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Epidemiology and Clinical Approach to Aortic Valve Disease
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Diagnosis and Evaluation
Echocardiography allows to diagnose acute AR, assess its severity, and in some cases to
identify the underlying cause (such as infective endocarditis or aortic dissection). Color
Doppler echocardiography demonstrates the backflow of blood across the aortic valve in
diastole. The regurgitant jet is either central or eccentric, and the vena contracta width might
be >6 mm. Holodiastolic flow reversal can be observed in the descending thoracic and
proximal abdominal aorta [5]. In very severe cases, the late diastolic velocity approaches
zero, indicating that aortic diastolic pressure and LV diastolic pressure are virtually identical
[53, 54]. Signs of rapid pressure equalization of diastolic aortic and LV pressures include a
dense continuous wave Doppler signal with a steep diastolic slope (pressure half-time <200
ms), and a short mitral deceleration time (<150 ms) and premature closure of the mitral valve.
Importantly, the criteria for severe chronic AR may underestimate the severity of acute AR
[55]. Echocardiography also enables evaluation of LV size and systolic function (which are
often normal), and may provide information on the cause of valve dysfunction, by showing
for example aortic dilatation and dissection or the presence of valvular vegetations. TEE is
useful for identifying the mechanism of acute AR in the setting of aortic dissection, which
may affect decision-making about the surgical procedure [56]. ECG changes are nonspecific.
ST and T wave abnormalities are common, and patients may develop a myocardial infarction
because of coronary occlusion in the setting of aortic dissection. Chest radiograph may show
evidence of pulmonary edema, an enlarged cardiac silhouette because of pericardial effusion,
or aortic root dilation [5]. When aortic dissection is suspected, TEE or CT can be performed,
with high and similar values of sensitivity and specificity. CT imaging may help identify the
intimal flap, the site and extent of dissection and the possible involvement of major branch
arteries. Emergency valve surgery should not be delayed for coronary angiography if there is
severe acute AR with hemodynamic instability. If the patient is reasonably stable, coronary
angiography is generally performed in patients with CAD [18]. Aortography is indicated only
when the diagnosis cannot be established by noninvasive imaging [5].
Chronic Aortic Regurgitation
Symptoms
Patients with chronic AR may remain asymptomatic for decades, even if there is
progressive LV dilation. Symptoms that develop in some patients with severe AR include
exertional dyspnea, angina, and other symptoms of HF. Dyspnea on effort and other HF
symptoms (such as orthopnea or paroxysmal nocturnal dyspnea) are usually associated with
LV systolic dysfunction. Angina during exercise can occur in the absence of significant CAD
and is caused by reduced coronary flow reserve, as epicardial coronary flow shifts from
predominantly diastolic to predominantly systolic. Angina can also occur at night when the
heart rate slows, arterial diastolic pressure falls, and regurgitant volume increases, thus
reducing coronary diastolic perfusion pressure. Some patients with severe AR may complain
of symptoms related to the increased LV size and stroke volume. These include an
uncomfortable awareness of the heartbeat, and atypical chest pain. These symptoms are
especially pronounced when lying down or lying on the left side, which brings the LV apex
closer to the chest wall.
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Signs
The physical examination in patients with chronic severe AR provides many clues to the
diagnosis, though findings are frequently more subtle in patients with milder disease. A
variety of signs are caused by the wide pulse pressure in patients with chronic AR (Table 3).
Among the four signs with sufficient literature for review (Corrigan pulse, Duroziez sign, Hill
sign, and Austin Flint murmur), the Hill sign had a 75-100% sensitivity and a 71-100%
specificity [57]. On precordial inspection and palpation, the apical impulse is displaced
laterally and inferiorly and becomes diffuse and hyperdynamic. A prominent pulsation (and
occasionally a thrill) may be felt at the sternal notch due to concurrent dilation of the
ascending aorta. A diastolic murmur is a key sign favoring the diagnosis of AR, although the
absence of a diastolic murmur does not exclude the diagnosis. The presence of an early
diastolic murmur, as heard by a cardiologist, was the most useful finding for establishing the
presence of AR (positive likelihood ratio 8.8) and its absence the most useful finding for
reducing the likelihood of AR (negative likelihood ratio 0.2-0.3) [58]. On the other hand,
widely different frequencies of a diastolic murmur among patients with chronic AR have been
reported (14 to 73%) [59]. The diastolic murmur of AR begins immediately after A2. It has a
high pitch, often blowing quality, and may be sustained or having a decreasing intensity. It
may be soft and barely audible, often appreciated only when the patient is sitting up, leaning
forward, and holding his or her breath in end-expiration. The intensity of the diastolic murmur
does not correlate well with the severity of AR. The timing and duration of the murmur may
be helpful in assessing the severity of AR:
In mild AR, the murmur occurs only in early diastole and is blowing.
