Approach Considerations
Diagnostic studies in the emergency department should include electrocardiography (ECG), chest radiography, serum electrolyte levels, cardiac biomarkers, and a complete blood count (CBC). Arterial blood gas measurements are generally not necessary but may be obtained if hypoxemia or a mixed respiratory disease state is suspected.
Two-dimensional and Doppler echocardiography is the imaging modality of choice to diagnose and determine the severity of aortic stenosis. In general, cardiac catheterization is not necessary to determine the severity of aortic stenosis. However, in instances in which clinical findings are not consistent with echocardiogram results, cardiac catheterization is recommended for further hemodynamic assessment.
Go to Imaging in Aortic Stenosis for more complete information on this topic.
Echocardiography
The American College of Cardiology/American Heart Association (ACC/AHA) recommendations from the ACC/AHA 2006 valvular heart disease guidelines for echocardiography in aortic stenosis are summarized below, in Table 2.[11] LV size, mass, and function should also be evaluated in each patient.
Table 2. ACC/AHA Recommendations for Echocardiography (Imaging, Spectral, and Color Doppler) in Aortic Stenosis (Open Table in a new window)
| Indication | Class |
| Diagnosis and assessment of severity of aortic stenosis | I |
| Assessment of LV size, function, and/or hemodynamics | I |
| Reevaluation of patients with known aortic stenosis with changing symptoms or signs | I |
| Assessment of changes in hemodynamic severity and ventricular function in patients with known aortic stenosis during pregnancy | I |
| Reevaluation of asymptomatic patients with severe aortic stenosis | I |
| Reevaluation of asymptomatic patients with mild to moderate aortic stenosis and evidence of LV dysfunction or hypertrophy | IIa |
| Routine reevaluation of asymptomatic adult patients with mild aortic stenosis who have stable physical signs and normal LV size and function | III |
Two-dimensional transthoracic echocardiography can confirm the clinical diagnosis of aortic stenosis and provide specific data on LV function. The etiology of aortic stenosis (bicuspid, rheumatic, or degenerative calcific) may be assessed from the 2D echocardiographic, parasternal, short-axis view (see the image below). The structure and function of the other heart valves can also be assessed.
Calcific aortic stenosis (parasternal long-axis and short-axis views). The following 3 echocardiographic findings are indicative of severe aortic stenosis:
- An echo-dense aortic valve with no cusp motion (may be unreliable in congenital or rheumatic valvular stenosis)
- A decrease in the maximal aortic cusp separation (< 8 mm in the adult)
- The presence of otherwise unexplained LV hypertrophy
Although the presence of aortic stenosis is readily diagnosed with 2D echocardiography, the severity of aortic stenosis cannot be judged based on the 2D echocardiographic images alone. Doppler echocardiography is an excellent tool for assessing the severity of aortic stenosis.
Using the modified Bernoulli equation, a maximum instantaneous and mean aortic valve gradient can be derived from the continuous-wave Doppler velocity across the aortic valve. In a laboratory with experienced personnel, Doppler-derived aortic valve gradients are accurate and reproducible and correlate well with those obtained during cardiac catheterization.
The transvalvular gradient is dependent on the severity of obstruction and the flow across the valve. In patients with low cardiac output, the valvular stenosis may be severe even though the transvalvular gradient is low. To overcome this problem, 2D Doppler echocardiography can also provide a reliable estimation of aortic valve area (AVA). The echocardiographic criteria for assessment of aortic stenosis severity are outlined below, in Table 3.
Table 3. Criteria for Determining Severity of Aortic Stenosis (Open Table in a new window)
| Severity | Mean gradient (mm Hg) | Aortic valve area (cm2) |
| Mild | < 25 | >1.5 |
| Moderate | 25-40 | 1-1.5 |
| Severe | >40 | < 1 (or < 0.5 cm2/m2 body surface area) |
| Critical | >80 | < 0.5 |
The ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease include jet velocity (m/sec) in their criteria:[11]
- Mild (area 1.5 cm2, mean gradient less than 25 mm Hg, or jet velocity less than 3 m per second)
- Moderate (area 1-1.5 cm2, mean gradient 25-40 mm Hg, or jet velocity 3-4 m per second)
- Severe (area less than 1 cm2, mean gradient greater than 40 mm Hg, or jet velocity greater than 4 m per second).
