruction also may occur above the valve (supravalvular stenosis), below the valve (subvalvular aortic stenosis), or it may be caused by hypertrophic obstructive cardiomyopathy. Valvular aortic stenosis has a prevalence of approximately 5 cases per 10,000 population. Although it can occur at any age, it most commonly affects those older than 60 years. Degenerative valve disease is the most common etiology in the elderly, whereas congenital bicuspid valve and rheumatic valve disease is not common in this age group. The prevalence of aortic stenosis increases with age. Degeneration of the aortic valve is present is 75% of people older than 85 years (Lindroos, 1994). Valvular stenosis occurs in 2% of those older than 65 years and in 4% over those older than 85 years (Stewart, 1997). In young people, a bicuspid valve is the most common cause. Overall, a bicuspid aortic valve occurs in 0.5-1.0% of people. Rheumatic valvular disease is rare in the United States, but it remains an important cause of valvular disease in the developing world. Aortic stenosis causes a pressure overload because the LV must generate pressure that is high enough to overcome the obstruction and to pump blood forward into the aorta. Patients present with asymptomatic murmur in the beginning. After symptoms develop, only one quarter of patients survive 3 years without valve replacement. The annual risk of sudden death ranges from 10% in patients with angina to 15% with syncope and 25% with heart failure. Recognition and evaluation of symptoms to determine the severity of aortic stenosis is crucial. In most patients, definitive therapy for severe valvular heart disease is mechanical restoration of valvular function. Pathophysiology: The normal area of the aortic valve is 3-4 cm2, and little hemodynamic disturbance occurs until the orifice is reduced to approximately one third of its normal size, at which time a systolic gradient develops between the LV and the aorta. LV and aortic pressures normally are almost equal during systole. In patients with aortic stenosis, intracavitary LV pressure must increase above aortic pressure to produce forward flow across the stenotic valve and to achieve acceptable downstream pressure. A geometric progression occurs in the magnitude of the gradient as the area of the valve narrows. Given a normal cardiac output, the gradient rises rapidly from 10-15 mm Hg at valvular areas of 1.5-1.3 cm2 to approximately 25 mm Hg at 1.0 cm2, 50 mm Hg at 0.8 cm2, 70 mm Hg at 0.6 cm2, and 100 mm Hg at 0.5 cm2. The rate of progression of aortic stenosis varies widely from patient to patient; it may remain stable for many years or increase as rapidly as 15 mm Hg per year. A major compensatory response to the increased LV pressure of aortic stenosis is the development of concentric LV hypertrophy. The Laplace equation is as follows: S = (P X R)/2T, where S is stress, P is the pressure, R is the radius, and T is the thickness. This equation indicates that the force on any unit of the LV myocardium (afterload) varies directly with the ventricular pressure and radius and inversely with the wall thickness. Thus, as pressure increases, it can be offset by increased LV wall thickness (concentric hypertrophy). The determinants of LV ejection fraction are contractility, preload, and afterload. By normalizing afterload, the development of concentric hypertrophy helps preserve ejection fraction and cardiac output despite the pressure overload. Hemodynamic effects Although the cardiac output at rest is within normal limits in most patients with severe aortic stenosis, it often fails to rise normally during exertion. Late in the course of the disease, the cardiac output, stroke volume, and, therefore, the LV-aortic pressure gradient all decline, whereas the mean left atrial, pulmonary capillary, pulmonary arterial, right ventricular systolic and diastolic, and right atrial pressures rise. LV hypertrophy Although hypertrophy clearly serves a compensatory function, it also has a pathologic role and is in part responsible for the classic symptoms of aortic stenosis. Atrial kick In patients with severe aortic stenosis, large a waves usually appear in the left atrial pressure pulse because of the combination of enhanced contraction of a hypertrophied left atrium and diminished LV compliance. Atrial contraction plays a particularly important role in filling of the LV in aortic stenosis. Atrial contraction raises LV end-diastolic pressure without causing a concomitant elevation of mean left atrial pressure. This booster-pump function of the left atrium prevents the pulmonary venous and capillary pressures from rising to levels that produce pulmonary congestion. Therefore, loss of appropriately timed vigorous atrial contraction, as occurs in atrial fibrillation or atrioventricular dissociation, may result in rapid clinical deterioration of patients with severe aortic stenosis. Diastolic dysfunction Although ventricular hypertrophy is a key adaptive mechanism to the pressure load imposed by aortic stenosis, it has an adverse pathophysiologic consequence. That is, it increases diastolic stiffness. As a result, increased intracavitary pressure is required for ventricular filling. This increased stiffness, however produced, contributes to the elevation of ventricular diastolic filling pressure at any level of ventricular diastolic volume and may be responsible for flash pulmonary edema in patients with aortic stenosis. Diastolic dysfunction may revert toward normal as hypertrophy regresses after aortic stenosis is relieved. Frequency:
Mortality/Morbidity: The presence or absence of the classic symptoms of aortic stenosis, including angina, syncope, and the symptoms of heart failure, is the key to the natural history of the disease. Before symptoms appear, survival rates are similar in patients and in the healthy population, and sudden death is rare. However, after classic symptoms develop, survival rates decline precipitously.