As the regurgitation becomes more severe, the murmur extends through more of
diastole, may become holodiastolic, and is often rougher in quality. Patients with a
longer diastolic murmur, a displaced LV impulse, a wide pulse pressure, and the
peripheral findings of a wide pulse pressure cited in the previous section are
considered to have severe AR.
In very severe regurgitation with ventricular decompensation, the murmur may
become soft or even absent. This change in character reflects the near equalization of
aortic diastolic and LV diastolic pressures, which diminish regurgitant flow. A
similar situation can occur when AR is acute and the LV diastolic pressure is very
high. The intensity of the murmur can also be affected by certain maneuvers. For
example, the intensity of the murmur increases with squatting and decreases with the
Valsalva maneuver. The site at which the murmur is best heard varies with the cause.
The murmur is heard best along the left sternal border, at the third and fourth
intercostal space, when AR is due to valvular disease. In contrast, abnormalities of
the aortic root produce murmurs that are best heard at the right sternal border and
apex. A mid-systolic murmur is heard in many patients with AR [59, 60]. The
systolic murmur typically resembles the ejection type of murmur heard in aortic
stenosis, i.e., a crescendo-decrescendo harsh murmur beginning after S1. This
murmur is caused by a large ejection volume and thus does not necessarily reflect
concurrent AS. A second type of diastolic murmur (the Austin Flint murmur) may
also be appreciated. This murmur is a low-pitched, mid-to-late diastolic rumble, best
heard at the apex. The murmur has been attributed to the effects of competing
antegrade turbulent diastolic blood flow from the left atrium and the retrograde
Epidemiology and Clinical Approach to Aortic Valve Disease
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Sign
Manifestations
Corrigan pulse
“Water hammer” or “collapsing” pulse (rapidly rising and falling arterial pulse
with a wide pulse pressure). Best appreciated in correspondence of radial,
brachial, and carotid arteries.
de Musset’s sign
Head bob in correspondence of each heartbeat.
Traube’s sign
“Pistol shot” pulse (systolic and diastolic sounds) in correspondence of femoral
arteries.
Duroziez’s sign
Systolic and diastolic bruit heard when the femoral artery is partially
compressed.
Quincke’s pulses
Capillary pulsations in the fingertips or lips.
Mueller’s sign
Systolic pulsations of the uvula.
Becker’s sign
Visible pulsation of the retinal arteries.
Landolfi’s sign
Constriction and dilation of the pupils with each heartbeat.
Hill’s sign
Popliteal cuff systolic pressure exceeding brachial cuff pressure by more than
20 mmHg with patient in the recumbent position.
Mayne’s sign
>15 mmHg decrease in diastolic blood pressure with arm elevation from the
value obtained with the arm in the standard position.
Rosenbach’s sign
Systolic pulsations of the liver.
Gerhard’s sign
Systolic pulsations of the spleen.
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regurgitant flow from the aorta. The sensitivity and specificity of the Austin Flint
murmur is uncertain. A review found a higher sensitivity (57 to 100%) among
patients with severe AR compared with patients with mild to moderate disease (0 to
50%) [57]. The heart sounds typically have the following characteristics: S1 may be
soft, often reflecting a long PR interval; S2 is variable; it may be soft, absent, or
single; A2 is often soft or absent while P2 may be normal, but obscured by the
diastolic murmur; a systolic ejection sound may be due to abrupt aortic distension
caused by the large stroke volume; a third heart sound (S3 gallop) is heard when LV
function is severely depressed.
Table 3. Signs of aortic regurgitation
Adapted from: Babu et al., 2003 [57].