The major limitation of Doppler echocardiography in assessing the severity of aortic stenosis is underestimation of the gradient if the beam is not parallel to the aortic stenosis velocity jet. Thus, in a patient with clinical features of severe aortic stenosis but echo/Doppler findings of mild to moderate aortic stenosis, further evaluation with repeat Doppler or cardiac catheterization may be required.
Rarely, Doppler may overestimate the severity of aortic stenosis in patients with severe anemia (hemoglobin < 8 g/dL), a small aortic root, or sequential stenoses in parallel (coexistent LV outflow tract [LVOT] and valvular obstruction).
Furthermore, echocardiographic calculation of AVA is highly dependent on accurate measurement of the diameter of the LVOT. In patients with poor transthoracic echocardiographic images, transesophageal echocardiography (TEE) may be used to measure the mean and peak gradient and a planimeter may be used to assess the AVA.
In patients who are potential candidates for transcatheter aortic valve replacement (see below), the role of echocardiography is critical. For this reason, the European Association of Echocardiography (EAE) and American Society of Echocardiography (ASE) have published recommendations for the use of echocardiography in patients undergoing transcatheter aortic valve replacement.[12]
Cardiac Catheterization and Coronary Arteriography
Cardiac catheterization provides an accurate measure of aortic stenosis and is an important tool, particularly in patients who have discrepant clinical and echocardiographic findings.[4] In general, if clinical findings are not consistent with Doppler echocardiogram results, cardiac catheterization is recommended for further hemodynamic assessment. The recommendations of the ACC/AHA 2006 valvular heart disease guidelines for cardiac catheterization in aortic stenosis are summarized below, in Table 4.[11]
Table 4. Recommendations for Cardiac Catheterization in Aortic Stenosis (Open Table in a new window)
| Indication | Class |
| Coronary angiography before aortic valve replacement in patients at risk for coronary artery disease | I |
| Assessment of severity of aortic stenosis in symptomatic patients when aortic valve replacement is planned or when noninvasive tests are inconclusive or a discrepancy exists in the clinical findings regarding the severity of aortic stenosis or the need for surgery | I |
| Coronary angiography before aortic valve replacement in patients for whom a pulmonary autograft (Ross procedure) is contemplated and the origin of the coronary arteries was not identified by noninvasive tests | I |
| With infusion of dobutamine, can be useful for evaluation of patients with low-flow/low-gradient aortic stenosis and LV dysfunction | IIa |
| Not recommended for hemodynamic measurements for assessment of aortic stenosis severity when noninvasive techniques are adequate and concord with clinical findings | III |
| Not recommended for hemodynamic measurements for assessment of LV function and aortic stenosis severity in asymptomatic patients | III |
Measuring the LV end-diastolic and systolic volume and calculating the EF can quantitate the status of LV systolic pump function. However, EF may underestimate LV performance in the presence of the increased afterload associated with severe aortic stenosis. Since bolus administration of contrast may provoke hemodynamic compromise and assessment of LV function can usually be obtained via echocardiography, contrast ventriculography is rarely indicated.
Exclusion of coronary artery disease by coronary angiography is important in all patients older than 35 years who are being considered for valve surgery. Coronary angiography should also be performed in patients younger than 35 years if they have LV systolic dysfunction, symptoms or signs suggestive of coronary artery disease, or 2 or more risk factors for premature coronary artery disease, excluding sex. Generally, the incidence of associated coronary artery disease has been reported to be 50% in patients with aortic stenosis who are older than 50 years.
Radionuclide Ventriculography
Radionuclide studies to evaluate myocardial perfusion at rest and during exertion and exercise may be considered as part of the complete workup of aortic stenosis. Radionuclide ventriculography may provide information on LV function, including LVEF, ESV, and EDV. Perform these tests cautiously on symptomatic patients.[13]
Exercise Stress Testing
Exercise stress testing is contraindicated in symptomatic patients with severe aortic stenosis, but it may be considered in asymptomatic patients with severe aortic stenosis. The ACC/AHA 2006 valvular heart disease guidelines state that exercise testing may be considered in asymptomatic patients (class IIb recommendation), and recommend that exercise testing not be performed in symptomatic patients with aortic stenosis without specifying severity (class III).[11] In asymptomatic patients, stress testing has been shown to be a low-risk procedure when it is performed under strict surveillance.[13]
Closely monitored exercise stress testing may be of value to assess exercise capacity in asymptomatic patients. Abnormal results may prove greater disability than the patient would admit. In addition to watching for symptoms on the treadmill, one should also look for hemodynamic abnormalities, such as blood pressure decreases or failure to increase blood pressure normally, which can occur in the absence of symptoms. In this setting, the test is not used to screen for coronary disease.
