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CURRENT Diagnosis & Treatment in Cardiology > Chapter 7. Aortic Stenosis >

Essentials of Diagnosis

  • Angina pectoris.
  • Dyspnea (left ventricular heart failure).
  • Effort syncope.
  • Systolic ejection murmur radiating to the carotid arteries.
  • Carotid upstroke delayed in reaching its peak and reduced in amplitude (parvus et tardus).
  • Echocardiography shows thickened, immobile aortic valve leaflets.
  • Doppler echocardiography quantifies increased transvalvular pressure gradient and reduced valve area.

General Considerations & Etiology

Aortic stenosis is the narrowing of the aortic valve orifice, caused by failure of the valve leaflets to open normally. This reduction in orifice area produces an energy loss as laminar flow is converted to a less efficient turbulent flow, in turn increasing the pressure work that the left ventricle must perform in order to drive blood past the narrowed valve. The concentric left ventricular hypertrophy that develops as a major compensatory mechanism helps the left ventricle cope with the increased pressure work it must perform. These factors—turbulence, energy loss, and hypertrophy—constitute the pathophysiologic underpinnings for the patient’s symptoms. The disease is confirmed through history and physical examination, Doppler echocardiography, and cardiac catheterization.

Bicuspid Aortic Valve

This is the most common congenital cardiac abnormality, occurring in approximately 2% of the population. It is believed that the bicuspid valve has hemodynamic disadvantages compared with the normal tricuspid valve, leading to valvular degeneration by mechanisms that are still not fully understood. At least mild aortic stenosis develops in approximately 50% of all patients with bicuspid aortic valves, usually by age 50. Bicuspid aortic valve is associated with aortic dilatation and an increased risk of dissection and rupture, independent of any associated valve disease.

Tricuspid Aortic Valve Degeneration

Many patients born with normal tricuspid aortic valves eventually develop senile degeneration of the valve leaflets and leaflet calcification, thus producing valvular stenosis. Although hypercholesterolemia and diabetes have been defined as risk factors for this degeneration, these conditions account for only a small percentage of all cases. The mechanisms by which some valves degenerate and become stenotic while others remain relatively normal are unknown but are probably related to genetic polymorphisms.

Congenital Aortic Stenosis

Fusion of the valve leaflets before birth produces congenital aortic stenosis that is occasionally detected for the first time in adulthood. In many respects, however, congenital aortic stenosis appears to differ from acquired adult aortic stenosis. The hypertrophy in congenital aortic stenosis is more exuberant, yet heart failure symptoms. The first clinical manifestation of the disease can be sudden death without the development of premonitory symptoms in about 15% of patients.

Rheumatic Fever

Rheumatic fever still occasionally causes aortic stenosis in the United States, although this cause is more common in developing nations. Rheumatic heart disease almost never attacks the aortic valve in isolation, usually also affecting the mitral valve to some degree. A patient with aortic stenosis and a perfectly normal mitral valve is considered to have degenerative rather than rheumatic aortic stenosis.

Other Causes

Systemic lupus erythematosus, severe familial hypercholesterolemia, and ochronosis have occasionally been reported to cause valvular aortic stenosis.

Grotenhuis HB et al. Reduced aortic elasticity and dilatation are associated with aortic regurgitation and left ventricular hypertrophy in nonstenotic bicuspid aortic valve patients. J Am Coll Cardiol. 2007 Apr 17;49(15):1660–5. [PMID: 17433959]

O’Brien KD. Epidemiology and genetics of calcific aortic valve disease. J Investig Med. 2007 Sep;55(6):284–91. [PMID: 17963677]

Clinical Findings

Symptoms and Signs

Angina, effort syncope, and congestive heart failure are the classic symptoms in patients with acquired aortic stenosis. Angina is the presenting symptom in approximately 35% of patients, effort syncope in 15%, and congestive heart failure in 50%. The onset of these symptoms heralds a dramatic increase in the mortality rate for these patients if aortic valve replacement is not performed. Symptoms are therefore the guidepost for intervention, and understanding them is key to understanding and managing the disease.


Angina occurs in response to myocardial ischemia, which develops when left ventricular oxygen demand exceeds supply. It should be noted that although epicardial coronary artery disease may coexist with aortic stenosis, angina frequently occurs in aortic stenosis in the absence of coronary artery disease.

As noted earlier, concentric left ventricular hypertrophy develops as a compensatory response to the pressure overload of aortic stenosis. The load on individual myocardial fibers can best be described as left ventricular wall stress and defined by the Laplace equation:

As left ventricular pressure increases, a parallel increase in left ventricular wall thickness (concentric hypertrophy) helps offset the pressure overload and maintain stress in the normal range. The left ventricular myocardium must produce stress in order to shorten; maintaining normal stress facilitates shortening. This compensatory mechanism is attended by negative pathophysiologic sequelae, however. Despite normal epicardial coronary arteries, the coronary blood flow is reduced; although the flow may be normal at rest, the reserve needed to offset increased oxygen demands during stress or exercise is inadequate, and thus ischemia develops. The exact mechanism by which the coronary blood flow reserve is reduced in aortic stenosis is uncertain, but low capillary density per unit of muscle is at least one operative factor.

Oxygen demand is best estimated clinically by the product of heart rate and wall stress. As noted earlier, the hypertrophy initially maintains wall stress in the normal range, and despite the pressure overload, myocardial oxygen demand is not increased. Eventually, however, the hypertrophy cannot keep pace with the pressure demands of the ventricle, and wall stress increases. This increases oxygen demand and is another factor contributing to ischemia and the symptoms of angina.

