AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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) or below the valve (subvalvular aortic stenosis). Aortic stenosis may be caused by hypertrophic obstructive cardiomyopathy.

Valvular aortic stenosis has a prevalence of approximately 5 cases per 10,000 population. Although it may occur in patients of any age, it most commonly affects those older than 60 years. Degenerative valve disease is the most common etiology in the elderly; congenital bicuspid valve disease and rheumatic valve disease are not common in patients of this age group. The prevalence of aortic stenosis increases with age. Degeneration of the aortic valve is present in 75% of people older than 85 years.¹ Valvular stenosis occurs in 2% of those older than 65 years and in 4% of those older than 85 years.² In young people, a bicuspid valve is the most common cause. Overall, a bicuspid aortic valve occurs in 0.5-1.0% of the population. Rheumatic valvular disease is rare in the United States, but it remains an important form 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. Early in the course of disease, patients present with asymptomatic murmur. 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% of patients with syncope and 25% of those 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.^{3, 4, 5, 6, 7}

Related eMedicine topics:
Aortic Stenosis (from Cardiology)
Aortic Stenosis (from Emergency Medicine)
Aortic Regurgitation
Mitral Regurgitation

Related Medscape topics:
EVEREST I and II: Percutaneous Approach to Mitral Regurgitation

Specialty Site Radiology
Specialty Site Cardiology

Pathophysiology

The normal area of the aortic valve is 3-4 cm². 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 the 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 it may 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 the amount of stress, P is the amount of 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 may 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.⁸

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 it may be 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

United States

Aortic stenosis is primarily a disease of the elderly; its incidence is increasing in the population. An estimated 3 million Americans have some degree of aortic stenosis. A bicuspid aortic valve is the single most common congenital cardiac defect; it occurs in approximately 0.5-1.0% of the population. Degenerative and bicuspid aortic valvular stenoses are most common in the Western world.

International

Rheumatic valvular stenosis is most common in developing countries.

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 to those in the healthy population, and sudden death is rare. However, after classic symptoms develop, survival rates decline precipitously.

• Approximately 35% of patients with aortic stenosis present with angina. Of these, 50% die within 5 years unless aortic valve replacement (AVR) is performed.
• Approximately 15% of patients present with syncope; of these, 50% die within only 3 years unless the aortic valve is replaced.
• Of the 50% of patients who present with symptoms of congestive heart failure, 50% die within 2 years without AVR.
• Because cardiac output is usually well maintained for many years in patients with severe aortic stenosis, marked fatigability, debilitation, peripheral cyanosis, and other clinical manifestations of low cardiac output usually are not prominent until late in the course of the disease.
• Other late findings in patients with isolated aortic stenosis include atrial fibrillation, pulmonary hypertension, and systemic venous hypertension.
• Aortic stenosis may be responsible for sudden death; sudden death usually occurs in patients who were previously symptomatic.

Race

No particular predilection for race has been identified in aortic stenosis.

Sex

Valvular aortic stenosis without accompanying mitral valve disease is more common in men than in women; rarely, it has a rheumatic etiology. Sex-based differences in the response of the LV to aortic stenosis have been reported.

• In women with valvular aortic stenosis, ventricular performance is usually normal, or even supernormal. The LV is often small, thick-walled, and concentrically hypertrophied. Diastolic dysfunction occurs, and systolic wall stress is normal or even subnormal.
• In men, eccentric LV hypertrophy, excessive systolic wall stress, systolic dysfunction, and ventricular dilatation are characteristic.

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 decade of life.