Race: No particular predilection for race has been identified. Sex: Valvular aortic stenosis without accompanying mitral valve disease is more common in men than in women and rarely occurs due to a rheumatic etiology. Sex-based differences in the response of the LV to aortic stenosis are reported.
Age: In the natural history of aortic stenosis in adults, a long latent period is observed. Cardinal manifestations of acquired aortic stenosis most commonly appear in the fifth or sixth decades of life.
Anatomy:
Clinical Details: Clinical history Patients with aortic stenosis have a long latent period during which obstruction gradually increases and the pressure load on the myocardium increases while the patient remains asymptomatic. Cardinal manifestations of acquired aortic stenosis, which commence most commonly in the fifth or sixth decades of life, are angina pectoris, syncope, exertional dyspnea and, ultimately, heart failure.
Physical examination Physical examination may yield the following findings:
Laboratory studies
Preferred Examination: Echocardiography Echocardiography is the preferred imaging test. Echocardiography is indispensable to the assessment of the extent of LV hypertrophy, systolic ejection performance, and anatomy of the aortic valve. Doppler interrogation of the aortic valve makes use of the modified Bernoulli equation (gradient = 4 X velocity2) to assess the severity of the stenosis. As blood flows from the body of the LV across the stenotic valve, the flow rate must accelerate for the volume to remain constant. Doppler interrogation of the valve detects this increase in velocity and helps estimate the valvular gradient. In summary, echocardiography may demonstrate the following findings:
Chest radiography Chest radiographs may show several significant findings consistent with aortic stenosis. The aortic valve may appear calcified. With plain images, calcification is best detected on the lateral view. Calcification of the aortic valve is found in almost all adults with hemodynamically significant aortic stenosis. The LV may be slightly enlarged with a rounded apex, which is a nonspecific finding. The left atrium may be enlarged as well. Visible calcification on plain chest films usually indicates a gradient of 50 mm Hg or more across the valve, which is severe enough to require surgery. CT scanning CT scans may exhibit chamber enlargement and calcification of the aortic valve. This calcification is a reliable indicator of severe stenosis, particularly when it is present in a young patient. Magnetic resonance imaging Cine MRI can be used to depict the signal void caused by high-velocity jet flow across a narrow valvular orifice associated with the opened valve in aortic stenosis. The signal void is projected into the ascending aorta in systole. Despite the good anatomic detail obtainable by using MRI, echocardiography has superseded MRI because of its improved portability. Cardiac catheterization and angiography During catheterization, the transvalvular pressure gradient across the aortic valve is measured, with a catheter in the LV and another in the proximal aorta or femoral artery. A mean pressure gradient of greater than 30 mm Hg usually represents clinically significant aortic stenosis. Limitations of Techniques: During determination of aortic gradient using Doppler echocardiography, mitral regurgitation is occasionally difficult to differentiate.