Effort Syncope

In general, syncope results from inadequate cerebral perfusion. The syncope of aortic stenosis usually occurs during exercise. One theory for exertional syncope in aortic stenosis is that during exercise total peripheral resistance decreases, but cardiac output cannot increase as it normally does because the narrowed aortic valve restricts the output. Blood pressure is the product of peripheral resistance and cardiac output, so this imbalance causes a drop in blood pressure, leading to syncope.

Another theory is that the very high left ventricular pressure that develops during exercise triggers a reflexive vasodepressor response, leading to a fall in blood pressure. In addition, exercise can cause both ventricular and supraventricular arrhythmias, which in aortic stenosis lead to a fall in effective output and consequently a decrease in blood pressure.

Congestive Heart Failure

Both left ventricular systolic and diastolic failure occur in aortic stenosis and produce the symptoms of dyspnea on exertion as well as orthopnea and paroxysmal nocturnal dyspnea. In some patients, the attendant high left-sided filling pressure leads to pulmonary hypertension, which overloads the right ventricle and thereby produces right ventricular failure and the symptoms of edema and ascites.

Impaired diastolic left ventricular filling in aortic stenosis is primarily due to the increased wall thickness caused by concentric hypertrophy. Because the increased thickness makes the ventricle harder to fill, producing any left ventricular volume requires increased filling pressure. The increased diastolic filling pressure is referred to the left atrium and to the pulmonary veins, where pulmonary venous congestion develops, leading to increased lung water, increased lung stiffness, and dyspnea. The wall composition also changes. Collagen content increases (Figure 7–1), creating a compensatory mechanism that helps translate the increased force generated by the myocardium into chamber contraction. Unfortunately, the increase in collagen further increases ventricular stiffness.

Figure 7–1.

Scanning electron microscopy of normal myocardium (A and C) and pressure-overloaded hypertrophied myocardium (B and D). B shows denser perimysial collagen connections in the hypertrophied myocardium (compared with A, D) shows the thickened tendons in the hypertrophied myocardium (compare with normal myocardium in C).

(Adapted, with permission, from Weber KT. J Am Coll Cardiol. 1989;13:1637.)

Systole is governed by two mechanical properties: contractility and afterload. Contractility is the ability of the myocardium to generate force; afterload is the force the ventricle must overcome to contract. Either property can impair ventricular systole, and both are operative in aortic stenosis. Although the initial concentric hypertrophy normalizes wall stress (afterload), as the disease progresses, the hypertrophy may not keep pace with the increase in pressure and wall stress increases. As stress increases, ejection fraction (EF) decreases:

Reduced ejection fraction is more common in men than women. Inexplicably, women tend to generate more hypertrophy, keeping wall stress low and thus maintaining normal or even supernormal ejection fraction.

Ejection fraction may also decline if contractility falls; however, the exact mechanism of reduced contractility in aortic stenosis is unclear. In the simplest sense, reduced contractility is the result of prolonged overload on the heart. Loss of contractile elements and ischemia from abnormal coronary blood flow are two of the mechanisms that have been postulated to explain the reduction.

Physical Examination

Systolic Ejection Murmur

The classic murmur of aortic stenosis is a medium-pitched and often harsh systolic ejection murmur, heard best in the aortic area and radiating to the carotid arteries. In mild disease, the murmur peaks early in systole. As the disease worsens, the murmur peaks later, increases in intensity, and may be associated with a thrill palpated in the aortic area. With further progression of aortic stenosis, the murmur peaks very late in systole. It may decrease in intensity as cardiac output begins to fall, and the thrill may disappear. In advanced but still correctable disease, the murmur may become very unimpressive and be reduced to a grade II/VI or even a grade I/VI murmur, sometimes misleading the examiner into believing that severe disease is not present.

Sometimes the murmur is heard well over the aortic area, fades over the midsternum, and reappears over the apex (Gallavardin phenomenon). The diagnostician may be misled into believing that two separate murmurs—one of aortic stenosis and one of mitral regurgitation—are present. Distinguishing between Gallavardin phenomenon and two separate murmurs is difficult but important: The appearance of even mild mitral regurgitation in aortic stenosis is an ominous prognostic sign. If the diagnosis cannot be settled at the bedside, color-flow Doppler examination of the mitral valve will resolve the issue.

Carotid Upstroke

Carotid upstroke in aortic stenosis is typically low in volume and delayed in reaching the peak amplitude (Figure 7–2). Palpation of this parvus et tardus pulse is probably the single best way to estimate the severity of aortic stenosis at the bedside. The examiner should palpate his or her own carotid artery with one hand while palpating the patient’s carotid artery with the other, thus gauging the difference between normal and abnormal. A palpable shuddering sensation of the carotid pulse may also be noted. In elderly patients, increased stiffness of the carotid arteries may falsely normalize the upstroke, making it feel relatively brisk in nature. Even in this circumstance, however, the upstroke is rarely completely normal in character.

Figure 7–2.

A: A carotid pulse tracing from a normal subject. B: A tracing from a patient with aortic stenosis. The upstroke in B is quite delayed and demonstrates a shudder.

Second Heart Sound

Paradoxic splitting of the second heart sound is due to the prolonged ejection time required to expel stroke volume through the stenotic valve, which delays the closure of the aortic valve (A2) past closure of the pulmonic valve (P2). Although paradoxic splitting is emphasized in many texts, a more common finding is that the reduced movement of the aortic valve renders A2 inaudible and only a soft, single second sound (P2) is heard.

