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Chapter 12
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Chest X-Ray in Aortic Disease
Anneke Damberg, Bulat A. Ziganshin, John A. Elefteriades
Aortic Institute at Yale-New Haven Hospital, Yale University School of Medicine, New Haven, CT, United States
Chapter Outline
Introduction 129
Capabilities of the Plain Chest X-Ray 129
Diagnosis of Acute Aortic Syndrome 129
INTRODUCTION
Today’s trainees are raised in a three-dimensional, computed tomographic (CT) radiographic imaging world. Recent trainees tend to “look down” on the chest X-ray for the imaging of the aorta. This chapter is written specifically to bring home
the point that important, although at times subtle, clues to the aortic contour are indeed available on the plain chest X-ray
[1]. They can be detected by knowing where to look and being interested in looking at the chest X-ray. The information to
be garnered can be of vital importance, providing important diagnostic and therapeutic clues even before the CT scan is
ordered or performed.
Conclusions 131
References 131
CAPABILITIES OF THE PLAIN CHEST X-RAY
The plain chest X-ray derives its ability to discern the contours of the aorta because of the contrast between the airfilled lungs and the fluid-filled aorta. The normal contours of the aorta are quite familiar and generally very well seen.
See Fig. 12.1; it displays a normal chest X-ray as well as one with sites marked where the dilated aorta can make itself
known. Also see Fig. 12.2, for example, of thoracic aneurysms diagnosed by chest X-ray.
l The ascending aorta, if substantially enlarged, will appear outside the upper right cardiac silhouette.
l The aortic knob should normally be small and distinct in the upper left mediastinum. This knob will enlarge in the case
of arch aneurysm. The knob becomes indistinct in patients with aortic dissection, due to edema and hemorrhage in the
tissues.
l The descending aorta normally makes a clean, crisp stripe to the left of the vertebral column. Aneurysmal dilatation of
the descending aorta will be clearly seen, with bulging of this stripe to the right.
Also, in cases of severe aortic enlargement, the trachea, left main bronchus, or esophagus may be seen to be displaced
on a plain chest X-ray.
Of course, when aortic pathology is suspected on chest radiography, supplementary imaging should be performed using
computed tomography angiography (CTA) or magnetic resonance imaging (MRI) [2].
DIAGNOSIS OF ACUTE AORTIC SYNDROME
Chest X-ray can, for the reasons mentioned above, be an important part of the work-up in a patient with acute aortic syndrome. A few specific findings on the chest X-ray may suggest aortic dissection. These include displacement of intimal
calcifications, the presence of a double density, or a blurred aortic knob [2,3].
The American Heart Association and American College guidelines for thoracic aortic disease (2010) do recommend the
evaluation of mediastinal width in patients being evaluated for aortic dissection if index of suspicion is low [4]. However, it
has to be kept in mind that its diagnostic value in aortic dissection is limited and that more than 10% of patients may have a
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00012-2
Copyright © 2018 Elsevier Inc. All rights reserved.
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(A) (B) (C)
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(A) (B)
FIGURE 12.1 (A) Normal chest X-ray. (B) Same chest X-ray with areas where ascending, arch, and descending aortic aneurysm shadows may appear.
FIGURE 12.2 Aneurysms diagnosed by chest X-ray. (A) Ascending; (B) Arch; (C) Descending.
normal chest X-ray [5,6]. In the International Registry of Aortic Dissection (IRAD) report on the diagnosis of acute aortic
dissection, 11.3% and 15.8% of patients had no abnormalities on chest X-ray in acute Type A and B dissection, respectively
[6]. Luker et al. reported the evaluation of 75 chest X-rays of patients with aortic dissection and found that only 48% patient
chest X-rays evidenced sufficient information to diagnose aortic dissection, exemplifying the known limited sensitivity. In
five patients, sufficient findings were overlooked and accurate diagnosis was delayed [5].