Congenital aortic stenosis
Findings: Routine chest radiography may demonstrate normal or nondiagnostic findings in patients with critical aortic stenosis. Findings include those described below.
Degree of Confidence: Chest radiograph findings are usually nondiagnostic in aortic stenosis, unless valvular calcification is present. In almost one half of patients (in whom stenosis is minimal to moderate), no detectable abnormal radiograph findings are demonstrated except for the slight prominence of the ascending aorta. When present, the findings are characteristic. Subaortic stenosis is particularly difficult to diagnose radiographically because little if any poststenotic dilation occurs in idiopathic hypertrophic subaortic stenosis. In the membranous type of stenosis, often no poststenotic dilatation occurs, and LV hypertrophy is often minimal. False Positives/Negatives: No clinically significant false-positive or false-negative findings are encountered because this test is nonspecific. |
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Findings: The presence of valvular calcification is specific for aortic-valve disease. Calcification is most readily detected by using CT scans. Calcification of the aortic valve is also a reliable indication that stenosis is severe, particularly when it is present in a young patient. If the patient does not have decompensation, visible calcification on plain chest images usually indicates a gradient of 50 mm Hg or more across the valve. This degree of stenosis usually is treated with surgery. Supravalvular aortic stenosis is a rare condition that is seen as an element of Williams syndrome, which consists of mental and physical retardation, elfin facies, hypercalcemia, and peripheral pulmonary artery stenoses. In supravalvular aortic stenosis, a tight hourglass constriction of the ascending aorta occurs just cephalic to the valve. Degree of Confidence: CT findings in aortic stenosis may be diagnostic, but in some patients, they must be supported by clinical findings to make the diagnosis. False Positives/Negatives: Subaortic stenosis is particularly difficult to diagnose radiologically because in idiopathic hypertrophic subaortic stenosis, little if any poststenotic dilation occurs. In the membranous type of stenosis, no poststenotic dilatation may be noted, and LV hypertrophy is often minimal.
Findings: MRI is uniquely advantageous for imaging the cardiovascular structures. High contrast is demonstrated between the moving blood pool and the static cardiovascular structures. Imaging techniques include spin-echo (SE) and cine gradient echo (GRE) imaging. On SE MRI the blood appears black, while the static internal cardiac structures, such as chamber walls and valves, appear bright. In contrast, high signal intensity is noted on cine GRE MRI, on which the blood pool appears white and has signal intensity higher than that of the myocardium. The latter can be used to quantify the flows and gradients in valvular stenoses by imaging and analyzing the signal void caused by high-velocity jet flow across the narrow aortic valvular orifice that is projected into the ascending aorta in systole. Various planes can be used for imaging. A long-axis view through the LV apex and aortic outflow tract in a coronal plane is most useful in assessing aortic stenosis. SE MRI SE imaging can clearly demonstrate the structural details of the aortic valve cusps, supravalvular and subvalvular structures, and dimensions of the LV and aortic root. It can show a bicuspid valve, thickened or bulging leaflets, reduced valve excursion, LV hypertrophy, and ascending aortic dilatation due to the impact from the stenotic jet. Cine GRE MRI Cine GRE images can be used to determine the severity of aortic stenosis by measuring the size and extent of the stenotic jet into the ascending aorta imaged in coronal plane centered on the LV outflow tract. Velocity-encoded MRI is one of the best ways to quantify the transvalvular pressure gradient and valvular area. The valvular area can also be directly traced on the transverse axial cine GRE images obtained with a velocity-encoded sequence. The maximal velocity in the stenotic jet can be determined on planes perpendicular to the flow (through-plane measurement) or parallel to the flow (in-plane measurement). As with Doppler echocardiography, the pressure gradient across the stenotic aortic valve can be calculated by using the modified Bernoulli equation: P = 4 X (Vmax)2, where P = pressure gradient, and Vmax = maximal velocity. In addition, the area of the aortic valve (AAo) can be calculated by determining area of the aortic outflow tract (AOT), maximum velocity in the aortic outflow tract (VOT), and maximum velocity in the aortic stenotic jet (VAo) by using the following continuity equation: AAo = (AOT X VOT)/VAo. The calculated area of the aortic valve and the pressure gradient are well correlated with the data obtained from Doppler echocardiography and hemodynamic monitoring in the catheterization laboratory. Degree of Confidence: MRI is useful, and the degree of confidence is high. During cine GRE imaging, the echo time (TE) must be kept long because shorter TEs may miss or not show the signal void produced by the stenotic jet well. False Positives/Negatives: Velocity-encoded MRI has certain potential sources of error. Imaging plane must be as close to perpendicular and parallel to the jet as possible. Also, because of the cyclic quality of phase shift, aliasing may appear, especially when the velocity range is lowered.