Apical Impulse

Because in aortic stenosis the left ventricle is usually concentrically hypertrophied and its volume is not increased, the point of maximum impulse is usually felt in its normal position. The apex beat, however, is abnormally forceful and sustained in nature. The left atrial contribution to left ventricular filling may be both visible and palpable; it corresponds to the fourth heart sound and is usually present in aortic stenosis as a result of increased left ventricular stiffness.

Other Findings

In far-advanced disease with congestive heart failure, a third heart sound is often heard. Pulmonary hypertension may develop, increasing the intensity of the pulmonic component of the second sound. At their initial visit, patients with aortic stenosis may also have right ventricular failure manifested as edema and ascites.

Diagnostic Studies


The concentric left ventricular hypertrophy that develops in aortic stenosis is often reflected in the electrocardiogram (ECG) as increased QRS voltage, left atrial abnormality, and ST and T wave abnormalities. The ECG, however, does not always demonstrate left ventricular hypertrophy even though the heart is actually hypertrophied. No ECG findings are, therefore, either sensitive or specific for aortic stenosis.

Chest Radiography

Patients with aortic stenosis usually show a normal-sized heart on a chest radiograph. The left heart border may develop a rounded appearance consistent with concentric left ventricular hypertrophy; the aortic shadow may become enlarged because of post-stenotic dilation. Occasionally, calcification of the aortic valve can be seen on the lateral view.


Echocardiographic examination of the heart combined with Doppler investigation of the aortic valve usually can confirm the diagnosis of aortic stenosis; a technically adequate study can accurately quantify its severity. Echocardiography shows thickening of the aortic valve, reduced leaflet mobility, and concentric left ventricular hypertrophy, demonstrating the presence of aortic stenosis but not quantifying its severity.

The Doppler study can be used to determine the gradient across the aortic valve and to calculate aortic valve area. Doppler quantification of aortic stenosis is based on the ability to measure blood velocity. Flow through an orifice is equal to cross-sectional orifice area times velocity. As shown in Figure 7–3, velocity must increase when a moving stream of a given flow reaches a narrowed area if the flow is to remain constant when it reaches the constriction. That is, the product of the velocity times area at the first orifice must be equal to that at the second orifice.

Figure 7–3.

Constant flow through a tube of different diameters. As the flow reaches the narrowed orifice A 2, velocity must increase in order for the flow to remain constant.

Measuring the area of the aortic outflow tract (A  1), the velocity of flow there (V  1), and the velocity at the stenosis (V  2), the aortic valve area (A 2) can be calculated as follows:

The velocity of flow at the stenosis can also be used to calculate the aortic pressure gradient using the modified Bernoulli equation:

Figure 7–4 shows the velocity profile from Doppler examination of a patient with aortic stenosis. The velocity of 4 m/s thus translates to a gradient of 64 mm Hg.

Figure 7–4.

The Doppler wave form; flow across a stenotic aortic valve. Flow accelerates to 4 m/s, which translates to a gradient of 64 mm Hg.

(Adapted, with permission, from Assey et al. The patient with valvular heart disease. In: Pepine CJ, Hill JA, Lambert CR, eds. Diagnostic and Therapeutic Cardiac Catheterization. Philadelphia: Williams & Wilkins, 1998.)

This technique is remarkably accurate compared with gradients measured invasively by catheter. In general, a mean gradient greater than 50 mm Hg or an aortic valve area less than 0.8 cm2 indicates that the aortic stenosis is severe enough to cause the patient’s symptoms. Many exceptions to this rule exist, however. Some patients remain asymptomatic despite higher gradients and smaller valve areas, and others become symptomatic with lower gradients and larger valve areas.

Cardiac Catheterization

Although Doppler echocardiography is an accurate means of determining the severity of aortic stenosis in most patients, other noninvasive techniques are generally not recommended. Stress testing, for example, can be dangerous, and left-ventricular hypertrophy makes cardiac perfusion imaging and the interpretation of ECGs problematic. Cardiac catheterization (whose main purpose is coronary angiography) is indicated when symptoms such as angina pectoris could be caused by coronary disease or aortic stenosis or when valve replacement surgery is planned. The presence and severity of coronary disease will influence the course of therapy, tipping the balance toward surgery when the aortic stenosis is of borderline severity.

During cardiac catheterization, cardiac output and aortic valve gradient are measured; these data are used to assess stenosis severity by calculation of aortic valve area. Great care must be used in assessing both parameters because errors in estimating the stenosis will be proportional to any measurement errors. The cardiac output is measured using the Fick principle or the indicator-dilution principle (usually thermodilution). The gradient is obtained by placing one catheter in the left ventricle (by retrograde or transseptal technique) and a second catheter in the proximal aorta on the other side of the stenotic valve. The pressure difference (gradient) is measured by recording the two pressures simultaneously. Recent studies discredit the use of a femoral artery sheath to record the downstream pressure. Left ventricular and femoral artery pressure waves occur at different times, so the tracings are aligned to compensate for this. This practice, however, may underestimate the true gradient by as much as 50%.