Similarly, Hartnell et al. compared chest radiographs of 25 patients with myocardial infarction and 18 patients with
acute Type A dissection and came to the conclusion that no individual or combination of radiological signs can accurately
discriminate between the two diseases [7].
Somewhat higher accuracy measures were reported by Jagannath et al. and von Kodolitsch et al. [8,9]. Jagannath
reviewed chest X-rays of 36 patients with aortic dissection and 36 normal controls. Overall radiologist’s impression was a
better predictor than individual signs investigated, but interobserver agreement was poor. They found an overall sensitivity
of 81% and a specificity of 89% [8]. In the study performed by von Kodolitsch, the authors reevaluated chest X-rays of 216
patients with acute aortic syndrome. They found an overall sensitivity of 64% and a specificity of 86%, with much lower
accuracy if the pathology was isolated to the ascending aorta [9].
These findings go in line with a review performed by Klompas, which concluded that chest X-ray is usually abnormal (with
a pooled sensitivity of 90%), and that, therefore, a normal chest X-ray substantially lowers the risk of aortic dissection [10].
Thoracic Aortic Aneurysm—Guilt by Association Chapter | 12 131
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Mediastinal widening, the most established radiographic sign of aortic dissection, was present in 62.6% of patients with
Type A dissection and 56% of patients with Type B dissections in the IRAD report [6]. Pooled sensitivity for mediastinal
widening in the review by Klompas was 64% [10].
An abnormal aortic contour, known as a further potential sign of aortic dissection, was present in 46.6% (Type A dissection) and 53% (Type B dissection) of patients in the IRAD study [6]. The review by Klompas reached a pooled sensitivity
of 71% for this finding. Displaced intimal calcification is not reliably present in aortic dissection, with a pooled sensitivity
of only 9% [10].
CONCLUSIONS
Chest X-ray is a broadly used and easily accessible diagnostic test, which often reveals radiographic signs of aortic disease.
Chest X-ray does have an important role in the evaluation of the aorta.
Chest X-ray alone, however, is not a sufficiently accurate diagnostic tool to confirm or exclude aortic pathology, and
neither does it offer sufficient anatomic detail to depict accurately the detailed anatomy and complications of aortic aneurysms or allow the planning of therapeutic management. Therefore, the radiographic signs of aortic disease on chest X-ray
should lead to further imaging using CTA or MRI. Nevertheless, if a patient is evaluated for aortic dissection and the index
of suspicion is high, a CT scan should not be delayed for a chest x-ray.
On the authors’ aortic service, we encourage residents trained in computerized tomographic imaging and MRI not to
ignore the chest X-ray. The plain film can, upon careful reading, not only raise the suspicion of aortic disease, but also
predict, with surprising accuracy, the findings that will obtain on more advanced imaging modalities.
REFERENCES
[1] Eleferiades JA. Editor’s Counterpoint Danias PG. Imaging of aneurysms and dissections. In: Elefteriades JA, editor. Acute aortic disease. New York,
London: Informa; 2007.
[2] Goldstein SA, Evangelista A, Abbara S, Arai A, Asch FM, Badano LP, et al. Multimodality imaging of diseases of the thoracic aorta in adults: from
the American Society of Echocardiography and the European Association of Cardiovascular imaging: endorsed by the Society of Cardiovascular
computed tomography and Society for Cardiovascular magnetic resonance. J Am Soc Echocardiogr 2015;28(2):119–82.
[3] Danias P. Imaging of aneurysms and dissections: chest X-ray, echo, computed tomography, magnetic resonance imaging. Boca Raton (Florida,
USA): CRC Press; 2007.
[4] Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey Jr DE, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM
guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/
American Heart Association Task Force on Practice Guidelines, American Association for thoracic Surgery, American College of Radiology,
American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular angiography and Interventions, Society of
Interventional Radiology, Society of thoracic Surgeons, and Society for Vascular Medicine. Circulation 2010;121(13):e266–369.