• The initial insult responsible for stenosis of the bicuspid aortic valve is unknown. However, thickening and calcification of the leaflets eventually inhibit opening; stenosis usually develops in the fourth, fifth, and sixth decades of life.
• Congenital aortic stenosis from a unicuspid, bicuspid, or even an abnormal tricuspid valve occasionally causes symptoms during childhood and requires correction by adolescence.⁹

Anatomy

• Congenital aortic stenosis
• • Congenital malformations of the aortic valve may be unicuspid, bicuspid, or tricuspid, or a dome-shaped diaphragm may be noted. Overall, approximately 30% of patients with aortic stenosis have congenital deformation of their valve, the vast majority of which are bicuspid.
  • Unicuspid valves produce severe obstruction in infancy and are the most frequent malformations found in fatal valvular aortic stenosis in children younger than 1 year.
  • Congenitally bicuspid valves are not often severely stenotic during childhood. The abnormal architecture induces turbulent flow, which traumatizes the leaflets and leads to fibrosis, increased rigidity, calcification of the leaflets, and narrowing of the aortic orifice in adulthood.
  • A tricuspid valve with cusps of unequal size and with some commissural fusion may develop turbulent flow, which may lead to fibrosis and, ultimately, to calcification and stenosis. In adults, tricuspid stenotic aortic valves may be congenital, rheumatic, or degenerative in origin.
• Acquired aortic stenosis
• • Acquired aortic stenosis accounts for more than 70% of cases. Over 90% are the result of age-related degeneration.
  • Rheumatic aortic stenosis: Rheumatic aortic stenosis results from adhesions and fusions of the commissures and cusps and neovascularization of the leaflets or the valvular ring, leading to retraction and stiffening of the free borders of the cusps. Calcific nodules develop on both surfaces, and the orifice is reduced to a small round or triangular opening. With the decline in rheumatic fever in industrialized nations, rheumatic aortic stenosis is decreasing in frequency.
  • Age-related degenerative-calcific aortic stenosis
  • • Formerly termed senile aortic stenosis, this form currently is the most common cause of aortic stenosis in adults, and it is the most frequent reason for AVR in patients with aortic stenosis. It appears to result from years of normal mechanical stress on a valve that sometimes exhibits inflammatory changes with infiltration of macrophages and T lymphocytes. The cusps are immobilized, and stenosis is caused by deposits of calcium along the bases of the flexion lines.
    • Immunohistochemical evidence of Chlamydia pneumoniae infection has been found in early lesions of age-related degenerative aortic stenosis. This form of aortic stenosis may be accompanied by calcifications of the mitral annulus and coronary arteries and, rarely, by aortic regurgitation. Both diabetes mellitus and hypercholesterolemia are risk factors for the development of age-related aortic stenosis or degenerative-calcific aortic stenosis.
    • Age-related sclerosis of the aortic valve and calcific aortic stenosis appear to be associated with traditional risk factors for atherosclerosis, such as cigarette smoking and hypertension. A relationship with lower high-density lipoprotein cholesterol (HDL-C) levels (hypoalphalipoproteinemia) has not been demonstrated convincingly. Of no surprise, age-related aortic-valve sclerosis is associated with an increase in the risk of cardiovascular death and myocardial infarction.
  • In patients with atherosclerotic aortic-valve stenosis, severe atherosclerosis involves the aorta and other major arteries. This form of aortic stenosis occurs most frequently in patients with severe hypercholesterolemia and is observed in children with homozygous type II hyperlipoproteinemia.
  • Calcific aortic stenosis is observed in a number of other conditions, including Paget disease of the bone and end-stage renal disease.
  • Rheumatoid involvement of the valve is an infrequent cause of aortic stenosis. It involves nodular thickening of the valvular cusps and involvement of the proximal portion of the aorta.
  • Ochronosis with alkaptonuria is another rare cause of aortic stenosis.

Clinical Details

With aortic stenosis, there occurs a long latent period during which obstruction gradually increases and the pressure load on the myocardium increases; during this period, 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.^{10, 11, 12, 13, 14, 15, 16, 17}