The cardiac output and gradient are then used to calculate the aortic valve area using the Gorlin formula:

where AVA = aortic valve area, CO = cardiac output, G = mean aortic valve gradient, SEP = systolic ejection period (in seconds), and HR = heart rate. A valve area of less than 0.7–0.8 cm2 usually indicates critical aortic stenosis, a severity of disease capable of causing symptoms, morbidity, and death. A symptomatic patient with a valve area of less than 0.8 cm2 will usually require aortic valve replacement because the presence of symptoms connotes a poor prognosis and the constricted valve area suggests that the aortic stenosis is causing those symptoms. A caveat: Although the Gorlin formula is reasonably accurate in predicting the orifice area in severe disease, it was validated in patients with mitral—not aortic—stenosis. When used to calculate the aortic valve area, the Gorlin formula is flow-dependent; that is, the valve area varies directly with the flow. This dependence can be the result of the increased flow physically increasing the orifice; the increased calculated area and flow can also represent a problem with the formula. In either case, the calculated area depends on the patient’s cardiac output at the moment. This is not a factor in severe disease with a large transvalvular gradient for which the formula almost always correctly predicts a critically narrowed valve. In some patients with very low cardiac outputs and low transvalvular gradients, however, the formula calculates a severely narrowed aortic valve area when no severe aortic stenosis is actually present. In such cases, increasing the cardiac output by infusion of dobutamine allows for recalculation of the valve area at a higher output. If the aortic valve area then exceeds 1.0 cm2 or the gradient fails to increase markedly despite an increase in output, the stenosis is probably relatively mild and not the cause of the patient’s symptoms or cardiac failure. Dobutamine infusion can be used with echocardiography or cardiac catheterization.

Valve resistance, which is simply the gradient divided by flow, is gaining credibility as another measure of stenosis severity. A resistance greater than 250 dynes x s x cm–5 probably indicates severe stenosis. Valve resistance (VR) is calculated using the following formula:

and is expressed as dynes x s x cm–5.

Patient Examples of Aortic Stenosis

The following cases are examples of patients with varying degrees of aortic stenosis (PCW = pulmonary capillary wedge):

Case 1

Symptoms: angina, dyspnea

PCW: 16 mm Hg

CO: 4.5 L/min

HR: 70 bpm

SEP: 0.33 s

G: 72 mm Hg

EF: 55%

Both calculations indicated severe aortic stenosis; the gradient was large and the patient symptomatic. Surgery was therefore mandatory because this patient undoubtedly suffered from severe symptomatic aortic stenosis.

Case 2

Symptoms: dyspnea, orthopnea

PCW: 26 mm Hg

CO: 3.3 L/min

HR: 70 bpm

SEP: 0.28 s

G: 30 mm Hg

EF: 30%

In this case, the calculated aortic valve area indicated moderately severe aortic stenosis that required surgery; the valve resistance was borderline, suggesting the stenosis might be less severe. To evaluate the patient further, nitroprusside was cautiously infused and titrated. The repeat hemodynamics showed the following:

PCW: 16 mm Hg

CO: 4.5 L/min

HR: 80 bpm

SEP: 0.25 s

G: 30 mm Hg

AVA: 0.93 cm2

VR: 177 dynes x s x cm–5

Both indexes now indicated moderate—but not critical—aortic stenosis. That the disease was only moderate is further suggested by the lack of an increase in gradient when the cardiac output increased. It was also indicated by improvement in the hemodynamics with infusion of a vasodilator (which, in true aortic stenosis, could be expected to cause deterioration rather than improvement). In this case, an independent cardiomyopathy was probably responsible for the reduced ejection performance. The moderate aortic stenosis played a detrimental role but was not responsible for the patient’s condition. He subsequently improved with long-term administration of an angiotensin-converting enzyme (ACE) inhibitor, a result that would not have been anticipated in severe outflow tract obstruction.

Cardiac Computed Tomography (CT)

The progression of aortic sclerosis (calcium deposits in the aortic valve) can be monitored by cardiac CT, and it can be used to quantify the amount of calcium in the aortic valve. However, there is poor correlation between valve calcium and the hemodynamic severity of aortic stenosis. One study has found that the severity of calcification of the valve in aortic stenosis is associated with worse clinical outcomes.

Attenhofer Jost CH et al. Echocardiography in the evaluation of systolic murmurs of unknown cause. Am J Med. 2000 Jun 1;108(8):614–20. [PMID: 10856408]

Freeman RV et al. Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies. Circulation. 2005 Jun 21;111(24):3316–26. [PMID: 15967862]

Monin JL et al. Low-gradient aortic stenosis: operative risk stratification and predictors for long-term outcome: a multicenter study using dobutamine stress hemodynamics. Circulation. 2003 Jul 22;108(3):319–24. [PMID: 12835219]

Nishimura RA et al. Low-output, low-gradient aortic stenosis in patients with depressed left ventricular systolic function: the clinical utility of the dobutamine challenge in the catheterization laboratory. Circulation. 2002 Aug 13;106(7):809–13. [PMID: 12176952]

Phoon CK. Estimation of pressure gradients by auscultation: an innovative and accurate physical examination technique. Am Heart J. 2001 Mar;141(3):500–6. [PMID: 11231450]

Popovic AD et al. Echocardiographic evaluation of valvular stenosis: the gold standard for the next millennium? Echocardiography. 2001 Jan;18(1):59–63. [PMID: 11182784]

Rifkin RD. Physiological basis of flow dependence of Gorlin formula valve area in aortic stenosis: analysis using an hydraulic model of pulsatile flow. J Heart Valve Dis. 2000 Nov;9(6):740–51. [PMID: 11128779]

Rosenhek R et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000 Aug 31;343(9):611–7. [PMID: 10965007]


The only effective therapy for severe aortic stenosis is relief of the mechanical obstruction posed by the stenotic valve. Figure 7–5 shows the natural course of aortic stenosis: Survivorship is excellent until the classic symptoms of angina, syncope, or congestive heart failure develop. At that point, survival declines sharply. Treatment includes such modalities as aortic balloon valvotomy, valve débridement, and valve replacement.