Provocative stress testing is used in cases when the severity of the aortic stenosis is uncertain because of a small stroke volume and a small mean aortic valve gradient (low-gradient aortic stenosis). Infusion of an inotropic agent such as dobutamine, which results in an increase in stroke volume and heart rate, is usually helpful in establishing the correct diagnosis. Cardiac output and LV and aortic pressures are measured simultaneously and AVA is calculated before and during dobutamine infusion.
In patients with an initially low-pressure gradient but severe aortic stenosis, the measured AVA does not change with an intravenous dobutamine infusion, but the mean-pressure gradient increases significantly. In contrast, in patients who have a low cardiac output due to concomitant myocardial dysfunction rather than due to severe aortic stenosis alone, a small increase in the measured AVA and the aortic valve gradient usually occurs with dobutamine infusion.
Investigational Imaging Modalities
Three-dimensional (3D) volume quantification of aortic valve calcification using multislice computed tomography (CT) scanning demonstrates a close, nonlinear relationship to echocardiographic parameters for the severity of aortic stenosis.[14] This method is not yet clinically validated.
In a study by Shah et al that compared multidetector CT scanning with TEE, multidetector CT scanning was found to be an accurate modality for determining aortic valve measurements in patients with aortic stenosis.[15]
Cardiac magnetic resonance imaging (MRI) has also been investigated for assessment of aortic stenosis. AVA measurements made with cardiac MRI have shown excellent correlation with those made with Doppler echocardiography. This method is not yet clinically validated.
Chest Radiography
Even in the presence of significant aortic stenosis, the cardiac size often is normal, with rounding of the LV border and apex. Poststenotic dilatation of the ascending aorta is common.
On lateral views, aortic valve calcification is found in almost all adults with hemodynamically significant aortic stenosis. Although its absence on fluoroscopy in individuals older than 35 years rules out severe valvular aortic stenosis, its presence does not prove severe obstruction in individuals older than 60 years.
The left atrium may be slightly enhanced, and pulmonary venous hypertension may be seen. In later, more severe stages of aortic stenosis, radiographic signs of left atrial enlargement, pulmonary artery enlargement, right-sided enlargement, calcification of the aortic valve, and pulmonary congestion may be evident.
Electrocardiography
Generally, ECG is not a reliable test for aortic stenosis. The results vary widely in patients with this disorder and overlap with other cardiac conditions.
Although the ECG findings may be entirely normal, the principal finding is left ventricular hypertrophy (LVH), which is found in 85% of patients with severe aortic stenosis; however, its absence does not preclude critical aortic stenosis. Patients with significant aortic stenosis who may not show clear ECG evidence of ventricular hypertrophy include elderly persons with significant myocardial fibrosis and adolescents, who may experience ST-segment changes before QRS changes.
T-wave inversion and ST-segment depression in leads with predominantly positive QRS complexes are common. ST depression exceeding 0.3 mV in patients with aortic stenosis indicates LV strain and suggests severe LVH. Occasionally, a septal pseudoinfarct pattern can be seen. Left atrial enlargement with a preterminal negative p wave in lead V1 is noted in 80% of cases of severe isolated aortic stenosis. The presence of left atrial enlargement suggests an associated mitral valve process.
The correlation between absolute voltages in precordial leads and the severity of obstruction, unlike in children with congenital aortic stenosis, is poor in adults.
The rhythm usually is normal sinus. Atrial fibrillation can be seen at late stages or as a consequence of coexistent MV disease or hyperthyroidism.
Extension of calcification into the conduction system can cause atrioventricular or intraventricular block in 5% of cases of aortic stenosis. Approximately 10% of all cases of left anterior fascicular block are secondary to calcific aortic valve disease. Ambulatory ECG monitoring frequently shows complex ventricular arrhythmias, particularly in cases with myocardial dysfunction.
While the degree of severity of changes on a single ECG does not correlate well with the degree of hemodynamic compromise, serial ECGs performed over time (months to years) can be valuable in demonstrating the progression of the disease.