• Asymptomatic murmur: Asymptomatic patients with suggestive murmurs benefit from early diagnosis; early diagnosis allows both the patient and the physician to be most vigilant regarding possible early signs and symptoms and to guide the use of prophylactic regimens to prevent bacterial endocarditis.
• Angina
• • Angina occurs in approximately two thirds of patients with critical aortic stenosis. Approximately one half of these patients have associated clinically significant coronary artery obstruction.
  • The supply of oxygen to the LV depends on coronary blood flow; angina occurs in association with myocardial ischemia, as LV oxygen demand exceeds supply. In persons without aortic stenosis, coronary blood flow may increase 5- to 8-fold under maximum metabolic demand, but in patients with aortic stenosis, this reserve is limited.
  • In patients with aortic stenosis who do not have coronary artery disease, coronary blood-flow reserve may be reduced through either of 2 mechanisms: it may occur as a result of the relative diminution of ingrowth of capillaries, which serve the needs of the hypertrophied LV, or it may occur as a result of a reduction in the transcoronary gradient for coronary blood flow. Such a reduction in the transcoronary gradient occurs as a result of an elevation in LV end-diastolic pressure. Restricted coronary blood-flow reserve appears to be responsible for angina in many patients with aortic stenosis whose epicardial coronary arteries are normal.
  • • In other patients, angina is a result of an increase in oxygen demand. Wall stress is a key determinant of myocardial oxygen consumption. When hypertrophy is inadequate, wall stress increases. This increase in wall stress causes an increase in oxygen demand, which in turn leads to angina.
    • In rare cases, angina results from calcium emboli occurring in the coronary vascular bed.
• Syncope

• • Syncope usually occurs because cerebral perfusion is inadequate. In patients with aortic stenosis, syncope is usually related to exertion. It may occur when exertion causes a fall in total peripheral resistance that cannot be compensated for by increased cardiac output, owing to the fact that output is limited by the obstruction to LV outflow. This combination reduces systemic blood pressure and cerebral perfusion.
  • In addition, during exercise, high LV pressures may trigger a systemic vasodepressor response that lowers blood pressure and produces syncope. Cardiac arrhythmias, possibly caused by exertional ischemia, also cause hypotension and syncope.
  • With exertional hypotension, the patient may experience graying-out spells or dizziness on exertion.
  • Syncope at rest may result from the following:

•  

  • • Transient ventricular fibrillation, from which the patient recovers spontaneously
    • Transient atrial fibrillation with loss of the atrial contribution to LV filling, which causes a precipitous decline in cardiac output
    • Transient atrioventricular block caused by extension of the calcification of the valve into the conductive tissue
• Heart failure
• • In patients with aortic stenosis, both contractile dysfunction (systolic failure) and failure of normal relaxation (diastolic failure) occur and cause symptoms.
  • The extent of ventricular contraction depends on contractility and afterload. In patients with aortic stenosis, contractility (ie, the ability to generate force) often is reduced. The mechanisms of contractile dysfunction may include abnormal calcium handling, microtubular hyperpolymerization, and myocardial ischemia.
  • In some patients, contractile function is normal, but hypertrophy is inadequate to normalize wall stress, resulting in high afterload. Excessive afterload in turn inhibits ejection, reduces forward cardiac output, and leads to heart failure. The increase in wall thickness that helps normalize stress unfortunately increases diastolic stiffness. Even if the muscle properties remain normal, high filling pressure must be generated to distend a thickened ventricle.
  • As aortic stenosis advances, collagen deposition also stiffens the myocardium and adds to diastolic dysfunction.
• Gastrointestinal bleeding: Gastrointestinal bleeding, either idiopathic or occurring as a result of angiodysplasia (most commonly of the right colon) or other vascular malformations, occurs more often in patients with calcific aortic stenosis than in persons without this condition. Bleeding may cease after AVR.
• Infective endocarditis is a greater risk in younger patients with mild valvular deformity than in older patients with rocklike, calcific aortic deformities.
• Microthrombi may be present in thickened bicuspid valves; embolization of these microthrombi to the brain may result in stroke or transient ischemic attacks. Calcific aortic stenosis may cause embolization of calcium in various organs, including the heart, kidneys, and brain. Abrupt loss of vision may occur when calcific emboli occlude the central retinal artery.

• Systolic ejection murmur radiating to neck
• Delayed carotid upstroke
• S₄ heart sound
• • Audibility of the S₄ sound is a clinically significant feature, but it is nonspecific.
  • The S₄ sound is a result of LV hypertrophy and a reduction in LV compliance. Therefore, the S₄ sound is also audible in the aging heart and in patients with hypertension and infiltrative heart disease.
  • A soft or paradoxic S₂ sound is audible.
• Murmur in aortic stenosis
• • The diagnosis of aortic stenosis usually is first suggested when the classic systolic ejection murmur is heard during physical examination.

