Thoracic Imaging 2003 - Society of Thoracic Radiology

as well as separation of the cusps due to involvement of the
annulus. Dilatation of the aortic root can occur in patients with
aortitis, aortic dissection, systemic hypertension, cystic medial
necrosis and connective tissue disease.
When the aortic valve is regurgitant, the left ventricle
receives the normal blood volume from the left atrium as well
as the regurgitant volume from the aorta. To compensate for this
increased blood volume, the left ventricle enlarges in order to
maintain cardiac output. However, over time, the increased
stroke volume leads to decreased systolic function. The left
ventricle requires an increased oxygen demand due to the
increased stroke volume and increased wall tension as a result
of dilatation. This may result in angina. Left ventricular
enlargement might be identified on chest radiograph. However,
the ventricle must enlarge almost twice its size before this is
reliably seen. Cross-sectional imaging will show dilatation of
the left ventricle and aorta.
Mitral Stenosis
Rheumatic heart disease accounts for nearly all cases of
mitral stenosis. Women are affected much more frequently than
men. Mitral stenosis occurs several years after the initial endocarditis
and is a result of fibrotic thickening of the valve and
scarring and retraction of the chordae tendinae. The stenotic
valve increases the left atrial pressure, which is transmitted to the
pulmonary vasculature resulting in pulmonary venous hypertension.
The left atrium also dilates with dilatation of the left atrial
appendage. If the left atrial appendage is not dilated, it may represent
a prevalvular lesion such as atrial myxoma or mobile
thrombus or may represent chronic clot that has retracted the
appendage. The left ventricle, which is distal to the site of stenosis,
will be normal in size. With progression of mitral stenosis,
patients will develop interstitial edema. With continued elevated
venous pressure, pulmonary arterial hypertension develops with
increase in size of the main pulmonary artery. With longstanding
mitral stenosis, pulmonary valve regurgitation, right ventricular
failure and tricuspid regurgitation may occur.
The chest radiograph and cross-sectional imaging will show
redistribution of the pulmonary vasculature, mild left atrial
enlargement, with enlargement of the left atrial appendage and
may show prominence of the main pulmonary artery.
Calcification of the left atrium is a late sequelae of rheumatic
endocarditis.
Patients with mitral stenosis may initially be asymptomatic.
As the left atrial pressure increases, the patient experiences dyspnea
on exertion. Dyspnea is also a symptom when pulmonary
arterial hypertension develops. Once the right ventricle fails,
symptoms include peripheral edema and ascites. Right heart
failure also leads to decreased left ventricular cardiac output
leading to fatigue.
Mitral Regurgitation
Although mitral regurgitation can result from rheumatic
heart disease, unlike mitral stenosis, there are multiple additional
causes of mitral regurgitation. Abnormality of the mitral
valve leaflets (fusion, calcification, retraction) is frequently seen
in patients with rheumatic hart disease. Calcific or myxomatous
degeneration of the valve, and endocarditis can also result in a
regurgitant mitral valve. If the left ventricle, and therefore the
mitral annulus are dilated, the mitral valve leaflets may fail to
close. Usually the left ventricle is dilated secondary to ischemic
heart disease or cardiomyopathy. Abnormality of the tensor
apparatus can result in mitral valve regurgitation. This can
occur with rupture of the papillary muscle following myocardial
infarction or papillary muscle dysfunction secondary to
ischemia. Rupture of the chordae tendinae can occur in patients
with endocarditis and mitral valve prolapse. Rheumatic heart
disease can result in shortening and thickening of the chordae
tendinae resulting in mitral valve regurgitation. Occasionally,
exuberant calcification of the mitral annulus may adhere to and
immobilize the posterior mitral leaflet resulting in regurgitation.
The chest radiograph and cross-sectional imaging will show
evidence of left atrial enlargement, which is usually more pronounced
than in patients with isolated mitral stenosis.
Enlargement of the left atrial appendage can be seen in patients
with mitral regurgitation secondary to rheumatic heart disease.
Because the left ventricle also sees the increased stroke volume,
left ventricular enlargement will be present although this is not
as reliably demonstrated on chest radiographs as left atrial
enlargement. Redistribution of the pulmonary vasculature and
mild interstitial edema will also be present. If mitral regurgitation
occurs acutely, such as in papillary muscle rupture, cardiac
decomposition occurs. However, the chest radiograph may not
show evidence of left atrial and left ventricular enlargement as
in patients with slowly developing mitral regurgitation, since the
cardiac chambers do not have time to adapt. Patients with left
atrial enlargement may develop atrial fibrillation. Occasionally,
patients with mitral regurgitation may show evidence of edema
localized to the right upper lobe. This is thought to be secondary
to the regurgitant blood being directed toward the right
superior pulmonary vein.
Pulmonary Stenosis
Pulmonary stenosis usually results from a congenital lesion
in which there is thickening of the leaflets with or without
fusion of the commissures, or there is a congenitally bicuspid
pulmonary valve. Abnormalities associated with congenital pulmonary
stenosis include ASD, VSD, TOGV, single ventricle and
tetralogy of Fallot. Rare causes of pulmonary stenosis include
rheumatic heart disease and carcinoid tumor, metastatic to the
liver. In the setting of carcinoid, vasoactive amines result in
thickened valve leaflets. Pulmonary valve stenosis results in
increased right ventricular systolic pressure. The right ventricle
responds by hypertrophying. The right atrial pressure increases
due to the elevated right ventricular filling pressures. With elevation
of the right atrial pressure, the foramen ovale can become
patent resulting in a right-to-left shunt. In the setting of right
ventricular failure secondary to pressure overload, the right ventricle
dilates which can lead to stretching of the tricuspid annulus
and resultant tricuspid regurgitation. In the absence of rightto-left
shunt and right ventricular failure, patients may be
asymptomatic.
In patients with congenital pulmonary stenosis, the chest
radiograph and cross-sectional imaging shows enlargement of
the main pulmonary artery and left pulmonary artery. This is
due to a high velocity jet directed at the anterior wall of the
main pulmonary artery with turbulence extending into the left
pulmonary artery. The right pulmonary artery, which takes off
at a more acute angle to the main pulmonary artery, is unaffected.
Right ventricular hypertrophy may be identified on the lateral
view, with filling of the retrosternal space. Subpulmonary
narrowing may occur due to hypertrophy of the crista supraventricularis.
This may cause outflow obstruction that can persist
after valve replacement.
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