Chapter 18
Congenital and Acquired Cardiac Disease
Learning Objectives
- Identify and describe the findings of the following on a chest radiograph or computed tomography (CT):
- Atrial septal defect
- Ventricular septal defect
- Patent ductus arteriosus
- Identify and describe the findings of the following on a chest radiograph:
- Enlarged left atrium
- Enlarged right ventricle
- Enlarged left ventricle
- Identify and describe the chest radiographic findings and state the most common etiologies of each of the following valvular diseases:
- Aortic stenosis
- Aortic insufficiency
- Mitral stenosis
- Mitral insufficiency
- Tricuspid stenosis
- Tricuspid insufficiency
- Pulmonic stenosis
- Pulmonic insufficiency
- Recognize an enlarged ascending aorta and aortic valve calcification on a chest radiograph and suggest the diagnosis of aortic stenosis when these findings are present.
- Recognize an enlarged left atrium, vascular redistribution, and mitral valve calcification on a chest radiograph and suggest the diagnosis of mitral stenosis when these findings are present.
- Describe the radiographic appearance of mitral annulus calcification and name the cardiac diseases associated with mitral annulus calcification.
- Define the types of cardiomyopathy (dilated, hypertrophic, restrictive) and list the common causes of each.
- Identify on CT and describe the CT findings and clinical significance of lipomatous hypertrophy of the interatrial septum.
- Define arrhythmogenic right ventricular dysplasia, describe the role of magnetic resonance imaging (MRI) in its diagnosis, and identify MRI findings that support the diagnosis.
- Name the most common benign primary cardiac tumors, including myxoma, lipoma, fibroma, and rhabdomyoma.
- Distinguish cardiac tumor from thrombus on CT and MRI.
- Name the most common malignancies to metastasize to the heart; describe their appearance on chest radiography and CT.
- Describe the anatomy of the coronary arteries and identify the following on chest CT:
- Right coronary artery
- Left main coronary artery
- Left anterior descending coronary artery
- Left circumflex coronary artery
- Identify on chest CT and describe the clinical significance of aberrant coronary artery origins.
- Describe the clinical significance of coronary arterial calcification on a chest radiograph.
- Recognize coronary arterial calcification on CT and describe the current role of coronary artery calcium scoring with CT.
- Identify the following postoperative findings on chest radiography and CT:
- Coronary artery stents
- Coronary artery grafts (normal and aneurysmal)
- Cardiac valve replacement
- Poststernotomy infection
- Describe the difference between a left ventricular aneurysm and pseudoaneurysm and distinguish between the two on chest CT.
- Recognize pericardial calcification on a chest radiograph and CT and name the most common causes.
- Identify and describe two chest radiographic signs of a pericardial effusion.
- Name five causes of a pericardial effusion.
- Identify and describe the findings of each of the following on a chest radiograph and CT:
- Constrictive pericarditis
- Pericardial metastases
- Pneumopericardium
- Describe the role of MRI in diagnosing constrictive pericarditis and differentiating constrictive pericarditis from restrictive cardiomyopathy.
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Heart disease is the leading cause of morbidity and
mortality in industrialized countries. Echocardiography, single photon
emission computed tomography (SPECT), scintigraphy, positron emission
tomography (PET), and cardiac catheterization with cineangiography have
long been used to assess the anatomy and function of the normal and
diseased heart. Recent advances in CT and magnetic resonance imaging
(MRI) have generated a renewed interest in cardiac imaging,
particularly among radiologists. CT in particular is an examination
with which radiologists are very comfortable, and it now provides a
means to globally assess the heart and lungs simultaneously. This
chapter will focus on the chest radiographic and CT findings of common
congenital cardiac diseases seen in the adult, normal and abnormal
cardiac anatomy, valvular disease, cardiomyopathies, cardiac tumors,
complications of myocardial infarction and cardiac surgery, and
pericardial disease.
Congenital Cardiac Disease
Whereas congenital abnormalities are the predominant
form of heart disease in childhood, in adults, congenital disorders
represent only 1% of recognized heart disease (1).
In general, adults with newly discovered congenital heart disease are
those whose anomalies produced no symptoms or mild symptoms in
childhood, or those who were misdiagnosed in childhood only to become
symptomatic in adult life. A discussion of all congenital heart defects
that can be diagnosed in adults is beyond the scope of this chapter.
What will be presented is a brief discussion of common left-to-right
shunts that are diagnosed in adulthood and the developmental anomalies
of the aorta that can be associated with congenital heart diseases.
Atrial Septal Defect
Atrial septal defect (ASD) accounts for 80% to 90% of congenital left-to-right shunts found in adults (2,3)
and is three times more common in women than in men. Almost half of the
patients with ASD in all age groups are asymptomatic, and in these
cases the ASD is discovered incidentally on a routine chest radiograph.
There are different types of ASD, with the ostium secundum type
(consisting of an absence or deficiency of tissue in the region of the
fossa ovalis) being the most common type seen in adult patients. In
uncomplicated ASD, the chest radiograph shows enlargement of the right
ventricle and all segments of the pulmonary arteries (“shunt
vascularity”) (Fig. 18-1). The right atrium is
also enlarged, but it is usually not distinguished from right
ventricular enlargement on the chest radiograph. Because the radiograph
does not accurately reflect the size of the right atrium and ventricle,
the overall heart size may appear normal. On the lateral view, right
ventricular enlargement results in a filling in of the retrosternal
clear space and posterior displacement of the left ventricle toward the
spine (4). There is no enlargement of the left
heart in a simple ASD. The aorta appears small, relative to the
pulmonary artery, and the superior vena cava appears small or "absent"
because of rotation of the heart from right-sided cardiac enlargement (Fig. 18-2).