[5] Luker GD, Glazer HS, Eagar G, Gutierrez FR, Sagel SS. Aortic dissection: effect of prospective chest radiographic diagnosis on delay to definitive
diagnosis. Radiology 1994;193(3):813–9.
[6] Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The international registry of acute aortic dissection
(IRAD): new insights into an old disease. JAMA 2000;283(7):897–903.
[7] Hartnell GG, Wakeley CJ, Tottle A, Papouchado M, Wilde RP. Limitations of chest radiography in discriminating between aortic dissection and
myocardial infarction: implications for thrombolysis. J Thorac Imaging 1993;8(2):152–5.
[8] Jagannath AS, Sos TA, Lockhart SH, Saddekni S, Sniderman KW. Aortic dissection: a statistical analysis of the usefulness of plain chest radio-
graphic findings. AJR Am J Roentgenol 1986;147(6):1123–6.
[9] von Kodolitsch Y, Nienaber CA, Dieckmann C, Schwartz AG, Hofmann T, Brekenfeld C, et al. Chest radiography for the diagnosis of acute aortic
syndrome. Am J Med 2004;116(2):73–7.
[10] Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA 2002;287(17):2262–72.
Chapter 13
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Echocardiography in Aortic Valve Stenosis
Ioan Tiberiu Nanea
1
University of Medicine and Pharmacy “Carol Davila” Bucharest, Romania; 2“Prof. Dr. Th. Burghele” University Hospital, Bucharest, Romania
1,2
Chapter Outline
Degenerative Aortic Stenosis 133
Rheumatic Aortic Stenosis 133
Congenital Aortic Stenosis 133
Quantification of Aortic Stenosis 133
Calculating the Jet Velocity and the Transaortic
Pressure Gradient 134
Aortic Valve Area 135
Special Varieties of Valvular Aortic Stenosis 138
Low-Flow, Low-Gradient Aortic Stenosis With Reduced Left
Ventricular Ejection Fraction 138
Paradoxical Low-Flow, Low-Gradient Aortic Stenosis 138
Aortic Stenosis Associated With a Noncompliant Left Ventricle,
With Reduced Ejection Fraction 138
Aortic Stenosis Associated With Systolic Aortic Regurgitation 138
Stress Echocardiography in Asymptomatic Aortic Stenosis 138
Conclusions 142
References 143
Aortic valve stenosis or aortic stenosis (AS) is the most common valvular heart disease, with an incidence of 2%–9% in sub-
jects aged 65 years or older [1]. AS etiology includes degenerative, congenital, and rheumatic AS.
DEGENERATIVE AORTIC STENOSIS
Degenerative AS develops progressively, the valvular degenerative process being similar to atherosclerosis.
Calcifications of the valvular tissue, without commissural involvement, are characteristic for degenerative AS (Fig. 13.1A)
RHEUMATIC AORTIC STENOSIS
Rheumatic AS is remarkable because of the diffuse thickening of valve leaflets associated with commissure fusion,
followed by calcific changes.
The rheumatic process leads to fibrosis, sclerosis, and valvular retraction (Fig. 13.1B).
CONGENITAL AORTIC STENOSIS
In bicuspid aortic valve disease, the number of leaflets, commissure position, intervalvular raphe are analyzed, as well as
the actual leaflet opening (dome-shaped) [2].
The morphofunctional assessment of the aortic valves is performed in diastole, when commissure functionality is best
evaluated. In systole, three cusps may be differentiated, but two of these have nonfunctional commissures because of the raphe.
Magnetic resonance imaging with a contrast agent is necessary to observe the effective valve opening [3] (Fig. 13.2).
There are tricuspid aortic valves with one hypoplastic cusp, behaving as AS and aortic regurgitation (Fig. 13.1D).
Sometimes, the fusion raphe between two cusps does not exist and imaging only documents two cusps, in the so-called
pure (true) bicuspid aortic valve disease.
Pure (true) bicuspid aortic valve disease versus pseudo-bicuspid aortic valve (three cusps, two of which are fused) may
be significant in terms of surgical technique for valvular replacement.