B-type Natriuretic Peptide
B-type natriuretic peptide (BNP) may provide incremental prognostic information in predicting symptom onset in asymptomatic patients with severe aortic stenosis.[16] A high or steadily rising BNP may predict the short-term need for valve replacement in asymptomatic, severe aortic stenosis. Preoperative BNP provides prognostic information on postoperative outcome.[17] Go to Natriuretic Peptides in Congestive Heart Failure for more complete information on this topic.
Tzemos N, Therrien J, Yip J, Thanassoulis G, Tremblay S, Jamorski MT, et al. Outcomes in adults with bicuspid aortic valves. JAMA. Sep 17 2008;300(11):1317-25. [Medline].
Hughes BR, Chahoud G, Mehta JL. Aortic stenosis: is it simply a degenerative process or an active atherosclerotic process?. Clin Cardiol. Mar 2005;28(3):111-4. [Medline].
Roberts WC, Vowels TJ, Ko JM. Comparison of interpretations of valve structure between cardiac surgeon and cardiac pathologist among adults having isolated aortic valve replacement for aortic valve stenosis (+/- aortic regurgitation). Am J Cardiol. Apr 15 2009;103(8):1139-45. [Medline].
Townsend CM, et al. Sabiston Textbook of Surgery. 18th ed. Saunders; 2008:1841-1844..
Kerstjens-Frederikse WS, Du Marchie Sarvaas GJ, et al. Left ventricular outflow tract obstruction: should cardiac screening be offered to first-degree relatives?. Heart. Aug 2011;97(15):1228-32. [Medline].
Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol. Jan 17 2012;59(3):235-43. [Medline].
Jander N, Minners J, Holme I, et al. Outcome of patients with low-gradient "severe" aortic stenosis and preserved ejection fraction. Circulation. Mar 1 2011;123(8):887-95. [Medline].
Tintinalli JE, Kelen GD, Stapczynski JS, eds. Valvular emergencies. In: 6th ed. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill; 2004:54.
Rodrigues Tda R, Sternick EB, Moreira Mda C. Epilepsy or syncope? An analysis of 55 consecutive patients with loss of consciousness, convulsions, falls, and no EEG abnormalities. Pacing Clin Electrophysiol. Jul 2010;33(7):804-13. [Medline].
Topol EJ, Califf RM, et al, eds. Aortic valve disease. In: Textbook of Cardiovascular Medicine. Section Two. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2007:Chap 23.
[Guideline] Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. Aug 1 2006;48(3):e1-148. [Medline].
Zamorano JL, Badano LP, Bruce C, et al. EAE/ASE recommendations for the use of echocardiography in new transcatheter interventions for valvular heart disease. Eur Heart J. Sep 2011;32(17):2189-214. [Medline].
Piérard LA, Lancellotti P. Stress testing in valve disease. Heart. Jun 2007;93(6):766-72. [Medline]. [Full Text].
Messika-Zeitoun D, Aubry MC, Detaint D, Bielak LF, Peyser PA, Sheedy PF, et al. Evaluation and clinical implications of aortic valve calcification measured by electron-beam computed tomography. Circulation. Jul 20 2004;110(3):356-62. [Medline].
Shah RG, Novaro GM, Blandon RJ, Whiteman MS, Asher CR, Kirsch J. Aortic valve area: meta-analysis of diagnostic performance of multi-detector computed tomography for aortic valve area measurements as compared to transthoracic echocardiography. Int J Cardiovasc Imaging. Aug 2009;25(6):601-9. [Medline].
Bergler-Klein J. Natriuretic peptides in the management of aortic stenosis. Curr Cardiol Rep. Mar 2009;11(2):85-93. [Medline].
Bergler-Klein J, Klaar U, Heger M, Rosenhek R, Mundigler G, Gabriel H, et al. Natriuretic peptides predict symptom-free survival and postoperative outcome in severe aortic stenosis. Circulation. May 18 2004;109(19):2302-8. [Medline].
Brown DW, Dipilato AE, Chong EC, Gauvreau K, McElhinney DB, Colan SD, et al. Sudden unexpected death after balloon valvuloplasty for congenital aortic stenosis. J Am Coll Cardiol. Nov 30 2010;56(23):1939-46. [Medline].