Long-standing large shunts lead to pulmonary arterial
hypertension; when pulmonary arterial pressure exceeds systemic
arterial pressure, a reversal of shunting of blood from left-to-right
to right-to-left occurs (Eisenmenger physiology). In these cases, there
is marked central pulmonary artery dilatation and narrowing of
peripheral pulmonary artery branches (5). The central pulmonary arteries can become aneurysmal and, rarely, can be calcified (Fig. 18-3).
 |
FIGURE 18-1. Atrial septal defect. A:
Posteroanterior (PA) chest radiograph shows marked enlargement of the
central and all segments of the pulmonary arteries. The cardiac
silhouette is enlarged. B: Lateral view
shows filling in of the retrosternal clear space, secondary to right
ventricular enlargement, and pulmonary artery enlargement. |
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 |
FIGURE 18-2. Atrial septal defect. A:
PA chest radiograph of a 17-year-old boy with a heart murmur since
birth shows enlargement of the cardiac silhouette, enlarged central and
peripheral pulmonary arteries ("shunt vascularity"), a normal- to
small-sized aorta, and "absent" superior vena cava shadow. B: Lateral view shows enlargement of the right ventricle, as evidenced by increased opacification posterior to the sternum. |
 |
FIGURE 18-3. Atrial septal defect with Eisenmenger physiology. PA (A) and lateral (B)
chest radiographs of a 52-year-old woman with a large, long-standing
ASD that has resulted in a reversal of shunting of blood and pulmonary
arterial hypertension. There is aneurysmal enlargement and
calcification of the central pulmonary arteries, enlargement of the
right heart, and "absence" of the superior vena cava shadow. C: CT shows large main (M), right (R), and lower (L)
lobe pulmonary arteries. Long-standing left-to-right shunting of blood
has resulted in pulmonary artery aneurysms, which contain
low-attenuation thrombus (arrowheads), and calcification (arrows). D: CT at a level inferior to (C) shows enlarged lower lobe pulmonary arteries containing thrombus (T) and calcification (C), enlarged right atrium (RA), and enlarged right ventricle (RV), causing leftward bowing and hypertrophy of the interventricular septum (arrows). The pulmonary artery lumina are outlined by high-attenuation contrast material (L). |
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ASD closure can be accomplished with a variety of
percutaneously placed devices. A catheter that is placed via the common
femoral vein is fed through the cardiac defect into the left atrium
using fluoroscopic and echocardiographic guidance. A commonly used
device is the Amplatzer Septal Occluder (AGA Medical Corporation,
Golden Valley, MN) (Fig. 18-4). This is a
two-part closure device. One of two nitinol mesh disks is pushed out
through the catheter into the left atrium; this is followed by release
of the second disk into the right atrium to close the defect.
Ventricular Septal Defect
Ventricular septal defect (VSD) is the most common congenital heart disease in childhood, but it represents only 10% of
congenital cardiac lesions in the adult patient. Surgical correction and spontaneous closure of the defect account for the decreased incidence in the adult patient (6). Most patients with VSD who survive into adulthood without intervention have small and physiologically inconsequential defects. Patients who reach adult life with large VSDs have pulmonary arterial hypertension, progressive right-to-left shunting (Eisenmenger physiology), and cyanosis. Small shunts cannot be identified on chest radiography. With large shunts (VSDs with a shunt ratio greater than 2:1) and normal pulmonary vascular resistance, the chest radiograph shows “shunt vascularity,” enlargement of the left atrium and both ventricles, a normal or small aorta, and a normal right atrium. The left ventricular apex projects to the left, inferiorly and posteriorly. On frontal chest radiographs, enlargement of the left atrium is seen as a “double density” behind the right atrium, and straightening or focal convexity of the left mediastinal border is seen below the pulmonary artery shadow.
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congenital cardiac lesions in the adult patient. Surgical correction and spontaneous closure of the defect account for the decreased incidence in the adult patient (6). Most patients with VSD who survive into adulthood without intervention have small and physiologically inconsequential defects. Patients who reach adult life with large VSDs have pulmonary arterial hypertension, progressive right-to-left shunting (Eisenmenger physiology), and cyanosis. Small shunts cannot be identified on chest radiography. With large shunts (VSDs with a shunt ratio greater than 2:1) and normal pulmonary vascular resistance, the chest radiograph shows “shunt vascularity,” enlargement of the left atrium and both ventricles, a normal or small aorta, and a normal right atrium. The left ventricular apex projects to the left, inferiorly and posteriorly. On frontal chest radiographs, enlargement of the left atrium is seen as a “double density” behind the right atrium, and straightening or focal convexity of the left mediastinal border is seen below the pulmonary artery shadow.
 |
FIGURE 18-4. Atrial septal defect occluder. A:
PA chest radiograph of a 50-year-old woman with a history of transient
ischemic attacks shows an Amplatzer Septal Occluder device (AGA Medical
Corporation, Golden Valley, MN) (arrow) in the location of the foramen of ovale. B: Lateral view confirms appropriate placement of the device (arrow). |
Patent Ductus Arteriosus
The ductus arteriosus is a portion of the sixth aortic
arch in the fetus that connects the left pulmonary artery to the
descending thoracic aorta. Twelve to 24 hours after birth, the ductus
is functionally closed, and anatomic closure occurs 1 to 2 weeks later.