Findings: Evaluation of patients with known or suggested aortic valve disease requires integration of anatomic information from 2-dimensional echocardiography and physiologic information from Doppler studies. Bicuspid valve Transthoracic echocardiography is a reliable method for detecting the bicuspid aortic valve. With this technique, the hallmark of the bicuspid valve is eccentric closure of the leaflets in the aorta. In approximately 80% of patients, 2 rather than 3 leaflets can be visualized directly. On close scrutiny with transesophageal echocardiography, what at first appears to be a true bicuspid valve is often found to be a 3-leaflet valve with unequal leaflet sizes and fusion of 1 of the 3 commissures resulting in a functional bicuspid valve. Coarctation of the aorta is strongly associated with a bicuspid valve. When clinical findings suggest either of these conditions, the other should be evaluated as well. Calcific aortic stenosis Degenerative calcific valves appear as 3-leaflet structures with marked thickening of the leaflets. Thickening and calcification may be most prominent at the base of the leaflets than at the tips. The range of immobility and stenosis is broad and depends on the duration and severity of disease. Rheumatic stenosis Rheumatic aortic stenosis typically results in thickening of the leaflet along the commissural edges. It is seen almost exclusively in the presence of rheumatic mitral stenosis. Secondary effects of aortic stenosis After aortic stenosis is defined anatomically, secondary effects can be evaluated. These include poststenotic dilatation of the aorta and LV hypertrophy. LV systolic function also should be assessed. Assessment of the severity of aortic stenosis Continuous Doppler echocardiography is essential for assessing the physiologic significance of aortic stenosis. In clinically significant aortic stenosis, the gradient is likely to exceed 50 mm Hg. This value corresponds to a Doppler velocity of approximately 3.5 m/s, which is out of the range for accurate quantitation by using pulsed-wave Doppler study. For this reason, use of continuous-wave Doppler imaging is essential for quantitation. Doppler interrogation of the aortic valve makes use of the modified Bernoulli equation (gradient = 4 X velocity2) to assess the severity of the stenosis. As blood flows from the body of the LV across the stenotic valve, the flow rate must accelerate for the volume to remain constant. Doppler interrogation of the valve depicts this increase in velocity and helps in estimating the valvular gradient. An additional method for determining the area of the aortic valve relies on the continuity equation with pulsed Doppler echocardiography. In aortic stenosis, the LV outflow tract area can typically be derived from the diameter of the annulus if a circular geometry is assumed. Then, pulsed Doppler echocardiography is used to determine the velocity of flow at that site. The product of the 2 values is volumetric flow in the outflow tract. At the stenotic orifice, continuous-wave Doppler imaging is used to determine the mean velocity. Then, the algebraic equation can be solved for the area of the aortic valve. In a modification of this technique mitral-valve flow is used instead of LV outflow. Because the velocity of flow increases at the restrictive orifice, several investigators have suggested using the ratio of the V1/V2 leads as a marker for clinically significant aortic stenosis. Variations in the valve area and gradients From a practical standpoint, determining the area of the aortic valve is often unnecessary. In a patient with thickened, restricted leaflets and a mean gradient exceeding 50 mm Hg, severe aortic stenosis is clinically ensured. Likewise, in patients with normal ventricular function and with low gradients, the likelihood of clinically significant aortic stenosis becomes negligible. Low ejection fraction Patients with reduced LV function, typically with ejection fractions of 25-35%, and a modest transvalvular gradient of 25-30 mm Hg have a serious problem. This situation may represent either mild disease of the aortic valve and unrelated LV dysfunction or critical aortic stenosis with secondary LV dysfunction. While LV function and valvular gradients are being monitored, and infusion of dobutamine can be helpful in differentiating these 2 entities. If LV function improves with dobutamine infusion and if the gradient increases, aortic stenosis is severe and associated with secondary LV dysfunction. Patients with this condition benefit from AVR. If ventricular function improves without a change in the gradient, aortic stenosis is unlikely to be the limiting factor. Patients with this condition can be treated medically. Degree of Confidence: The gradients determined using Doppler echocardiography are very well correlated with simultaneously determined invasive measurements. By using transthoracic echocardiography, the orifice of the valve is usually not visualized to a reliable degree. By using transesophageal echocardiography and planimetry, a direct measurement of the aortic valve orifice can be obtained in many patients with aortic stenosis. False Positives/Negatives: On occasion, Doppler echocardiography causes underestimation of the gradient measured. This is common with nonsimultaneous recordings, but it also occurs when the angle of interrogation exceeds approximately 20°. Off-angle interrogation is the most common cause for underestimation of a gradient in aortic stenosis.