Agarwal A, Kini AS, Attanti S, Lee PC, Ashtiani R, Steinheimer AM, et al. Results of repeat balloon valvuloplasty for treatment of aortic stenosis in patients aged 59 to 104 years. Am J Cardiol. Jan 1 2005;95(1):43-7. [Medline].
Rahimtoola SH. Choice of prosthetic heart valve in adults an update. J Am Coll Cardiol. Jun 1 2010;55(22):2413-26. [Medline].
[Best Evidence] Stassano P, Di Tommaso L, Monaco M, Iorio F, Pepino P, Spampinato N, et al. Aortic valve replacement: a prospective randomized evaluation of mechanical versus biological valves in patients ages 55 to 70 years. J Am Coll Cardiol. Nov 10 2009;54(20):1862-8. [Medline].
Leon MB, Smith CR, Mack M, Miller DC, Moses JW, Svensson LG, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. Oct 21 2010;363(17):1597-607. [Medline].
Clavel, MA, et al. Comparison Between Transcatheter and Surgical Prosthetic Valve Implantation in Patients With Severe Aortic Stenosis and Reduced Left Ventricular Ejection Fraction. Circulation. Nov 9 2010Vol;. 122 No.19.
Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. Jun 9 2011;364(23):2187-98. [Medline].
Daneault B, Kirtane AJ, Kodali SK, et al. Stroke associated with surgical and transcatheter treatment of aortic stenosis: a comprehensive review. J Am Coll Cardiol. Nov 15 2011;58(21):2143-50. [Medline].
[Guideline] Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. May 21 2003;289(19):2560-72. [Medline].
[Guideline] Nishimura RA, Carabello BA, Faxon DP, et al. ACC/AHA 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology. August 2008;52:676-85. [Medline].
Moura LM, Ramos SF, Zamorano JL, Barros IM, Azevedo LF, Rocha-Gonçalves F, et al. Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis. J Am Coll Cardiol. Feb 6 2007;49(5):554-61. [Medline].
Chan KL, Teo K, Dumesnil JG, Ni A, Tam J. Effect of Lipid lowering with rosuvastatin on progression of aortic stenosis: results of the aortic stenosis progression observation: measuring effects of rosuvastatin (ASTRONOMER) trial. Circulation. Jan 19 2010;121(2):306-14. [Medline].
Rossebo AB, Pedersen TR, Boman K, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med. Sep 25 2008;359(13):1343-56. [Medline].
Cowell SJ, Newby DE, Prescott RJ, et al. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med. Jun 9 2005;352(23):2389-97. [Medline].
[Guideline] Wann LS, Curtis AB, Ellenbogen KA, et al. 2011 ACCF/AHA/HRS Focused Update on the Management of Patients With Atrial Fibrillation (Update on Dabigatran): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. Mar 15 2011;123(10):1144-50. [Medline]. [Full Text].
[Best Evidence] Bagur R, Webb JG, Nietlispach F, Dumont E, De Larochellière R, Doyle D, et al. Acute kidney injury following transcatheter aortic valve implantation: predictive factors, prognostic value, and comparison with surgical aortic valve replacement. Eur Heart J. Apr 2010;31(7):865-74. [Medline]. [Full Text].
Eltchaninoff H, Prat A, Gilard M et al,. Transcatheter aortic valve implantation: early results of the FRANCE (FRench Aortic National CoreValve and Edwards) registry. Eur Heart Jl. 2011;32:191–197.
Lefevre T, Kappetein AP, Wolner E, et al. One year follow-up of the multi-centre European PARTNER transcatheter heart valve study. Eur Heart Jl. 2011;32:148–157.
Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. Oct 21 2010;363(17):1597-607. [Medline].
Prasad Y, Bhalodkar NC. Aortic sclerosis--a marker of coronary atherosclerosis. Clin Cardiol. Dec 2004;27(12):671-3. [Medline].
[Best Evidence] Rosenhek R, Zilberszac R, Schemper M, Czerny M, Mundigler G, Graf S, et al. Natural history of very severe aortic stenosis. Circulation. Jan 5 2010;121(1):151-6. [Medline].
Tamburino C, Capodanno D, Ramondo A, Petronio AS, Ettori F, Santoro G, et al. Incidence and predictors of early and late mortality after transcatheter aortic valve implantation in 663 patients with severe aortic stenosis. Circulation. Jan 25 2011;123(3):299-308. [Medline].
