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.
Multimodality imaging is essential for preoperative planning and postoperative detection of potential complications. [20] 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.
Echocardiography
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 2.
Table 2. Criteria for Determining Severity of Aortic Stenosis (Open Table in a new window)
Severity |
Mean gradient (mmHg) |
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 |
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%. [21]
The major limitation of Doppler echocardiography in assessing the severity of aortic stenosis is underestimation of the gradient if the sound 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. [22]
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.
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 gender. 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]
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. [23]
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. In asymptomatic patients, stress testing has been shown to be a low-risk procedure when it is performed under strict surveillance. [23]
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. [5, 24] 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. [25]
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. [2] 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. [26]
In evaluating data from a Japanese multicenter registry comprising 3815 patients with severe aortic stenosis, investigators assessed BNP levels in the 387 patients who had asymptomatic severe aortic stenosis with normal left ventricular ejection fraction and who were not referred for aortic valve replacement. [3] They found that increased BNP levels were associated with a greater risk for aortic stenosis-related adverse events (aortic valve-related death or heart failure hospitalization) in these patients, whereas there was a relatively low event rate in asymptomatic patients with BNP levels below 100 pg/mL. [3]
Go to Natriuretic Peptides in Congestive Heart Failure for more complete information on this topic.
-
Stenotic aortic valve (macroscopic appearance).
Tables
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%) |
Severity |
Mean gradient (mmHg) |
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 |
Symptomatic severe high-gradient AS (Stage D1) |
I |
Asymptomatic severe AS (Stage C2) with and LVEF < 50% |
I |
Severe AS (Stage C or D) undergoing other cardiac surgery |
I |
Asymptomatic, very severe AS (Stage C1, aortic velocity ≥5.0 m/s) and low surgical risk |
IIa |
| Asymptomatic, severe AS (Stage C1) and decreased expercise tolerance or an exercise fall in blood pressure | IIa |
| Symptomatic severe low flow/low gradient AS with reduced LVEF (Stage D2) with a low-dose dobutamine stress study with aortic velocity ≥4.0 m/s with a value are ≤1.0 cm2 at any dobutamine dose | IIa |
| Symptomatic severe low flow/low gradient AS (Stage D3) who are normotensive and have an LVEF ≥50% if clinical, hemodynamic and anatomic data support valve obstruction as the most likely cause of symptoms | IIa |
| Moderate AS (Stage B) who are undergoing other cardiac surgery | IIa |
| Asymptomatic severe AS (Stage C1) with rapid disease progression and low surgical risk | IIb |
Intervention Selection |
AHA/ACC (2014) [6] |
ESC/EACTS (2012) [5] |
STS(2013) [56] |
Surgical AVR in patients with low or intermediate surgical risk |
Class I |
Class I |
|
Transcatheter aortic valve replacement (TAVR) for patients who have a prohibitive surgical risk and a predicted post-TAVR survival >12 mo |
Class I |
Class I |
Class I |
TAVR for patients who have high surgical risk |
Class IIa-Reasonable |
Class IIa-Reasonable |
|
TAVR is not recommended in patients in whom existing comorbidities would preclude the expected benefit from correction of AS |
Class III |
Class III |
|
Balloon aortic valvuloplasty (BAV) as a bridge to surgical AVR or TAVR in severely symptomatic patients |
Class IIb-Consider |
Class IIb-Consider |
Class IIa-Reasonable |
BAV as bridge to AVR in hemodynamically unstable patients with severe AS where immediate AVR is not feasible |
Class IIb-Consider |
Class IIa-Reasonable |
|
BAV in severely symptomatic patients where AVR is not an option for symptom relief |
Class IIb-Consider |
||
BAV as a palliative measure when surgery is contraindicated because of severe comorbidities |
Class IIb-Consider |
Class IIb-Consider |
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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Guidelines
- 2021 ACC/AHA Valvular Heart Disease Clinical Practice Guidelines
- 2021 ESC/EACTS Management of Valvular Heart Disease (VHD) Clinical Practice Guidelines
- 2017 Multisociety Appropriate Use Criteria
- 2017 AHA/ACC Guidelines for the Management of Patients with Valvular Heart Disease
- 2014 Multisociety Guidelines for the Management of Valvular Heart Disease
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