However, for unknown reasons, the ductus arteriosus may remain patent,
creating a left-to-right shunt and varying degrees of overcirculation
to the lungs, left atrium, left ventricle, and the ascending and arch
portions of the aorta. If the ductus does not close, Eisenmenger
physiology develops when pulmonary vascular resistance exceeds systemic
resistance and causes a right-to-left shunt across the ductus
arteriosus. The radiographic features of an uncomplicated patent ductus
arteriosus (PDA) are similar to those of a VSD, except for the size of
the aorta. In PDA, the ascending and arch portions of the aorta can
enlarge (with the degree of enlargement dependent on the size of the
shunt), indicating that the shunt is extracardiac, as opposed to an
intracardiac shunt, such as a VSD, with which the size of the aorta is
normal or small. However, aortic size is not always a reliable
criterion, and in practice it can be difficult to distinguish VSD from
PDA on chest radiography. Another finding of PDA in an adult is
calcification of the ductus.
Anomalies of the Thoracic Aorta
Congenital bicuspid aortic valve is a relatively common
malformation. As the valve thickens and becomes fibrotic, it becomes
stenotic. When this occurs, the valve becomes calcified. A densely
calcified aortic valve, as seen on chest radiography or CT in a patient
under the age of 55, should prompt consideration of this anomaly.
In left aortic arch with aberrant right subclavian
artery, the right subclavian artery, instead of the first branch, takes
off as the final branch of the aorta. Patients with this common anomaly
are usually asymptomatic but may present with dysphagia as a result of
the retroesophageal course of the aberrant artery. The frontal chest
radiograph often shows an abnormal mediastinal contour at the level of
the aortic arch, where the proximal portion of the aberrant artery is
dilated - the so-called "diverticulum of Kommerell." The lateral chest
radiograph may show anterior displacement of the trachea.
A right aortic arch occurs when there is interruption of
the embryonic left aortic component of the hypothetical double aortic
arch. Two types are described: Type 1 is a mirror image of left aortic
arch and is associated with cyanotic congenital heart disease in more
than 95% of patients, most of whom have tetralogy of Fallot (7).
Type 2 right aortic arch - a right aortic arch with an aberrant left
retroesophageal subclavian artery - is common, occurring in 1 in 2,500
persons, and is usually found incidentally (1).
Additional cardiac anomalies occur in only 5% to 15% of patients with
type 2. Chest radiographs of a right aortic arch show that the trachea
is bowed to the left at the level of the right aortic arch, producing a
convex bulge just above the azygous vein (Figs. 18-5 and 18-6).
It is typical for a right-sided arch to be high riding and present as a
"mass" in the right paratracheal area. An aortic diverticulum, or
proximal arterial dilation, is seen to the left and slightly below the
usual site of a left-sided aortic arch. The diverticulum may be of
sufficient size to produce a large bulge immediately above the left
main pulmonary artery and simulate a left aortic arch or a nonvascular
mediastinal mass. Most often, the left mediastinal bulge is a result of
the aortic diverticulum rather than the aberrant left subclavian artery
itself. As the left subclavian artery crosses from right to left, it
will cause a posterior impression on the air-filled esophagus and the
trachea, which is seen best on the lateral chest radiograph. The right
aortic arch usually crosses to the left side posteriorly, in the middle
of the thorax behind the right pulmonary artery, to descend into the
abdomen on the left side. A double aortic arch forms a complete
vascular ring and on occasion can first present in adulthood.
Pseudocoarctation is a term
used to denote a focal narrowing of the aortic arch that has the same
morphology as classic coarctation but does not produce obstruction.
This anomaly is a buckling of the aorta at the isthmus with little or
no pressure gradient across the buckled portion (less than 30 mm Hg) (8).
Because there is no obstruction, there is no collateral flow, and there
is no rib notching as is seen with classic coarctation. The chest
radiograph shows a left "mediastinal mass" that represents an
elongated, redundant, and high aortic arch. Sagittally reconstructed CT
of the chest can show the high arch with a kink at the isthmus,
resembling the numeral 3, in which the midportion of the 3 corresponds
to the attachment of the ligamentum arteriosum (Fig. 18-7).
A "cervical aortic arch" can resemble pseudocoarctation of the aorta on
chest radiographs, but with a cervical arch, the aortic arch lies in
the neck, above the clavicles, usually on the right side.
Acquired Heart Disease
Valvular Disease
The radiologic signs of uncomplicated valvular lesions are relatively straightforward (Table 18-1).
Valve stenosis produces pressure overload and myocardial hypertrophy
without dilatation. Dilatation indicates that heart failure has
developed. Valve insufficiency produces volume overload and a
combination of dilatation and hypertrophy of the involved cardiac
chambers. With insufficiency, a dilated heart does not indicate cardiac
decompensation.