Findings: Myocardial perfusion imaging may be helpful for assessing concomitant atherosclerosis of the coronary arteries. Treadmill stress testing or pharmacologic imaging can usually be performed safely in patients with mild-to-moderate aortic stenosis, though it may be contraindicated in patients with severe aortic stenosis. Radionuclide ventriculography can be used to determine LV function in patients with aortic stenosis. Degree of Confidence: Nuclear medicine findings are reliable for the assessment of myocardial ischemia or for the assessment of LV function if needed. False Positives/Negatives: False findings are rare.
Findings: Cardiac catheterization and hemodynamics When echocardiography demonstrates severe aortic stenosis and when the patient has 1 or more of the classic symptoms of the disease, AVR should be performed. Because most patients with aortic stenosis are at the age at which coronary disease is common, cardiac catheterization to perform coronary arteriography is usually accomplished before surgery. When the hemodynamic diagnosis is unclear, right- and left-sided heart catheterization should be performed to obtain the transaortic valvular pressure gradient and cardiac-output readings. This information is used to calculate the aortic valve area by the Gorlin equation, as follows: Aortic valve area = [CO/(SEP X HR)]/(44.3 X h1/2), where CO = cardiac output (in milliliters per minute), SEP = systolic ejection period (in seconds), HR = the heart rate, and h = the mean gradient. Methods In patients with aortic stenosis, the transvalvular pressure gradient should be measured, whenever possible, by using a catheter in the LV and another in the proximal aorta. Although measuring the gradient between the LV and the femoral artery is convenient, downstream augmentation of the pressure signal and delay in pressure transmission between the proximal aorta and femoral artery may alter the pressure waveform substantially and introduce errors into the measured gradient. Still, in many patients, LV–femoral artery pressure gradients may suffice as an estimate of the severity of aortic stenosis to confirm a severely stenotic valve. If the side port of the arterial introducing sheath is used to monitor femoral pressure, the inner diameter of the sheath should be 1F larger than the outer diameter of the catheter used. The LV–femoral artery pressure gradient may not always be relied on in the calculation of the area of the valve orifice in patients with equivocal valve gradients. A careful single-catheter pullback from the LV to the aorta often is preferred to simultaneous measurement of LV and femoral-artery pressures. As an alternative, a single catheter with distal and proximal lumina or a micromanometer catheter with distal and proximal transducers may be used for simultaneous measurement of LV and central aortic pressures. In patients with atrial fibrillation, several beats should be taken and averaged. The preferred method may be to obtain simultaneous pressure recordings from the LV and aorta, with the averaging of several beats, to reduce errors caused by beat-to-beat variations due to changes in stroke volume. Another possibility that might be considered is the use of temporary transvenous pacing to regularize the R-R interval and therefore reduce this error. The mean pressure gradient across the aortic valve is determined by means of planimetry of the area separating the LV and aortic pressures by using multiple beats. This gradient is applied to the calculation of the area of the valve orifice. The peak-to-peak gradient, measured as the difference between peak LV pressure and peak aortic pressure, is commonly used to quantify the valve gradient because this measurement is rapidly obtained and can be visually estimated. Degree of Confidence: Some risk is associated with the rapid injection of a large volume of contrast material into a high-pressure LV; therefore, this procedure is usually not advisable in patients with aortic stenosis and critical obstruction. In patients in this situation, angiographic studies of the LV and the aortic valve are best performed by injecting contrast material into the pulmonary artery and by imaging in the 30° right anterior oblique and 60° left anterior oblique projections. These examinations often make it possible to ascertain the number of cusps of the stenotic valve and to demonstrate doming of a thickened valve and a systolic jet. In patients with very severe aortic stenosis, the LV catheter may reduce the effective area of the orifice, resulting in an artifactual increase in the measured pressure gradient. This overestimation of the severity of aortic stenosis is rarely important because the diagnosis of severe aortic stenosis is usually apparent already in these patients. False Positives/Negatives: False findings are rare.