•  

  • The murmur is loudest in the aortic area and radiates to the neck.
  • In some patients, the murmur disappears over the sternum and reappears over the LV apex, giving the false impression that a murmur of mitral regurgitation is also present (Gallavardin phenomenon).
  • The intensity of the murmur increases with cycle length because long cycles are associated with increased aortic flow.
  • In mild disease, the murmur peaks in intensity in early or mid systole. As the stenosis worsens in severity, the murmur peaks progressively later in systole.
  • Dynamic effects: The intensity of the systolic murmur varies from beat to beat in relation to variations in the duration of diastolic filling; such variations in the duration of diastolic filling occur after a premature contraction or in association with atrial fibrillation. This characteristic is helpful in differentiating aortic stenosis from mitral regurgitation, in which the murmur usually is unaffected.
  • The murmur of valvular aortic stenosis is augmented by squatting, which causes an increase in stroke volume. It is reduced in intensity during the strain of the Valsalva maneuver and during standing, which reduce transvalvular flow.

  •  

• Additional signs of aortic stenosis
• • Findings on physical examination that correlate with severe stenosis include a delay in the carotid upstroke; a loud, long systolic murmur; and a single S₂ sound.
  • Perhaps the most helpful clue to the severity of aortic stenosis on physical examination is the characteristic delay in the carotid pulse in association with diminution in volume. However, in elderly patients with aortic stenosis, an increase in carotid stiffness may cause the carotid upstrokes to appear normal.
  • The LV apical impulse in aortic stenosis is not displaced but is enlarged and forceful. Simultaneous palpation of a forceful LV apex beat along with a delayed and weak carotid upstroke usually represent severe aortic stenosis.
  • In patients with aortic stenosis, the S₁ sound usually is normal. In patients with congenital aortic stenosis, in which the valve is not calcified, the S₁ sound may be followed by a systolic ejection click.
  • In patients with calcific disease, the S₂ sound may be single and soft when the aortic component is lost because the valve neither opens nor closes well. In some patients, delayed LV emptying caused by LV dysfunction may create paradoxic splitting of the S₂ sound.
  • An S₄ gallop is common.
  • In advanced disease, pulmonary hypertension and signs of right-sided failure are surprisingly common.

• Electrocardiography
• • For patients with aortic stenosis, the ECG usually demonstrates LV hypertrophy; however, in some patients with severe aortic stenosis, LV hypertrophy is absent on ECG, possibly owing to the lack of LV dilatation. Left atrial abnormality is common because the stiff LV increases left atrial afterload and causes the left atrium to dilate.
  • In summary, ECG findings demonstrate left atrial abnormality and LV hypertrophy.
• Imaging techniques are described in detail in sections below.

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 (see Image 1).

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:

• Concentric LV hypertrophy
• Reduced separation of the cusp of the aortic valve
• Mean gradients greater than 50 mm Hg in patients with severe aortic stenosis on Doppler echocardiography

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; this 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 may 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 with 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 by use of a catheter in the LV and another in the proximal aorta or femoral artery (see Image 3). A mean pressure gradient greater than 30 mm Hg usually represents clinically significant aortic stenosis.

Limitations of Techniques

During measurement of the aortic gradient with Doppler echocardiography, mitral regurgitation is occasionally difficult to discern.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems To Be Considered

Congenital aortic stenosis
Supravalvular aortic stenosis
Rheumatic aortic stenosis
Aortic sclerosis
Subvalvular stenosis
Asymmetric septal hypertrophy
Aortic sclerosis

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Routine chest radiography may demonstrate normal or nondiagnostic findings in patients with critical aortic stenosis. Findings include those described below.