Aortic Stenosis
Aortic stenosis (AS) can exist at the valvular,
subvalvular, or supravalvular level. The chest radiographic
abnormalities depend on the age of the patient as well as on the
severity of the stenosis. The adult heart is of normal size and the
lungs are normal, because left ventricular failure and dilatation occur
only in terminally ill patients. Radiographically detectable
calcification in the aortic valve occurs in all types of aortic
stenosis and marks the stenosis as clinically severe. Dilatation of the
ascending aorta is frequent in aortic stenosis but correlates poorly
with severity or with the site of the stenosis. Poststenotic dilatation
of the ascending aorta is caused by the jet of blood through the
stenotic valve striking the lateral aortic wall. The lateral wall
of the aorta becomes both dilated and elongated, accentuating the rightward displacement of the aorta. In most children and adults with pure, severe aortic stenosis, the left ventricle is a small cavity that is hypercontractile and has the usual signs of hypertrophy. In the absence of other anomalies, left ventricular dilatation in pure aortic stenosis is direct evidence of heart failure.
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of the aorta becomes both dilated and elongated, accentuating the rightward displacement of the aorta. In most children and adults with pure, severe aortic stenosis, the left ventricle is a small cavity that is hypercontractile and has the usual signs of hypertrophy. In the absence of other anomalies, left ventricular dilatation in pure aortic stenosis is direct evidence of heart failure.
 |
FIGURE 18-5. Right aortic arch. A:
PA chest radiograph shows a right-sided aortic arch and descending
aorta. The trachea is not deviated to the right, as is usually seen
with a left aortic arch. B: Lateral view
shows a posterior impression on the tracheal air column, secondary to
compression from the aberrant left subclavian artery crossing from
right to left. |
 |
FIGURE 18-6. Right aortic arch with aberrant left subclavian artery. A: Scout view from a CT of a 29-year-old man with dysphagia shows deviation of the trachea to the left (arrowheads) and a right-sided descending thoracic aorta (arrows). B: CT shows the right-sided aortic arch (A) and an aberrant left subclavian artery (SCA) arising from the posterior arch and coursing posterior to the trachea (T) and esophagus (E).
Note the compression of the esophagus from the aberrant vessel, causing
the patient's dysphagia. There is also a persistent left superior vena
cava (arrow), in addition to a right superior vena cava (arrowhead). C: CT at a level inferior to (B) shows the persistent left superior vena cava (arrow)
coursing in a left paramediastinal location before draining into the
coronary sinus more inferiorly. The descending aorta is midline at this
level. |
 |
FIGURE 18-7. Pseudocoarctation of the aorta. A: PA chest radiograph of a 50-year-old woman shows a left paratracheal "mass" (arrows). Sternotomy wires are present from previous coronary artery bypass graft surgery. B: CT shows the left subclavian artery (S), right (R) and left (L) brachiocephalic veins, and the high-riding, "buckled" aortic arch (A). C: Sagittal reconstruction shows the buckled aortic arch (arrows) and focal kinking of the aorta at the isthmus (arrowhead). This reconstruction shows how an axial view at the level of the aortic arch (dashed line) will show "two" rounded, contrast-enhanced structures adjacent to each other. |
Calcific AS in the adult can be caused by rheumatic
heart disease, a congenital bicuspid aortic valve, or advanced age and
degeneration of the valve (8). The average age
at which aortic valve calcification is first detected is 25 years for
congenital AS, 47 years for rheumatic AS, and 54 years for degenerative
AS (9). Valve calcification is best seen on the
lateral chest radiograph, because the valve usually projects over the
spine in the frontal projection. An important clue to the diagnosis of
rheumatic disease in the aortic valve is the presence of mitral
stenosis or regurgitation.
AS in elderly patients results from degeneration of the
valve leaflets, with subsequent thickening and calcification. These
aortic valves are tricuspid and have clumps of calcium within the webs
of the leaflets. Some of these elderly patients also have coronary
artery calcification and calcification in the mitral annulus and aortic
arch.
Aortic Insufficiency
Stenotic aortic valves generally also have some
insufficiency. If the aortic insufficiency (AI) is both chronic and
severe, the chest radiograph shows left ventricular enlargement and
dilatation of the entire aorta. This pattern follows the principle that
insufficiency of any of the heart valves enlarges structures on both
sides of the insufficient valve. Isolated AI most commonly results from
a congenital bicuspid aortic valve. Other rare causes of AI include
syphilitic aortitis (presenting between 45 and 65 years of age and
associated with calcification of the ascending aortic aneurysm), Marfan
syndrome (presenting before age 30 and not associated with
calcification of the aneurysm), ankylosing spondylitis, relapsing
polychondritis, and traumatic rupture of the aortic valve.
Mitral Stenosis
Most mitral stenosis (MS) is acquired and usually
results from rheumatic carditis that occurred at least 5 to 10 years
previously. Less common etiologies include left atrial myxoma,
thrombus, or a tumor that may prolapse through the mitral orifice
during diastole and create functional stenosis. Early in the course of
rheumatic MS in the adult, the pulmonary blood flow
redistributes to the upper lobes. Later, the pulmonary arteries enlarge as pulmonary arterial hypertension develops. Later still, the right ventricle fails, from both a pressure overload from pumping into hypertensive pulmonary arteries and from pulmonic insufficiency secondary to a dilated annulus (Fig. 18-8). The chest radiograph in MS physiologically reflects the left atrial hypertension. The left atrium is enlarged, but the left ventricle is normal in size (unless there is coexisting mitral insufficiency). Left atrial enlargement can manifest as straightening of the left heart border or a convex shadow just below the left mainstem bronchus on the posteroanterior chest radiograph (indicating enlargement of the left atrial appendage), splaying of the tracheal carina, and posterior displacement of the pulmonary venous confluence and left lower lobe bronchus on the lateral chest radiograph (Fig. 18-9). The lungs show a diffuse increase in interstitial markings that is likely related to both fibrosis and edema. Patients with severe MS can have hemoptysis caused by bleeding of the engorged plexus of vessels around the middle to smaller bronchi, with a late sequela of pulmonary hemosiderosis, the deposits of which can calcify. The amount of calcium in the mitral valve roughly correlates with the degree of MS, but, unlike the aortic valve, the mitral valve may be severely stenotic and have no radiologically visible calcification. To distinguish aortic from mitral valve calcification on a lateral chest radiograph, one can draw a line from the inferior aspect of the right pulmonary artery along the right middle lobe branch to the tip of the xiphoid; the aortic valve is above this line, and the mitral valve is below this line.