QUANTIFICATION OF AORTIC STENOSIS
Essentially, AS severity is assessed by evaluating: the transvalvular blood flow velocity, the transvalvular pressure gradient,
and the aortic valve area (AVA).
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00013-4
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FIGURE 13.1 (A) Degenerative aortic stenosis (AS). Three-dimensional (3D) echocardiography. The absence of commissure fusion (arrows).
Hyperechogenicity of the valves suggests fibrosis and valvular tissue calcification. (B) Rheumatic AS. 3D echocardiography of the aortic valve. Stenotic
valvular orifice, fused commissures (arrow), hyperechoic areas on the noncoronary cusp, suggestive for calcific changes. (C) 3D echocardiography for the
quantification of the aortic valve area (AVA) by planimetry, in the same patient as (B). Tracing of the aortic orifice automatically calculates the valve area.
(D) Transesophageal echocardiography, short axis, at the level of the aortic valve; d, right coronary aortic cusp, n, noncoronary aortic cusp, s, hypoplastic
left coronary aortic cusp.
Severity stratification in AS is also achieved by determining atrial and ventricular dimensions, wall thickness, and
systolic and diastolic function, along with left ventricular (LV) mass, pulmonary hypertension, and the magnitude of other
associated valvular lesions.
CALCULATING THE JET VELOCITY AND THE TRANSAORTIC PRESSURE GRADIENT
Evaluating jet velocity through the stenotic aortic orifice (or the velocity–time integral, VTI) is accomplished by continuous wave Doppler (CWD), with the ultrasound beam parallel to the blood flow, when maximum velocity is calculated.
Two-dimensional echocardiography is used in the apical five-chamber or three-chamber views or the transducer may be
positioned in a suprasternal manner or on the right side of the sternum. The pressure gradient is calculated by using the
Bernoulli equation [4]:
Pressure (mmHg) = 4 × V
where V2 = maximum aortic velocity.
2
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FIGURE 13.2 Magnetic resonance imaging of the aortic valves: (A) three cusps are apparently differentiated by visualizing the raphes (arrow). (B) After
contrast agent administration, it can be observed that, in fact, the stenotic orifice is generated by the dome-shaped opening of the noncoronary and right coronary
cusps. The right coronary cusp is fused with the left coronary cusp, an image impossible to identify without a contrast medium [3].
Aortic valve opening is related to the transvalvular blood flow, the aortic cusps remain open to allow the systolic volume
to be ejected from the LV.
AORTIC VALVE AREA
Quantification of the AVA is attained by means of continuity equation. The physics principle involves mass conservation:
the stroke volume (SV) in the left ventricular outlet tract (LVOT) is equivalent to the SV through the aortic valve [5].
SV in the LVOT is the cross-sectional area of the LVOT (ALVOT) times the VTI in the LVOT (VTILVOT).
SV through the stenotic aortic valve is the AVA times the VTI in the stenotic aortic valve (VTIAS).
Thus, the continuity equation becomes [6]:
ALVOT × VTILVOT = AVA × VTIAS,
where
AVA (cm2) = (ALVOT × VTILVOT)/VTIAS,
and
ALVOT = 3.14 × RLVOT
and RLVOT = radius of the LVOT.
2
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Δ
2
−
2
)
,
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LVOT diameter is measured in mid-systole, in the two-dimensional parasternal long axis view (zoomed region), exactly
under the aortic cusps’ insertion. Incorrect assessments of the LVOT diameter and velocity are the main errors in estimating
AVA. The maximum LVOT velocity is measured by pulsed wave Doppler (PWD) two-dimensional (2D) echocardiography,
apical three or five chambers. The sample volume should be positioned just proximal to the stenotic valve, the blood flow
being laminar.
Using the maximum velocity and not the VTI is preferred for patients in atrial fibrillation, when 5 or 10 cardiac cycles
are used.