Zahn R, Gerckens U, EGrube E et al. Transcatheter aortic valve implantation: first results from a multi-centre real-world registry. Eur Heart Jl. 2011;32:198–204.
Zajarias A, Cribier AG. Outcomes and safety of percutaneous aortic valve replacement. J Am Coll Cardiol. May 19 2009;53(20):1829-36. [Medline].
- Table 1. Common Causes of Aortic Stenosis Among Patients Requiring Surgery
- Table 2. ACC/AHA Recommendations for Echocardiography (Imaging, Spectral, and Color Doppler) in Aortic Stenosis
- Table 3. Criteria for Determining Severity of Aortic Stenosis
- Table 4. Recommendations for Cardiac Catheterization in Aortic Stenosis
- Table 5. Recommendations for Aortic Valve Replacement in Aortic Stenosis
| Age < 70 years (n=324) | Age >70 years (n=322) |
| Bicuspid AV (50%) Postinflammatory (25%) Degenerative (18%) Unicommissural (3%) Hypoplastic (2%) Indeterminate (2%) | Degenerative (48%) Bicuspid (27%) Postinflammatory (23%) Hypoplastic (2%) |
| Indication | Class |
| Diagnosis and assessment of severity of aortic stenosis | I |
| Assessment of LV size, function, and/or hemodynamics | I |
| Reevaluation of patients with known aortic stenosis with changing symptoms or signs | I |
| Assessment of changes in hemodynamic severity and ventricular function in patients with known aortic stenosis during pregnancy | I |
| Reevaluation of asymptomatic patients with severe aortic stenosis | I |
| Reevaluation of asymptomatic patients with mild to moderate aortic stenosis and evidence of LV dysfunction or hypertrophy | IIa |
| Routine reevaluation of asymptomatic adult patients with mild aortic stenosis who have stable physical signs and normal LV size and function | III |
| Severity | Mean gradient (mm Hg) | Aortic valve area (cm2) |
| Mild | < 25 | >1.5 |
| Moderate | 25-40 | 1-1.5 |
| Severe | >40 | < 1 (or < 0.5 cm2/m2 body surface area) |
| Critical | >80 | < 0.5 |
| Indication | Class |
| Coronary angiography before aortic valve replacement in patients at risk for coronary artery disease | I |
| Assessment of severity of aortic stenosis in symptomatic patients when aortic valve replacement is planned or when noninvasive tests are inconclusive or a discrepancy exists in the clinical findings regarding the severity of aortic stenosis or the need for surgery | I |
| Coronary angiography before aortic valve replacement in patients for whom a pulmonary autograft (Ross procedure) is contemplated and the origin of the coronary arteries was not identified by noninvasive tests | I |
| With infusion of dobutamine, can be useful for evaluation of patients with low-flow/low-gradient aortic stenosis and LV dysfunction | IIa |
| Not recommended for hemodynamic measurements for assessment of aortic stenosis severity when noninvasive techniques are adequate and concord with clinical findings | III |
| Not recommended for hemodynamic measurements for assessment of LV function and aortic stenosis severity in asymptomatic patients | III |
| Indication | Class |
| Symptomatic patients with severe aortic stenosis | I |
| Patients with severe aortic stenosis undergoing coronary artery bypass surgery | I |
| Patients with severe aortic stenosis undergoing surgery on the aorta or other heart valves | I |
| Patients with severe aortic stenosis and LV systolic dysfunction (ejection fraction < 0.50) | I |
| Patients with moderate aortic stenosis undergoing coronary artery bypass surgery or surgery on the aorta or other heart valves | IIa |
| Patients with mild aortic stenosis undergoing coronary artery bypass surgery when there is evidence that progression may be rapid, such as moderate-to-severe valve calcification | IIb |
| Asymptomatic patients with severe aortic stenosis and abnormal response to exercise (eg, hypotension) | IIb |
| Asymptomatic patients with severe aortic stenosis and a high likelihood of rapid progression (based on age, calcification, and coronary artery disease) or if surgery might be delayed at the time of symptom onset | IIb |
| Asymptomatic patients with extremely severe aortic stenosis (valve area less than 0.6 cm2, mean gradient greater than 60 mm Hg, and jet velocity greater than 5 m per second) if the patient’s expected operative mortality is 1% or less | IIb |
| AVR is not useful for prevention of sudden death in asymptomatic patients with none of the findings listed under asymptomatic patients with severe aortic stenosis | III |