Intervention: Balloon aortic valvuloplasty In acquired calcific aortic stenosis, leaflet restriction results from heavy calcium deposition in the leaflets and not commissural fusion. Therefore, balloon aortic valvotomy (BAV) is relatively ineffective in improving aortic stenosis and usually results in a residual gradient of 30-50 mm Hg and a valvular area of 1.0 cm2. Mortality rates after this procedure are similar to those found in untreated patients. For this reason, BAV is used only palliatively in patients in whom AVR is impossible because of comorbidity or because it is impractical because immediate temporary relief is required to meet the demands of other noncardiac conditions. Overall intermediate-term (6-12 mo) results of BAV have been disappointing largely because of recurrence of stenosis. However, the procedure does have a role in the treatment of severe calcific aortic stenosis in patients who are not surgical candidates. Indications include the following:
In adults with calcified aortic stenosis, BAV is not a substitute for surgery (as balloon mitral valvuloplasty may be in patients with mitral stenosis). In children and adolescents with noncalcific congenital aortic stenosis, who most commonly have bicuspid aortic valves, simple commissural incision under direct visualization usually leads to substantial hemodynamic improvement with low risk (mortality rate <1%). Therefore, this procedure (or now, more commonly, balloon aortic valvuloplasty) is indicated not only in symptomatic patients but also in asymptomatic children and adolescents with severe aortic stenosis, which often is defined as a calculated effective orifice less than 0.8 cm2 or 0.5 cm2/m2 of the body surface area. Despite the salutary hemodynamic results after this procedure, the anatomy of valve is not made entirely normal. Turbulent blood flow through the valve may lead to further deformation, calcification, regurgitation, and stenosis that recurs after 10-20 years. Patients may probably require repeat operation and valve replacement later. AVR surgery At present, more than 100,000 aortic valve operations are performed each year in the United States according to the database of the Society of Thoracic Surgeons (STS). Approximately one half of patients undergoing AVR have additional procedures, with coronary artery bypass surgery being the most common concomitant procedure. Valve replacement is the procedure of choice, especially in adults. Valve-replacement surgery began in the 1950s, but the modern era began in the 1960s with the development of the ball-in-cage and tilting-disk mechanical devices. At present, bileaflet tilting disk valves are most commonly used and have superb durability. However, many patients who received ball-in-cage devices more than 30 years ago are still alive. Bioprosthetic valves were developed in the 1970s with the introduction of the stented porcine aortic and bovine pericardial valves. The range of bioprosthetic valves is wide and includes stentless porcine valves, new-generation stented valves, and homografts. Transplantation of the pulmonary valve into the aortic position (Ross procedure) is a useful option in young patients with suitable anatomy. Bioprosthetic devices are less durable than mechanical protheses, and they are reserved for older patients. Current bioprostheses last over 10 years on average, and many continue to perform in a satisfactory manner for 20 years after implantation. In most adults with calcific aortic stenosis, satisfactory long-term valvular function usually cannot be restored even with careful sculpturing procedures under direct visualization, and AVR is the surgical treatment of choice. In general, AVR should be performed in adults who have hemodynamic evidence of severe obstruction (aortic valve orifice <0.8-0.9 cm2 or <0.5-0.6 cm2/m2 of body surface area) and in adults whose symptoms are believed to result from aortic stenosis. In addition, AVR should be performed in asymptomatic patients with progressive LV dysfunction or those with a hypotensive response to exercise. Although a prospective randomized controlled study has not been performed, long-term mortality