An associated HOCM will induce a high LVOT and transaortic velocity due to velocity propagation from the obstruction
generated by the anterior mitral valve leaflet aspiration by the excessively hypertrophied septum.
LVOT velocity can be increased also by concomitant aortic regurgitation.
By using the disproportionately high aortic transvalvular and LVOT velocities, the stenotic AVA will be erroneously
evaluated. Therefore, the modified Bernoulli equation is applicable when the LVOT velocity exceeds 1.5 m/s. The modified
Bernoulli equation only appreciates the transaortic pressure gradient [6]:
PAo=4(VAo
VLVOT
where ΔPAo = transaortic pressure gradient, VAo = aortic valve velocity, VLVOT = velocity in the LVOT (Fig. 13.3).
FIGURE 13.3 Measurement of the transvalvular aortic gradient in aortic stenosis (AS) associated with hypertrophic obstructive cardiomyopathy (HOCM).
(A) Two-dimensional (2D) echocardiography with continuous wave Doppler (CWD) of the aortic valve, apical five-chamber view, maximum velocity
5.43 m/s. (B) 2D echocardiography with pulsed wave Doppler (PWD) of the obstruction: aspiration of the mitral valve, hypertrophy of the interventricular
septum. Characteristic “concave-to-the-left” (“yatagan”) shape of the Doppler flow (arrow), maximum velocity 1.81 m/s. (C) 2D echocardiography long
axis: Ao, aorta; arrow, aspiration of the anterior mitral valve leaflet to the interventricular septum; LV, left ventricle; RV, right ventricle; S, interventricular
septum. (D) 2D echocardiography, PWD at the LVOT, laminar Doppler flow, maximum velocity 1.62 m/s. LVOT, left ventricular outlet tract. The modified
Bernoulli equation indicates a maximum pressure gradient of 100.6 mmHg.
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Quantifying the AVA by planimetry can be achieved by two-dimensional transthoracic echocardiography, short axis
view, or transesophageal echocardiography, which offers a very good correlation with the area measured by cardiac
catheterization by the Gorlin equation [7].
Three-dimensional echocardiography, by the possibility to obtain different sectional planes at the aortic valve level,
improves the quality of AVA estimation.
Color Doppler echocardiography is useful for the accurate orientation of the aortic orifice (Fig. 13.1C).
Table 13.1 presents the classification of AS severity according to the American and European academic societies’
guidelines [4,8].
Tables 13.2 and 13.3, respectively, show concepts regarding the pathophysiological classification of AS, as well as
remarkable varieties of AS.
Surgical indications in asymptomatic AS are reviewed by current guidelines [4,8].
TABLE 13.1 Classification of Aortic Stenosis Severity
Characteristic Mild Moderate Severe
Aortic jet velocity (m/s) [4,8] 2.6–2.9 3.0–4.0 >4.0
Mean gradient (mmHg)—American [8] <20 20–40 >40
Mean gradient (mmHg)—European [4] <30 30–50 >50
Aortic valve area (cm2) [4,8] >1.5 1.0–1.5 <1.0
TABLE 13.2 Pathophysiological Classification of Aortic Stenosis
Aortic Stenosis Ejection Fraction Comments
High-flow, high-gradient [4,8] Normal –
Low-flow, low-gradient [4,8] Reduced
Paradoxical low-flow, low-gradient [4,8] Normal
l
Afterload mismatch
l
Primary left ventricle contraction dysfunction
l
Discordance between aortic valve area (AVA) and
pressure gradient
l
Discordance between AVA and pressure gradient
TABLE 13.3 Special Varieties of Aortic Stenosis
Variety Characteristics
Aortic stenosis (AS) associated with aortic annulus rigidity Aortic valve area increases, but the pressure gradient does
not increase with dobutamine
AS associated with secondary hypertrophic obstructive
cardiomyopathy
AS associated with systolic aortic regurgitation Massive aortic regurgitation with an increase in transaortic velocity
AS associated with a hypertrophied noncompliant left
ventricle (LV), with reduced ejection fraction
Excessive left ventricular outlet tract velocity by propagation from the
obstruction formed by the interventricular septum and
anterior mitral valve leaflet
Presystolic flow in outflow tract due to atrial contraction against a
highly noncompliant hypertrophied LV
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SPECIAL VARIETIES OF VALVULAR AORTIC STENOSIS
Valvular AS associated with secondary HOCM has been previously described (Fig. 13.3). It is difficult to assess whether
septal hypertrophy is the result of the valvular lesion severity or is the consequence of the activation of genetic mechanisms
developed under the hemodynamic effect imposed by the AS.