Diagnosis and Evaluation
Chronic AR should be suspected in patients with physical examination findings
consistent with AR, as symptoms develop only in a late disease stage. In addition, AR should
be suspected in patients with dilated aortic sinuses or ascending aorta and in patients with
bicuspid aortic valve, even if no murmur is apparent [18]. A TTE examination confirms the
diagnosis of AR, establishes its severity, provides an assessment of aortic root and ascending
aorta dilation, and evaluates LV size and function. Characteristic echocardiographic findings
include the following:
valve leaflets may be abnormal or may be normal but stretched due to aortic dilation,
depending on the etiology of the AR. Abnormalities that may be seen include
thickening, vegetations, calcification, a bicuspid valve, and prolapsed or flail leaflets;
the aortic sinuses are often dilated with or without dilation of the ascending aorta. A
thoracic aortic aneurysm is defined as an aortic diameter is ≥50% greater than the
expected normal diameter but many patients have valve dysfunction due to aortic
enlargement with a smaller degree of dilation;
Claudio Passino, Valentina Galfo, Simone Gasparini et al.
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Qualitative
Semiquantitative
Quantitative
Valve morphology: abnormal/flail/large coaptation defect
Vena contracta width:
>6 mm
EROA:
≥30 mm2
Color flow regurgitant jet:
large in central jets, variable in eccentric jets
Pressure half-time:
<200 ms
Regurgitant volume:
≥60 mL/beat
CW signal of regurgitant jet: dense
Increased LV volume
Holodiatolic flow reversal in descending aorta:
EDV >20 cm/s
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there is often restriction of opening of the anterior mitral leaflet and M-mode
showing high frequency diastolic fluttering, which are due to the diastolic regurgitant
jet of blood from the aorta;
Doppler echocardiography (transthoracic or transesophageal) is the most sensitive
noninvasive technique for detecting the regurgitant AR jet;
the LV end-systolic and end-diastolic dimensions and volumes are increased in
chronic AR. Wall motion is increased in parallel with the large stroke volume, but
the ejection fraction does not increase. When LV decompensation occurs, the
ejection fraction declines and end-systolic dimension and volume increases. Together
with clinical evaluation of patient symptoms, echocardiography helps define the
disease stage according to valve anatomy, severity of AR, and LV size and function,
which in turn determines the need for AVR. The European Society of Cardiology
guidelines have proposed qualitative, semiquantitative and quantitative criteria to
define chronic AR as severe (Table 4). An ECG is not indicated for diagnosis of AR
but is commonly included in the evaluation of patients with AR. ECG findings may
reflect the adaptive changes that occur in the LV as a result of the volume overload,
and typically shows evidence of LV eccentric hypertrophy. Conduction abnormalities
are usually not seen, but can occur late in the course of AR when significant LV
dysfunction occurs. Isolated atrial and ventricular premature beats are common, but
sustained supraventricular or ventricular tachyarrhythmias are unusual in the absence
of significant LV dysfunction. A chest radiograph may be obtained in selected
patients with AR such as those in whom the cause of dyspnea is uncertain. In patients
with severe AR, chest radiograph shows cardiac enlargement in an inferior and
leftward direction. The ascending aorta (and often the aortic arch or knob) are often
dilated. Left atrial enlargement does not occur unless there is significant LV
dysfunction. In patients with a suboptimal or inconclusive TTE, CMR imaging is
indicated to quantify AR severity, measure LV diastolic and systolic volumes, and
assess LV systolic function [18]. Aortic regurgitant volume and regurgitant orifice
area can be quantified. Aortic root angiography and cardiac catheterization with
measurement of LV pressures are indicated when noninvasive tests are inconclusive
or provide discrepant results from clinical findings [18].
Table 4. Features of severe aortic regurgitation
CW, Continuous-wave; EROA, effective regurgitant orifice area; EDV, end-diastolic volume; LV, left ventricle.
Staging and Serial Monitoring
A staging system considering valve anatomy and hemodynamics as well as symptoms has
been proposed (Table 2) [18]. The frequency of serial clinical and echocardiographic
Epidemiology and Clinical Approach to Aortic Valve Disease
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monitoring in patients with asymptomatic aortic regurgitation varies with the severity of the
disease, LV dimensions and LVEF, and the rate of disease progression on previous
examinations.
CONCLUSION
Aortic valve disease is an important cause of morbidity in both industrialized and
developing countries, although the etiology is profoundly different in the two settings. A
careful search for signs and symptoms may provide the first clues to the presence of aortic
valve disease, which can then be verified and characterized by imaging techniques, starting
from TTE. In patients with known severe aortic valve disease, prompt detection of symptom
onset is crucial to refer them to AVR or TAVI (in the case of AS), or AVR (in AR).
Furthermore, a correct interpretation of the signs and symptoms of acute AR can result in a
rapid diagnostic workup and prompt patient referral to surgery.
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