Figure 7–5.

The natural history of aortic stenosis. There is little change in survival until the symptoms of angina, syncope, or heart failure develop. Then the decline is precipitous.

(Adapted, with permission, from Ross J Jr et al. Circulation. 1968;38(Suppl V):V-61.)

Pharmacologic Therapy

There is no effective pharmacologic treatment for severe aortic stenosis, and in some instances medication may be harmful. Although digitalis and diuretics may temporarily help improve congestive heart failure, unless the aortic valve is replaced, the heart failure will worsen and lead to death. It should also be noted that although ACE inhibitors prolong life in most cases of congestive heart failure, they are contraindicated in severe aortic stenosis. Vasodilators decrease total peripheral resistance, usually increasing cardiac output and providing a beneficial effect in other cardiac diseases. In severe aortic stenosis, however, because cardiac output across the stenotic valve cannot increase, the fall in total peripheral resistance leads to hypotension—which can be fatal. In milder disease (such as Case 2 [described earlier]) that is associated with other causes of heart failure, vasodilators can be used to treat the underlying independent cardiomyopathy. Nitrates can be used cautiously in severe disease to treat angina until surgery is performed. -Adrenergic blocking agents must be used with great caution or avoided entirely: They may unmask the left ventricle’s dependence on adrenergic support for pressure generation and thereby cause shock or heart failure.

Because patients with aortic stenosis share some risk factors with patients with atherosclerosis, there has been enthusiasm for using cholesterol lowering drugs to decrease the progression of aortic stenosis. Studies to date have shown mixed results. Clearly, if patients with aortic stenosis have elevated low-density lipoprotein (LDL) cholesterol levels, they should be treated.

The latest guidelines have eliminated the need for antibiotic prophylaxis in patients with aortic stenosis to prevent infective endocarditis except for prosthetic valves.

Aortic Balloon Valvuloplasty

This procedure involves a percutaneous catheterization in which a large-bore balloon is placed retrograde across the stenotic aortic valve. Inflating the balloon fractures calcium deposits in the leaflets and stretches the aortic annulus, increasing the valve area. Although the procedure is of some benefit in cases of congenital aortic stenosis, in which the leaflets are not calcified, the results in adults have been disappointing. The procedure produces no regression in left ventricular hypertrophy, the gradient is reduced acutely by only about 50%, and the valve area remains in the critical stenosis range. Six months after the procedure, 50% of the patients have completely lost even that modest benefit. The periprocedural mortality rate is 2–5%, and the ultimate mortality rate is the same as that of the natural course of the disease without intervention.

It is important that patients understand that balloon valvuloplasty is not an alternative to aortic valve replacement. Because the procedure produces only transient mild hemodynamic benefits at high risk and does not reduce the high mortality rate of untreated aortic stenosis, it should be considered only a palliative measure for patients whose other severe systemic illnesses preclude surgery. Occasionally, it may provide a bridge to surgery for severely symptomatic patients who need time to recover from another illness prior to aortic valve surgery.

Surgical Therapy

Aortic Valve Replacement


As noted earlier, survival in aortic stenosis drops sharply when the classic symptoms of angina, effort syncope, or congestive heart failure appear. Fifty percent of the patients with aortic stenosis in whom angina pectoris develops are dead within 5 years of its onset if aortic valve replacement is not undertaken. Half the patients with syncope will be dead within 3 years, and 50% of the patients with congestive heart failure will be dead within 2 years without surgical correction. The exact pathophysiologic changes that produce the onset of symptoms and begin this rapid downhill course are unknown. It is known that in some cases the stenosis can worsen relatively rapidly, going from mild to severe in a year or two. Worsening stenosis increases the pressure overload on the left ventricle, which presumably reaches a point of decompensation manifested as the onset of symptoms.

Recent studies confirm the benignity of the asymptomatic state in aortic stenosis. In asymptomatic patients with proven peak Doppler gradients equal to or greater than 50 mm Hg, the incidence of sudden death is less than 1% per year. Therefore, surgery is generally not indicated for asymptomatic patients with aortic stenosis. The surgical mortality is at least 2–3%, and even this low figure cannot be justified in the absence of symptoms. However, outcomes in asymptomatic patients vary widely. Some evidence suggests that those with severe valve calcification or rapidly increasing valvular velocity on repeated Doppler studies have a poor prognosis and perhaps should be considered for surgery despite a lack of symptoms.

It must be made clear, however, that benignity of the asymptomatic condition pertains only to adult-acquired aortic stenosis. Children in whom the disease has been present from birth respond differently, and sudden death in the absence of symptoms is common. Asymptomatic children with aortic stenosis should probably undergo surgery once a peak gradient of 75 mm Hg develops, and sooner if symptoms are present.

The mortality rate in adults rapidly increases to about 5% within 3 months of the onset of symptoms and is a remarkable 75% in 3 years if surgical correction is not undertaken. Adults with aortic stenosis should be operated on shortly after the development of symptoms. A reasonable strategy for patients with asymptomatic aortic stenosis is to obtain an initial Doppler echocardiographic study. If the mean gradient is more than 30 mm Hg, the patient should undergo a history and physical examination every 6 months—with instructions to alert the physician immediately if symptoms occur. When close questioning reveals that symptoms have developed, the Doppler echocardiographic study can be repeated to confirm that the aortic stenosis has worsened. If the patient is in the coronary-disease-prone age range, cardiac catheterization to confirm the hemodynamics and to define coronary anatomy should be performed at that time, with an eye toward aortic valve replacement in the near future.