rates in asymptomatic patients with critical aortic stenosis and LV dysfunction who undergo surgery appear to be lower than mortality rates in medically treated patients who do not undergo surgery. AVR is indicated in patients with severe stenosis who are undergoing another cardiovascular operation (eg, coronary artery bypass grafting or surgery of the aorta or another heart valve). The surgical risk is highest in patients with impaired LV function (ejection fraction <35%). However, because the prognosis is poor without surgery and because some patients in this group have clinical and functional recovery after AVR, the procedure should usually be offered to these patients. Octogenarians with LV dysfunction can have improved survival after AVR. Successful replacement of the aortic valve results in substantial clinical and hemodynamic improvement in patients with aortic stenosis, aortic regurgitation, or combined lesions. In patients without frank LV failure, the surgical risk is 2-5% in most centers, and in patients younger than 70 years, the surgical risk is reported to be as low as 1%. The STS National Database Committee reported an overall operative mortality rate of 4.3% in 26,317 patients undergoing isolated AVR and 8.0% in 22,713 patients undergoing AVR and coronary artery bypass surgery. Risk factors that increase the mortality rate include a high class according to the New York Heart Association (NYHA) system, impaired LV function, advanced age, and associated coronary artery disease. The 10-year actuarial hospital survival rate in surgically treated patients is approximately 85%. Symptoms of pulmonary congestion (exertional dyspnea) and myocardial ischemia (angina pectoris) are relieved in almost every patient. Hemodynamic results of AVR are impressive; elevated end-diastolic and end-systolic volumes are substantially reduced. Impaired ventricular performance returns to normal more frequently in patients with aortic stenosis than in patients with aortic or mitral regurgitation. Diastolic function is improved as well. However, the finding that the strongest predictor of postoperative LV dysfunction is preoperative dysfunction suggests that patients should undergo surgery before LV function becomes seriously impaired, if possible. In patients with aortic stenosis and obstructive coronary artery disease (a relatively common combination), AVR and myocardial revascularization should be performed together. Although the risk of AVR is increased when accompanied by coronary artery bypass grafting, the surgical risk increases even more when severe coronary artery disease is left untreated. Interest in performing AVR through a small incision, usually a transverse sternotomy had increased. This approach is called minimally invasive surgery. Although the advantages (eg, shortened hospital stay, decreased tissue damage, improved cosmetic results) are clear, the procedure is technically demanding, and the mortality rate may be higher than of a standard approach. The Ross procedure (aortic and pulmonary valve switch) usually is performed in somewhat young patients. Medical therapy The only medical therapy indicated in patients with aortic stenosis is antibiotic prophylaxis to prevent bacterial endocarditis. Otherwise, the patient is either asymptomatic and requires no therapy or symptomatic and requires surgery. In patients with heart failure who are awaiting surgery, diuretics can be used cautiously to relieve pulmonary congestion. Nitrates may carefully be used to treat angina pectoris. Although vasodilators, especially angiotensin-converting enzyme inhibitors, have become a cornerstone of the therapy for heart failure. They are not recommended in patients with aortic stenosis. With a fixed valvular obstruction to outflow, vasodilation reduces pressure distal to the obstruction without increasing cardiac output and may cause syncope. When surgery and valvoplasty are unsuccessful or impossible, digitalis and diuretics can be used to improve symptoms with the understanding that they do not improve life expectancy. Medical/Legal Pitfalls:
Special Concerns:
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