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redistributes to the upper lobes. Later, the pulmonary arteries enlarge as pulmonary arterial hypertension develops. Later still, the right ventricle fails, from both a pressure overload from pumping into hypertensive pulmonary arteries and from pulmonic insufficiency secondary to a dilated annulus (Fig. 18-8). The chest radiograph in MS physiologically reflects the left atrial hypertension. The left atrium is enlarged, but the left ventricle is normal in size (unless there is coexisting mitral insufficiency). Left atrial enlargement can manifest as straightening of the left heart border or a convex shadow just below the left mainstem bronchus on the posteroanterior chest radiograph (indicating enlargement of the left atrial appendage), splaying of the tracheal carina, and posterior displacement of the pulmonary venous confluence and left lower lobe bronchus on the lateral chest radiograph (Fig. 18-9). The lungs show a diffuse increase in interstitial markings that is likely related to both fibrosis and edema. Patients with severe MS can have hemoptysis caused by bleeding of the engorged plexus of vessels around the middle to smaller bronchi, with a late sequela of pulmonary hemosiderosis, the deposits of which can calcify. The amount of calcium in the mitral valve roughly correlates with the degree of MS, but, unlike the aortic valve, the mitral valve may be severely stenotic and have no radiologically visible calcification. To distinguish aortic from mitral valve calcification on a lateral chest radiograph, one can draw a line from the inferior aspect of the right pulmonary artery along the right middle lobe branch to the tip of the xiphoid; the aortic valve is above this line, and the mitral valve is below this line.
TABLE 18-1 RADIOGRAPHIC APPEARANCES OF CARDIAC VALVULAR DISEASE | ||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
Mitral Insufficiency
Acute mitral insufficiency (MI) can be traumatic,
infectious, degenerative, or idiopathic. The pathology is usually a
rupture of a chorda, a papillary muscle, or a mitral leaflet. Acute MI
leads to acute left ventricular failure with severe pulmonary edema and
a normal-sized heart or minimal cardiomegaly.
The major causes of chronic MI are rheumatic fever,
mitral valve prolapse, coronary heart disease, and cardiomyopathy.
Typical radiographic manifestations include a markedly dilated left
atrium, a well-contracting but only mildly enlarged left ventricle,
cephalization of the pulmonary vasculature without frank pulmonary
edema, and moderate pulmonary trunk and right ventricle enlargement. MI
can also be associated with focal edema in the right upper lobe. The
pathogenesis for this condition is the vector of the regurgitant jet of
blood flow from the left ventricle to the left atrium, toward the right
superior pulmonary vein, which locally accentuates the forces for edema
formation in the right upper lobe (10) (Fig. 18-10).
With coronary heart disease and cardiomyopathy, the left ventricle is
usually markedly dilated with poor contractility, with only mild
enlargement of the left atrium.
Mitral Annulus Calcification
The mitral valve ring may calcify in individuals over
age 60; this occurs more commonly in women than in men. The
calcification often forms a pattern resembling the letter "J," the
letter "O," or a reverse letter "C" (Fig. 18-11). In most instances, mitral annulus calcification has little clinical significance and is a
noninflammatory chronic degenerative process. AS and hypertension are associated with mitral annulus calcification, likely as a result of the increased strain exerted on the mitral valve apparatus from the left ventricular pressure overload. If the calcification grows posteriorly into the ventricular myocardium, heart block can occur. If it grows anteriorly into the mitral valve leaflets, MS and MI can occur. Mitral annulus calcification is also associated with increased risk of stroke.
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noninflammatory chronic degenerative process. AS and hypertension are associated with mitral annulus calcification, likely as a result of the increased strain exerted on the mitral valve apparatus from the left ventricular pressure overload. If the calcification grows posteriorly into the ventricular myocardium, heart block can occur. If it grows anteriorly into the mitral valve leaflets, MS and MI can occur. Mitral annulus calcification is also associated with increased risk of stroke.
 |
FIGURE 18-8. Rheumatic mitral stenosis. PA (A) and lateral (B)
chest radiographs of a 40-year-old woman show enlargement of the right
ventricle (note increased opacity posterior to the sternum on the
lateral view) and left atrium (note the convexity of the left heart
border inferior to the left pulmonary artery shadow; arrows).