In Advanced Disease

Because aortic valve replacement instantaneously reduces afterload by removing or substantially reducing the pressure gradient, left ventricular performance improves immediately. Thus, patients with far-advanced disease and severe congestive heart failure may respond to aortic valve replacement with a dramatically rapid improvement following surgery. Even patients with ejection fractions of less than 20% may experience a doubling in both ejection fraction and forward output, with a reduction in filling pressures and pulmonary edema early after aortic valve replacement. Over time, left ventricular hypertrophy regresses, contractile function may improve, and ejection fraction may return completely to normal—even though it was profoundly depressed before surgery (Figure 7–6). Therefore, even when the disease is far advanced and is attended by severe congestive heart failure, it is almost never too late to perform aortic valve replacement for patients with aortic stenosis except, of course, when it is inappropriate.

Figure 7–6.

The effect of aortic valve replacement on preoperatively depressed ejection fraction. With the exception of one patient who suffered an intraoperative myocardial infarction, all patients demonstrated improved ejection fraction as afterload was reduced following surgery.

(Adapted, with permission, from Smith N et al. Circulation. 1978;58:255.)


The amount of afterload reduction that can be effected by removing the aortic valve obstruction is proportional to the gradient. In patients with a low mean transvalvular gradient, the increase in ejection fraction and cardiac output that occurs after surgery is limited because afterload reduction is limited. In fact, most patients with a low transvalvular gradient (< 30 mm Hg) and far-advanced heart failure do not improve following aortic valve replacement. It is also clear, however, that some patients do improve—even dramatically—despite a low gradient. Why some patients improve and most do not is currently unknown. Unfortunately, at this time, the outcome for the patient with a low gradient and far-advanced heart failure cannot be predicted. What is known is that such patients are at high risk when undergoing aortic valve replacement, and such patients need to be advised of the precarious nature of the surgery if it is undertaken.

Effects of Age

Age should not be considered a major factor when deciding if surgery should be undertaken. Although advanced age increases the risks of surgical mortality and postsurgical morbidity, it must be recognized that age is a risk factor in even apparently healthy patients without aortic stenosis. Once age is corrected for, the mortality rate following aortic valve replacement surgery for aortic stenosis approaches that of the normal population for that age range. In fact, aortic valve replacement for aortic stenosis in patients older than age 65 is one of the few conditions where cardiac surgery returns the patient to the expected longevity of the general population of that age range.


Replacement of the aortic valve removes or greatly reduces the pressure overload placed on the left ventricle by aortic stenosis. Left ventricular systolic pressure and afterload are significantly reduced, leading to improved ejection performance and cardiac output and reduced left ventricular filling pressure. Subsequently, the left ventricular hypertrophy regresses, most of it in the first year following surgery; full regression, however, may not occur for as long as a decade. The abnormal coronary blood flow and blood flow reserve caused by aortic stenosis also improve as the hypertrophy regresses. Although diastolic function improves as the wall thins, it may not completely return to normal because the increased collagen content (see Figure 7–1) that developed in response to the pressure overload does not regress fully. A persistently increased collagen content causes the left ventricular stiffness to be greater than normal.


Aortic valve replacement can be accomplished using the patient’s own pulmonic valve, a bioprosthesis, or a mechanical prosthesis. Each has its own inherent risks and benefits.

Pulmonic valve transplantation (Ross procedure)

In this procedure, the patient’s native pulmonic valve (autograft) is removed and sewn into the aortic position. A prosthetic valve or a pulmonic homograft is then sewn into the pulmonic position. This maneuver improves the patient’s condition because the native, viable pulmonic valve with its excellent hemodynamic characteristics and durability is sewn into the high-pressure, high-stress, left-sided circuit where prostheses can fail. The bioprosthesis or homograft placed in the pulmonic position is under low pressure and low stress; it is more durable here than it would be in the aortic position.

The major disadvantage of the pulmonic autograph is the amount of surgery involved. It is a technically very demanding procedure and, although excellent results have been reported from a few centers, it may not be applicable to every hospital’s surgical program.


Two general types of bioprostheses are available: heterografts and homografts. Heterografts are constructed from either porcine aortic valve leaflets or bovine pericardium (both preserved with glutaraldehyde). Heterografts have had a wide application, and much is known about their advantages and disadvantages. The major advantage of this bioprosthesis is its low thromboembolic potential. In the absence of atrial fibrillation, the risk of thromboembolism following aortic valve bioprosthetic implantation is less than 1 event per 100 patient years, and anticoagulation is not required. Atrial fibrillation substantially increases thromboembolic risk, as it does in patients with native valves. In the absence of a contraindication, anticoagulation is therefore probably advisable in patients with atrial fibrillation. Anticoagulation is unnecessary in patients with normal sinus rhythm.

The major disadvantage of heterografts is their limited durability. Primary valve failure occurs in only 10% of patients 10 years following implantation of a bioprosthesis in the aortic position, but valve failure rapidly accelerates after that period; approximately 50% of valves have failed within 15 years. Calcification and degeneration of the valves leads to tears in the cusps or stenosis of the valve or flail leaflets. Degeneration is greatly accelerated in younger patients, and heterograft bioprostheses should not be used in patients younger than 35 years of age—except for young women who wish to become pregnant. Because anticoagulation with warfarin produces an unacceptable rate of fetal mortality, valve replacement with a bioprosthesis that does not require anticoagulation may be preferable. The patient must understand, however, that a second valve replacement will probably be required.

