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Aortic Stenosis Workup

  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Nov 10, 2014
 

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.[5] 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.

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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.[6] 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. The structure and function of the other heart valves can also be assessed.

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[6] :

  • Mild (area 1.5 cm 2, mean gradient less than 25 mm Hg, or jet velocity less than 3 m per second)
  • Moderate (area 1-1.5 cm 2, mean gradient 25-40 mm Hg, or jet velocity 3-4 m per second)
  • Severe (area less than 1 cm 2, mean gradient greater than 40 mm Hg, or jet velocity greater than 4 m per second).

According to the European Society of Cardiology (ESC)/European Association for Cardio-Thoracic Surgery (EACTS) 2012 guidelines on the management of valvular heart disease, the echocardiographic criteria for defining severe aortic stenosis also include valve area less than 1.0 cm2, mean gradient greater than 40 mm Hg, and maximum jet velocity greater than 4 m per second.[5]

Color Doppler valve analysis during transesophageal echocardiography (TEE) can be used to accurately diagnose bicuspid aortic valve in patients with severe symptomatic aortic stenosis, according to a prospective study of 51 patients. In detecting bicuspid aortic valve, color Doppler TEE had a sensitivity of 95.5%, a specificity of 96.5%, and a positive predictive value of 95.5%.[15]

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, 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.[16]

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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.[6]

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

 

The ESC/EACTS guidelines recommend restricting cardiac catheterization to use in patients in whom non-invasive evaluation is inconclusive or discordant with clinical findings.[5]

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. Coronary angiography need not be performed in young patients with no atherosclerotic risk factors and in circumstances where the risk involved outweighs the benefits.[5]

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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.[17]

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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).[6] In asymptomatic patients, stress testing has been shown to be a low-risk procedure when it is performed under strict surveillance.[17]

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.

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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.[5, 18] 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.[19]

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.

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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.

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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.

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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.[3] 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.[20] Go to Natriuretic Peptides in Congestive Heart Failure for more complete information on this topic.

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Contributor Information and Disclosures
Author

Xiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; Associate Director of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center

Xiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Society of Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

Jerry Balentine, DO Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St Barnabas Hospital

Jerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Daniel P Lombardi, DO Clinical Assistant Professor, New York College of Osteopathic Medicine; Attending Physician, Associate Department Director and Program Director, Department of Emergency Medicine, St Barnabas Hospital

Daniel P Lombardi, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

John A McPherson, MD, FACC, FAHA, FSCAI Associate Professor of Medicine, Division of Cardiovascular Medicine, Director of Cardiovascular Intensive Care Unit, Vanderbilt Heart and Vascular Institute

John A McPherson, MD, FACC, FAHA, FSCAI is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, Society of Critical Care Medicine, and Tennessee Medical Association

Disclosure: Abbott Vascular Corp. Consulting fee Consulting

Bekir H Melek, MD, FACC Assistant Professor of Clinical Medicine, Department of Medicine, Section of Cardiology, Tulane University School of Medicine

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

James V Talano, MD, MM, FACC Director of Cardiovascular Medicine, SWICFT Institute

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Stenotic aortic valve (macroscopic appearance).
Table 1. Common Causes of Aortic Stenosis Among Patients Requiring Surgery
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%)



Table 2. ACC/AHA Recommendations for Echocardiography (Imaging, Spectral, and Color Doppler) in Aortic Stenosis
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
Table 3. Criteria for Determining Severity of Aortic Stenosis
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
Table 4. Recommendations for Cardiac Catheterization in Aortic Stenosis
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
Table 5. Recommendations for Aortic Valve Replacement in Aortic Stenosis
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
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