The central pulmonary arteries are enlarged from pulmonary arterial
hypertension, and there is pulmonary vascular redistribution. Unlike
the aortic valve, the mitral valve may be severely stenotic and, as in
this case, have no radiographically visible calcification. |
 |
FIGURE 18-9. Mitral stenosis. A:
PA chest radiograph of a 43-year-old woman with atrial fibrillation and
a history of rheumatic fever as a child shows abnormal convexity to the
upper left heart border, indicating an enlarged left atrial appendage (arrow). B: Lateral view shows posterior displacement of the pulmonary venous confluence (arrows). |
 |
FIGURE 18-10. Mitral insufficiency. A:
PA chest radiograph of an 84-year-old woman shows an enlarged cardiac
silhouette and right upper lobe pulmonary opacity representing edema. B: CT shows an enlarged left atrium (LA) and bilateral pleural effusions. C: CT at a level inferior to (B) shows calcification of the mitral valve (arrow) and enlargement of the left ventricle (LV). D:
CT with lung windowing shows ground-glass opacity limited to the right
upper lobe. Right upper lobe edema in patients with mitral
insufficiency is thought to be caused by the regurgitant jet of blood
flow through the mitral valve to the right superior pulmonary vein. |
Tricuspid and Pulmonic Valve Disease
Acquired disease isolated to the tricuspid and pulmonic
valves is much less common than aortic and mitral valve disease.
Primary disease of the tricuspid valve is most commonly caused by
rheumatic disease and is associated with disease also involving the
left-sided cardiac valves. Pulmonic stenosis is almost always
congenital (Fig. 18-12), and pulmonary
insufficiency is most commonly a result of severe pulmonic arterial
hypertension of any etiology (e.g., severe MS and recurrent pulmonary
thromboembolic disease).
Multivalvular Disease
Multivalvular involvement is common in patients with
rheumatic heart disease, cardiomyopathies, and connective tissue
disorders (Fig. 18-13). In general, the proximal valvular lesions tend to obscure the distal ones, both clinically and radiographically.
Cardiomyopathy
Cardiomyopathies can be classified as dilated,
hypertrophic, or restrictive. Each can be further categorized as
primary (affecting the myocardium but not other organs) or secondary
(myocardial disease as one manifestation of systemic disease). Idiopathic dilated cardiomyopathy
is characterized by dilatation of both ventricles or only the left
ventricle, and it is either idiopathic or, in about half of cases, is
thought to have a viral or immune etiology. Secondary dilated cardiomyopathy
can be caused by ethanol toxicity, chemotherapeutic agents (e.g.,
doxorubicin), heavy metals, infection, connective tissue diseases,
sarcoidosis, neuromuscular diseases, metabolic or endocrine
abnormalities (e.g., hypocalcemia or hypothyroidism), nutritional deficiencies (e.g., vitamin B12 deficiency), pregnancy, hypertension, or chronic myocardial ischemia; or it may be familial in origin. Chest radiography shows global cardiac enlargement and pulmonary edema.
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abnormalities (e.g., hypocalcemia or hypothyroidism), nutritional deficiencies (e.g., vitamin B12 deficiency), pregnancy, hypertension, or chronic myocardial ischemia; or it may be familial in origin. Chest radiography shows global cardiac enlargement and pulmonary edema.
 |
FIGURE 18-11. Mitral annulus calcification. PA (A) and lateral (B) chest radiographs of an 87-year old woman show a C-shaped calcification in the expected location of the mitral annulus (arrows) and a dual-lead pacemaker. C: CT shows dense calcification of the mitral annulus (arrow). |
Genetic hypertrophic cardiomyopathy
is characterized by biventricular myocardial hypertrophy without
chamber dilatation and is distinguished from acquired hypertensive
heart disease. Initially this disease was called idiopathic
hypertrophic subaortic stenosis, but it was recognized that subaortic
obstruction was only one feature of cardiac hypertrophy. In some cases,
the left ventricle or interventricular septum is predominantly
involved. The disease is genetically transmitted as an
autosomal-dominant trait. The disease can cause sudden death in young
patients. Chest radiographs most commonly show normal heart size. This
is because the hypertrophy decreases ventricular capacity but does not
increase ventricular size. Acquired or secondary hypertrophic cardiomyopathy
can be caused by essential hypertension, renal and adrenal disease,
endocrine diseases, and left ventricular outflow obstruction (i.e.,
aortic stenosis).
Restrictive cardiomyopathy
is characterized by impaired filling of noncompliant ventricles and
diastolic dysfunction. Either right- or left-sided symptoms may
predominate. Causes in-clude amyloidosis, scleroderma, endomyocardial
fibrosis, carcinoid heart disease, sarcoidosis, radiation, and familial
or id-iopathic origins. Heart size and contour are usually normal on
chest radiography. As the disease progresses, a combination of both
enlargement and a thick left ventricular wall may develop. Because of
the stiff right and left ventricles, the right and left
atria dilate in response to filling the ventricles under increased diastolic pressure. Dilated venae cavae, large atria, and small ventricles are also features of constrictive pericarditis, and the two may be difficult to distinguish. The presence of a thickened and calcified pericardium is relatively specific for constrictive pericarditis. However, not all constrictive pericarditis is calcified, and some patients with restrictive cardiomyopathy may have mild thickening of the pericardium.