A second disadvantage to bioprosthesis is a modest obstruction to outflow and a residual pressure gradient in patients requiring implantation of small valves.

The ideal patient for heterograft bioprosthesis implantation is the elderly patient whose life expectancy is less than the durability span of the valve or the patient for whom anticoagulation poses a significant risk.

Cryopreserved homografts, which are harvested from human donors, have an excellent hemodynamic profile. They are ideal for use in patients with a small aortic root where other types of prostheses might cause a transvalvular gradient. They are also relatively resistant to bacterial endocarditis. Although homografts may be more durable than heterograft valves, long-term follow-up data on large numbers of cryopreserved homografts are currently unavailable. In addition, the use of homograft valves is limited by availability. Because many potential donors for homograft valves are also whole-heart donors, the number of available homografts is small.

Mechanical valves

Compared with bioprostheses, mechanical valves, such as the bileaflet valve, have superior durability. All mechanical valves require anticoagulation, however. Thromboembolic complications possible in the absence of anticoagulation include stroke and fixation of the valve in either the open or closed position. With proper anticoagulation, these events are reduced to 1 event per 100 patient years; the risk of anticoagulant hemorrhage is approximately 0.5%/year. Anticoagulation therapy should be targeted to maintain the prothrombin time at 1.5 times control (international normalized ratio [INR] 2.5–3.5). Mechanical valves are typically implanted in younger patients for whom long-term durability is important and in whom anticoagulation can be accomplished at lower risk than in elderly patients. Although caged-ball and tilting-disk valves were popular in the twentieth century, the bileaflet valves are most commonly used today.

Aortic Valve Débridement

Both mechanical and ultrasonic débridement of the aortic valve to remove calcium deposits and increase leaflet mobility have met with limited success in calcific aortic stenosis. Surgical débridement usually results in significant residual stenosis that worsens in time. Ultrasonic débridement, using sound waves to pulverize the calcium deposits, dramatically reduces the aortic valve gradient and produces excellent results 6 months after surgery. Unfortunately, aortic insufficiency develops in many patients shortly thereafter as the integrity of the leaflets is impaired. Most current data suggest either mechanical or ultrasonic débridement is a poor alternative to aortic valve replacement.

The development of new techniques for engaging the patient with the heart–lung pump and stabilizing the heart during surgery have allowed for heart operations through limited thoracic incisions. Although results similar to conventional sternotomy have been reported for aortic valve surgery in some centers, total surgical time, pump time, and aorta cross-clamp time are significantly increased. On the other hand, patients appreciate the smaller incisions. Whether these minimally invasive approaches will replace conventional techniques is not clear at this time.

Recently, a collapsible bioprosthetic valve mounted in a large stent has been deployed percutaneously for aortic stenosis. Although often successful, some have failed to stay put and damage to the left-sided conduction system can occur. Currently, such devices are experimental, but improvements with experience will eventually result in a percutaneous alternative to aortic valve surgery.

Aikawa K et al. Timing of surgery in aortic stenosis. Prog Cardiovasc Dis. 2001 May–Jun;43(6):477–93. [PMID: 11431802]

Connolly HM et al. Severe aortic stenosis with low transvalvular gradient and severe left ventricular dysfunction: result of aortic valve replacement in 52 patients. Circulation. 2000 Apr 25;101(16):1940–6. [PMID: 10779460]

Cowell SJ et al; Scottish Aortic Stenosis and Lipid Lowering Trial Impact on Regression (SALTIRE) Investigators. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med. 2005 Jun 9;352(23):2389–97. [PMID: 15944423]

Cribier A et al. Early experience with percutaneous transcatheter implantation of heart valve prosthesis for the treatment of end-stage inoperable patients with calcific aortic stenosis. J Am Coll Cardiol. 2004 Feb 18;43(4):698–703. [PMID: 14975485]

Moura LM et al. Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis. J Am Coll Cardiol. 2007 Feb 6;49(5):554–61. [PMID: 17276178]

Oswalt JD et al. Highlights of a 10-year experience with the Ross procedure. Ann Thorac Surg. 2001 May;71(5 Suppl):S332–5. [PMID: 11388217]

Pereira JJ et al. Survival after aortic valve replacement for severe aortic stenosis with low transvalvular gradients and severe left ventricular dysfunction. J Am Coll Cardiol. 2002 Apr 17;39(8):1356–63. [PMID: 11955855]

Pessotto R et al. Midterm results of the Ross procedure. Ann Thorac Surg. 2001 May;71(5 Suppl):S336–9. [PMID: 11388218]

Pierri H et al. Clinical predictors of prognosis in severe aortic stenosis in unoperated patients > or = 75 years of age. Am J Cardiol. 2000 Oct 1;86(7):801–4. [PMID: 11018208]

Rosenhek R et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000 Aug 31;343(9):611–7. [PMID: 10965007]

Sundt TM et al. Quality of life after aortic valve replacement at the age of > 80 years. Circulation. 2000 Nov 7;102(19 Suppl 3):III70–4. [PMID: 11082365]


As noted earlier, the natural course and thus the prognosis of unoperated aortic stenosis are widely known. Once symptoms develop, aortic stenosis becomes a lethal disease with a 3-year mortality rate of 75%. Figure 7–7 compares the mortality rate of two groups of patients with symptomatic aortic stenosis: those who refused surgery, and patients who underwent it. The difference is dramatic. Overall, the 10-year survival rate following aortic valve replacement for pure aortic stenosis is 75%. The age-adjusted survivorship after surgery remains excellent even in octogenarians free of other cardiac or systemic diseases.