LOW-FLOW, LOW-GRADIENT AORTIC STENOSIS WITH REDUCED LEFT VENTRICULAR
EJECTION FRACTION
This type of AS is characterized by an AVA under 1 cm2, but with a low transaortic gradient, under 40 mmHg, associated
with an ejection fraction (EF) under 50% [9].
This type of AS is caused by two mechanisms: afterload mismatch or the primary LV contractility dysfunction. The
resistance in the LV emptying greatly increases LV work, LV function decreases, and EF becomes reduced (afterload
mismatch).
The second mechanism is the primary LV contractility dysfunction, induced by ischemia or in the context of nonischemic cardiomyopathy.
At rest, the two mechanisms cannot be differentiated: afterload mismatch and primary LV contractility dysfunction as
the cause of the reduced EF.
The hemodynamic stress test with dobutamine identifies the improvement in the segmental myocardial contractility, in
those with low-flow, low-gradient AS (LLAS) secondary to LV ischemia.
An increase in transaortic gradient over 40 mmHg in the dobutamine test signifies the existence of myocardial contractile reserve or flow reserve, separating severe AS from pseudosevere AS, where the gradient does not increase (Fig. 13.6).
LV flow reserve is defined by 20% increase in SV after dobutamine testing (5–20 μg/kg/min) [4].
Patients who do not have a flow reserve represent one-third of the LLAS with reduced LV EF patients and have a high
mortality at valvular replacement by prosthesis [10].
PARADOXICAL LOW-FLOW, LOW-GRADIENT AORTIC STENOSIS
Upon AVA estimation by continuity equation, paradoxical low-flow, low-gradient aortic stenosis (PLLAS) is defined by
AVA <1 cm2, transaortic gradient < 40 mmHg, SV index < 35 mL/m2, and EF >50% [11]. Although EF is normal, the LV
longitudinal strain is reduced under 16% [12].
PLLAS is produced in restrictive LV conditions, especially severe hypertrophy with a drop in LV cavity dimensions and
SV (Fig. 13.7).
AORTIC STENOSIS ASSOCIATED WITH A NONCOMPLIANT LEFT VENTRICLE, WITH
REDUCED EJECTION FRACTION
Afterload mismatch induced by AS generates a ventricular noncompliance that allows for an end-diastolic blood flow, sec-
ondary to the atrial contraction (Fig. 13.5). This phenomenon could lower the systolic aortic gradient even more, by increasing end-diastolic pressure (by diminishing lesion severity). For this special type of AS, I have described a transvalvular
mitral Doppler flow with a very low E wave velocity and greatly prolonged deceleration time (Fig. 13.5).
AORTIC STENOSIS ASSOCIATED WITH SYSTOLIC AORTIC REGURGITATION
I have described aortic regurgitation extended into the early systole in the context of a severe lesion. The early systolic pressure thus created could reduce the transaortic gradient, therefore decreasing AS severity (Fig. 13.4).
STRESS ECHOCARDIOGRAPHY IN ASYMPTOMATIC AORTIC STENOSIS
Exercise echocardiography in asymptomatic AS reflects
l more severe AS or
l rigid aortic valve orifice
An increase in the mean transaortic pressure gradient by 20 mmHg or more mandates valvular replacement [4,8,13].
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