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atria dilate in response to filling the ventricles under increased diastolic pressure. Dilated venae cavae, large atria, and small ventricles are also features of constrictive pericarditis, and the two may be difficult to distinguish. The presence of a thickened and calcified pericardium is relatively specific for constrictive pericarditis. However, not all constrictive pericarditis is calcified, and some patients with restrictive cardiomyopathy may have mild thickening of the pericardium.
 |
FIGURE 18-12. Pulmonic stenosis. A:
Anteroposterior chest radiograph of a 52-year-old man shows an abnormal
opacity in the expected location of the main and left pulmonary
arteries (arrow). B: CT shows marked enlargement of the main pulmonary artery (PA). C: CT at a level inferior to (B) shows marked enlargement of the left pulmonary artery (LPA) and a normal-size right pulmonary artery. |
 |
FIGURE 18-13. Multivalvular disease. PA (A) and lateral (B) chest radiographs of a 66-year-old woman with a history of rheumatic fever show mitral (solid arrows) and tricuspid (dashed arrows) valve prostheses. |
 |
FIGURE 18-14. Arrhythmogenic right ventricular dysplasia. MRI shows delayed hyperenhancement of the right ventricular free wall (arrows). (Image courtesy of David Bluemke, MD, PhD, Johns Hopkins Medical Institutions, Baltimore, MD.) |
Arrhythmogenic right ventricular dysplasia
(ARVD), an idiopathic cardiomyopathy, is a myocardial disorder of
primarily the right ventricle that is more common in males than females
and has a frequent familial occurrence (11).
The disorder is characterized by transmural or nontransmural
infiltration of the right ventricular myocardium with fat or fibrous
tissue, diffuse thinning of the right ventricular myocardium,
dyskinesia of the right ventricle, and abnormal enhancement on delayed
images (12) (Fig. 18-14).
MRI is the optimal technique for detection and follow-up of clinically
suspected ARVD. Clinically, ARVD is characterized by ventricular
arrhythmias with left bundle branch block that may lead to cardiac
arrest. It is recognized as a major cause of sudden death in young
adolescents. The differential diagnosis of ARVD includes idiopathic
dilated cardiomyopathy (usually presenting with a progressive decline
in left ventricular function, as opposed to the right ventricular
failure seen in ARVD) and the Uhl anomaly (characterized by a
paper-thin right ventricle owing to the nearly complete absence of
myocardial muscle fibers, with no gender predilection or familial
occurrence). The diagnosis of ARVD is based on the presence of
structural, histologic, electrocardiographic, and genetic factors.
Positive MRI findings serve as an important criterion in the clinical
diagnosis of ARVD, although negative MRI findings do not rule out ARVD.
Lipomatous Hypertrophy of the Interatrial Septum
Lipomatous hypertrophy of the interatrial septum (LHIS)
is a benign disorder characterized by the accumulation of fat in the
interatrial septum. The term is actually a misnomer, as the disorder is
caused by an increase in the number, and not hypertrophy, of adipocytes
(13). It typically occurs in elderly and obese patients. The thickness of the fatty septum is typically between 2 and 6 mm (14). CT shows a mass of fat attenuation with sharp margins and sparing of the fossa ovalis (Fig. 18-15),
resulting in a dumbbell shape. The diagnosis is most commonly made
incidentally and is usually unassociated with symptoms, although it can
lead to rhythm disturbances such as P-wave abnormalities, atrial
fibrillation, and even sudden death.
 |
FIGURE 18-15. Lipomatous hypertrophy of the interatrial septum. CT of a 72-year-old woman shows fatty infiltration of the interatrial septum (F), which spares the fossa ovalis (arrow). |
Cardiac Masses
The most common intracardiac mass is thrombus, which is
usually located within the left atrium or the left ventricle and is
associated with mitral valve disease, atrial fibrillation, or
cardiomyopathy. The distinction between tumor and thrombus is made on
MRI by the difference in signal characteristics or on MRI or CT by the
presence or absence of enhancement after administration of contrast
material. Tumor is usually hyperintense in comparison with myocardium
and skeletal muscle (and thrombus) on T2-weighted MRI images and
typically enhances with contrast on MRI or CT images (whereas thrombus
does not enhance).
In all age groups, benign primary cardiac neoplasms are more common than malignant ones (13).
Myxomas are the most common primary cardiac neoplasms, accounting for
about 50% of all primary cardiac tumors. They are located in the left
atrium in 75% of cases and in the right atrium in 20%. Unlike thrombus,
left atrial myxomas are typically attached by a narrow pedicle to the
area of the fossa ovalis (Fig. 18-16). They
usually have heterogenous low attenuation on CT and are frequently
calcified. Rhabdomyomas are the most common cardiac tumors in children,
with up to 50% occurring in children with tuberous sclerosis. They
typically occur in the left or right ventricle. Other benign cardiac
tumors include papillary fibroelastoma (usually attached to the valves
by a short pedicle); fibromas (arising in the myocardial walls,
commonly calcified, and associated with arrhythmias and sudden death);
lipoma; pheochromocytoma (most often located outside the cardiac
chamber); and hemangioma.
One fourth of primary cardiac tumors are malignant, with sarcomas representing the largest number, followed by primary
cardiac lymphomas. Malignant cardiac tumors typically involve more than one cardiac chamber; extend into pulmonary veins, pulmonary arteries, or vena cavae; have a wide point of attachment to the wall of a chamber or chambers; extend outside the heart; and are associated with internal necrosis and hemorrhagic pericardial effusion.
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cardiac lymphomas. Malignant cardiac tumors typically involve more than one cardiac chamber; extend into pulmonary veins, pulmonary arteries, or vena cavae; have a wide point of attachment to the wall of a chamber or chambers; extend outside the heart; and are associated with internal necrosis and hemorrhagic pericardial effusion.