Figure 7–7.

The effect of aortic valve replacement in patients with symptomatic severe aortic stenosis (solid circle) compared with the survivorship of similar patients who refused surgery (open circle).

(Adapted, with permission, from Schwarz F et al. Circulation. 1982;66:1105.)

Asymptomatic patients generally have a good prognosis; however, symptoms will develop within 5 years in most patients with hemodynamically significant aortic stenosis, and the risk of sudden death will be 1% per year. Certain factors, such as reduced left ventricular ejection fraction, an enlarged left ventricle, and severe valve calcification, are known to reduce patient’s survival. Also, patients with hypercholesterolemia, hypercalcemia, or elevated serum creatinine tend to progress more rapidly and should be monitored closely. Whether progressive stenosis can be delayed or halted by altering cholesterol levels or other biologic factors is unknown.

Coincident Disease

Coronary artery disease is the single most important coincident disease that affects the prognosis of aortic stenosis. Figure 7–8 shows that the prognosis for patients with aortic stenosis and coronary disease worsens almost immediately following surgery, compared with the prognosis of corrected isolated aortic stenosis. Coronary bypass surgery may improve this prognosis, but this point is controversial. What is not controversial is that even with complete revascularization the prognosis of combined aortic stenosis and coronary disease does not equal that of isolated aortic stenosis. Some experts have advocated correcting only the aortic stenosis in patients with combined disease because the addition of coronary bypass grafting has not been clearly shown to prolong survival. These results, however, were acquired before the more recent extensive use of artery grafts, which are superior to vein grafts. Modern results may be better. Therefore, because there is no definitive answer regarding the efficacy of combined coronary bypass grafting and aortic valve replacement, grafting seems prudent when angina is one of the patient’s symptoms or when left-main or three-vessel disease is present.

Figure 7–8.

The effects of coronary disease (open circle) on survivorship of patients with aortic stenosis (AS) or aortic stenosis and regurgitation (as/ar) following surgery shown and compared with that of isolated AS or as/ar (solid circle). CAD, coronary artery disease.

(Adapted, with permission, from Miller DC et al. Am J Cardiol. 1979;43:494.)

Acquired von Willebrand syndrome (type 2A) is observed in most patients with severe aortic stenosis and is associated with increased skin or mucosal bleeding in about 20%. Hemostatic abnormalities often disappear the first day after valve replacement surgery suggesting that they are related to high shear stress. These abnormalities can recur if there is a mismatch between patient and prosthesis size. Patients with severe aortic stenosis are at risk for bleeding before and during surgery, especially if they have Heyde syndrome with gastrointestinal angiodysplasia.


Implantation of a prosthetic heart valve is not curative. The severe risks of native valve aortic stenosis have instead been exchanged for the lesser risks inherent to prosthetic valves. Lifelong regular follow-up of patients with prostheses is therefore required. If anticoagulation therapy is used, periodic surveillance of the prothrombin time is needed, and alterations in dosage must be made to maintain it at 1.5 times control. The prothrombin time should be tested at least once a month and more frequently if a stable dose of warfarin and the degree of anticoagulation have not yet been obtained. Many avoidable complications of prostheses result from improper anticoagulation.

Endocarditis prophylaxis is more important in the presence of a prosthetic valve than in the presence of an abnormal native valve. Infection of a prosthesis is often fatal, and even when the infection is cured, the valve almost always requires re-replacement. Prevention of prosthetic valve endocarditis by antibiotic administration before and after dental and other surgery is therefore advised.

Implantation of a prosthesis makes the Doppler echocardiographic evaluation of valve function difficult. Although acoustic shadowing around the prosthesis hinders echocardiographic and Doppler interpretation, each valve has a characteristic Doppler profile that should be recorded early following surgery. If subsequent symptoms of congestive heart failure or syncope develop, another ultrasound study can be made for comparison. A significant deviation from the initial study may indicate that prosthetic stenosis or regurgitation is now present and responsible for the recurrence of the patient’s symptoms. Transesophageal echocardiography is usually better able to visualize morphologic details of a prosthetic valve than transthoracic echocardiography and is indicated for suspected valve failure, thrombosis, or endocarditis. Cinefluoroscopy is also useful for assessing valve motion and diagnosing leaflet or ball-motion abnormalities. The suspicion of valve dysfunction is usually confirmed by cardiac catheterization. It should be noted, however, that when prosthetic stenosis is suspected, the gradient across the valve may be difficult to obtain invasively. Retrograde passage of the catheter across a tilting disk valve may result in catheter entrapment, a potentially fatal complication. Retrograde passage of a catheter across a bileaflet valve may damage the leaflets; this practice should be avoided. Transseptal catheterization is often the safest way to obtain a transvalvular gradient if prosthetic aortic valve stenosis is suspected.

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Pellikka PA et al. Outcome of 622 adults with asymptomatic hemodynamically significant aortic stenosis during prolonged follow-up. Circulation. 2005 Jun 21;111(24):3290–5. [PMID: 15956131]

Rossi A et al. Echocardiographic prediction of clinical outcome in medically treated patients with aortic stenosis. Am Heart J. 2000 Nov;140(5):766–71. [PMID: 11054623]

Veyradier A et al. Abnormal von Willebrand factor in bleeding angiodysplasias of the digestive tract. Gastroenterology. 2001 Feb;120(2):346–53. [PMID: 11159874]

Vincentelli A et al. Acquired von Willebrand syndrome in aortic stenosis. N Engl J Med. 2003 Jul 24;349(4):343–9. [PMID: 12878741]

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