• Enlarged cardiac chamber
• • The cardiac silhouette is usually normal in size or slightly enlarged on the anteroposterior view. The edge of the LV and the apex may appear rounded, presenting a boot-shaped appearance. In the presence of aortic regurgitation or heart failure, substantial cardiomegaly is noted.
  • The left atrium may be slightly enlarged in patients with severe aortic stenosis, and radiologic signs of pulmonary venous hypertension may be demonstrated. However, when left atrial enlargement is marked, associated mitral valvular disease should be suspected.
• Valvular calcification
• • Calcification of the aortic valve is diagnostic of aortic stenosis.
  • Calcification is detected best by using fluoroscopy or CT scans (see Image 2). If seen on plain images, calcification is detected most readily on the lateral view.
  • Calcification of the aortic valve is found in almost all adults with hemodynamically significant aortic stenosis.
  • The absence of calcium in the region of the aortic valve on careful fluoroscopic examination in a patient older than 35 years essentially excludes severe valvular aortic stenosis. However, in patients older than 65 years who have degenerative aortic stenosis, severe calcification of the aortic valve may occur with no or only mild obstruction.
• Dilatation of the aorta
• • Poststenotic dilatation of the ascending aorta is a common finding.
  • The dilatation is characteristically located in the ascending aorta and increases convexity of the right lateral aspect of the ascending aorta.
  • The transverse arch or aortic knob is not enlarged.
  • LV hypertrophy and dilatation may occur in this condition and result in enlargement of the heart downward and to the left. The heart is usually not enlarged greatly unless it has begun to decompensate.
• Supravalvular stenosis

• 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 is present just cephalic to the valve.

Degree of Confidence

Chest radiograph findings are usually nondiagnostic in patients with 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, such findings are pathognomonic.

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.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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 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.^{18, 19, 20}

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.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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, whereas 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 may 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 may 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.

Spin-echo MRI

Spin-echo (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 caused by the impact of the stenotic jet.

Cine GRE MRI

Cine GRE images may 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 the 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 may also be directly traced on the transverse axial cine GRE images obtained with a velocity-encoded sequence.

The maximal velocity in the stenotic jet may 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 may be calculated by using the modified Bernoulli equation: P = 4 X (V_max)², where P = pressure gradient, and V_max = maximal velocity.

In addition, the area of the aortic valve (A_Ao) may be calculated by determining the area of the aortic outflow tract (A_OT), the maximum velocity in the aortic outflow tract (V_OT), and the maximum velocity in the aortic stenotic jet (V_Ao) by using the following continuity equation: A_Ao = (A_OT X V_OT)/V_Ao.

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 with shorter TEs, the signal void produced by the stenotic jet well may be missed or may not be apparent.

False Positives/Negatives

Certain potential sources of error are associated with the use of velocity-encoded MRI. The imaging plane must be as close to perpendicular and as 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.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

The 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.^{21, 22, 23, 24}

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 may 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 in which the leaflets are of different sizes and in which fusion of 1 of the 3 commissures has resulted 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 looked for as well.

Calcific aortic stenosis

Degenerative calcific valves appear as 3-leaflet structures with marked thickening of the leaflets. Thickening and calcification may be more 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 association with rheumatic mitral stenosis.

Secondary effects of aortic stenosis

After aortic stenosis is defined anatomically, secondary effects may 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 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 of determining the area of the aortic valve relies on the continuity equation with pulsed Doppler echocardiography. In aortic stenosis, the LV outflow tract area may 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 represents the 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 may 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 in whom the mean gradient exceeds 50 mm Hg, severe aortic stenosis is clinically ensured. Likewise, in patients with normal ventricular function in whom the gradients are low, the likelihood of clinically significant aortic stenosis becomes negligible.

Low ejection fraction

A serious caseis when the LV function is reduced, typically involving ejection fractions of 25-35%, and when there is a modest transvalvular gradient of 25-30 mm Hg. 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, an infusion of dobutamine may be helpful in differentiating these 2 entities. If LV function improves with dobutamine infusion and if the gradient increases, aortic stenosis is severe and is associated with secondary LV dysfunction. Patients with this condition benefit from aortic valve replacement. If ventricular function improves without a change in the gradient, aortic stenosis is unlikely to be the limiting factor. Patients with this condition may 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 may be obtained in many patients with aortic stenosis.

False Positives/Negatives

On occasion, the use of Doppler echocardiography may lead to an underestimation of the gradient. 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 of underestimation of a gradient in aortic stenosis.

NUCLEAR MEDICINE

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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 may 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 and for the assessment of LV function, if needed.

False Positives/Negatives

False findings are rare.

ANGIOGRAPHY

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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 with the Gorlin equation, as follows: Aortic valve area = [CO/(SEP X HR)]/(44.3 X h^1/2), 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 the femoral artery may alter the pressure waveform substantially and introduce errors into the measured gradient.

Nevertheless, in many patients, LV–femoral artery pressure gradients may suffice for estimating the severity of aortic stenosis in confirming 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 reliable when calculating 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 the aorta, with the averaging of several beats, to reduce errors caused by beat-to-beat variations caused by changes in stroke volume. Another possibility that may 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 through the use of 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 for 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 increase in artifacts in the measured pressure gradient. This is usually of no importance because the diagnosis of severe aortic stenosis is usually already apparent in these patients.

False Positives/Negatives

False findings are rare.

INTERVENTION

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Balloon aortic valvuloplasty

In acquired calcific aortic stenosis, leaflet restriction results from heavy calcium deposition in the leaflets, not commissural fusion. Therefore, balloon aortic valvotomy (BAV) is relatively ineffective in improving aortic stenosis; it 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 aortic valve replacement (AVR) is impossible because of comorbidity or because the use of AVR is impractical, owing to the fact that 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 the 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:

• Patients with cardiogenic shock caused by critical aortic stenosis
• Patients with critical aortic stenosis who require an urgent noncardiac operation
• Patients with severe heart failure who are at extremely high operative risk, as a bridge to AVR
• Patients who are pregnant and have critical aortic stenosis
• Patients with severe comorbid conditions that preclude surgery
• Patients with critical aortic stenosis who refuse surgical treatment

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 of this procedure, the anatomy of the 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 often require repeat operation and, later, valve replacement.

Aortic valve replacement 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.²⁵

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 for young patients with suitable anatomy. Bioprosthetic devices are less durable than mechanical protheses; 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 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 who experience 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 do experience clinical and functional recovery after AVR, the procedure should usually be offered to these patients. In octogenarians with LV dysfunction, survival may be improved 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; 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 classification status, in accordance with 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, has 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 with a standard approach.

The Ross procedure (aortic and pulmonary valve switch) usually is performed in somewhat young patients.²⁶

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 may 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 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 it may cause syncope. When surgery and valvoplasty are unsuccessful or impossible, digitalis and diuretics may be used to improve symptoms, although their use does not increase life expectancy.

Medical/Legal Pitfalls

• As a result of the dire consequences of missing the diagnosis of symptomatic aortic stenosis, the physician must have a low threshold for obtaining an echocardiogram whenever the possibility of aortic stenosis cannot be excluded during physical examination.
• Asymptomatic patients with suggestive murmurs benefit from early diagnosis, which allows both the patient and the physician to be most vigilant regarding possible early signs and symptoms and to guide the use of prophylactic regimens to prevent bacterial endocarditis.

Special Concerns

• The only effective therapy for aortic stenosis is AVR. After symptoms of aortic stenosis develop, the 3-year mortality rate is 75% in patients who do not undergo AVR; however, after the valve is replaced, survivorship returns to almost normal rates.
• Even octogenarians benefit from valve replacement unless other comorbid factors contraindicate surgery. Hence, AVR should not be denied on the basis of age or because the ejection fraction is reduced.
• • Valve replacement relieves the excess afterload caused by the stenotic valve, and the ejection fraction usually improves dramatically.
  • The exception to this outcome includes patients with a low LV ejection fraction and only a small aortic valve gradient in whom the severity of aortic stenosis may be overestimated. In these patients, LV muscle dysfunction either has another cause or is so severe that it fails to improve after valve replacement.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Aortic stenosis is seen on 2-dimensional echocardiography. Note thickened calcified leaflets.
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Media file 2:  Valvular calcification of aortic stenosis seen with cardiac fluoroscopy during catheterization.
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Media file 3:  Transvalvular gradient seen across the aortic valve during simultaneous recordings of aortic and left ventricular (LV) pressures (cardiac catheterization).
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REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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Article Last Updated: Aug 14, 2008