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FIGURE 18-16. Left atrial myxoma. CT of a 63-year-old man shows a low-attenuation mass (arrow) in the anterior left atrium (LA), along the interatrial septum. Note the right atrium (RA), aortic outflow track (Ao), right ventricle (RV), and left ventricle (LV). |
 |
FIGURE 18-17. Pericardial metastases. A:
PA chest radiograph of a 76-year-old woman with breast cancer shows an
enlarged cardiac silhouette and numerous pleural-based masses. The left
hemidiaphragm is elevated, and there is blunting of the left
costophrenic angle. B: CT shows pericardial and left pleural effusions, as well as a soft tissue mass infiltrating the anterior pericardium (arrow). C: Coronal reformatted CT shows left pleural-based masses (arrows) and pericardial effusion (P). The more inferior mass involves the pericardium. |
Metastases to the heart and pericardium are much more common than primary cardiac tumors (15). Melanoma, lymphoma, and breast cancer are the most common tumors to metastasize to the heart (Fig. 18-17). Tumors of the lung and mediastinum can locally invade the pericardium and heart (Fig. 18-18).
Focal obliteration of the pericardial line with or without effusion
indicates extension of tumor into the pericardial sac. If the effusion
is hemorrhagic, extension is almost certain.
Coronary Artery Disease
Coronary arteriography is the accepted method used to
examine the coronary arteries. However, technological advancements with
CT and MRI have dramatically improved the ability to noninvasively
image the coronary arteries. Electrocardiography-gated multidetector CT
shows promise as
a comprehensive method for evaluating cardiac and noncardiac chest pain in stable emergency department patients (16). Among the diagnoses that can be made on CT in addition to coronary artery disease are aortic dissection and pulmonary embolism (the so-called "triple rule-out"). Further hardware and software improvements will be necessary before CT can replace coronary arteriography and become widely used in clinical practice.
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a comprehensive method for evaluating cardiac and noncardiac chest pain in stable emergency department patients (16). Among the diagnoses that can be made on CT in addition to coronary artery disease are aortic dissection and pulmonary embolism (the so-called "triple rule-out"). Further hardware and software improvements will be necessary before CT can replace coronary arteriography and become widely used in clinical practice.
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FIGURE 18-18. Carcinoma invading the heart. CT shows a large right lung mass compressing the superior vena cava (arrow) and left atrium (LA). The right superior and inferior pulmonary veins are obliterated. |
Cardiac Anatomy
Multidetector CT, even in routine use to evaluate the
lungs, can provide information about the morphology of the heart and
coronary arteries. Therefore, it is important to have an understanding
of the normal anatomy and CT appearance of these structures. On axial
imaging, the right ventricle is anterior and has a triangular
appearance, whereas the left ventricle is posterior and more ovoid. The
maximum internal diameter of the right ventricle in its small axis
should be equivalent to that of the left ventricle (17).
The normal myocardial thickness of the right ventricle is 3 to 4 mm,
approximately three times thinner than that of the left ventricle. The
interventricular septum does not normally measure more than 13 mm in
thickness. Anterior and posterior trabecular muscles, and the smaller
medial papillary muscle, are connected to the tricuspid valve leaflets
via the chordae tendineae in the right ventricle. The moderator band
extends from the interventricular septum to the anterolateral aspect of
the right ventricle in the region of the ventricular apex, where it
inserts at the base of the anterior papillary muscle. It conveys the
electrical apparatus of the right bundle of His. Anterior and posterior
papillary muscles can also be seen in the left ventricle connecting to
the leaflets of the mitral valve via chordae tendineae.
The crista terminalis can be recognized as a muscular
prominence on the posterolateral aspect of the right atrium extending
from the orifice of the superior vena cava to that of the inferior vena
cava, and should not be mistaken for intracavitary tumor or thrombus on
CT. The atrioventricular valves are located at the base of each
ventricle.
The coronary arteries arise from the right and left
coronary cusps, which are anatomic dilations of the ascending aorta at
the aortic root, just above the aortic valve. (Figs. 18-19 and 18-20).
Each aortic sinus can also be referred to as a sinus of Valsalva. The
left main coronary artery arises from the left coronary cusp and passes
behind the pulmonary trunk. It divides into the left anterior
descending (LAD) and left circumflex (Cx) arteries. Occasionally, the
left main coronary artery terminates in a trifurcation, giving rise to
an intermediate coronary artery (ramus intermedius) that is directed
laterally. The LAD artery courses along the anterior interventricular
groove. Diagonal branches arise from the LAD and course at downward
angles to supply the anterolateral free wall of the left ventricle. The
LAD supplies the anterior two thirds of the septum, the anterior and
anterolateral walls, the apex, and the anterolateral papillary muscle.
The Cx artery extends laterally and posteriorly in the left
atrioventricular groove and gives rise to obtuse marginal branches that
extend on the lateral and posterior wall toward the apex. The Cx artery
supplies the lateral left ventricular wall and anterolateral papillary
muscle.
The right coronary artery typically arises from the
right coronary cusp. It passes between the right ventricular outflow
tract and the right atrial appendage and then runs in the right
atrioventricular sulcus. The right coronary artery supplies the
posterior one third of the septum, the inferior surface of the left
ventricular and right ventricular free wall and the posteromedial
papillary muscle. The distal right coronary artery courses along the
diaphragmatic surface of the heart. The right coronary artery branches
are the conus branch, the right ventricular branches, the acute
marginal branch and the posterior descending artery. The posterior
descending artery arises from a dominant right coronary artery in 85%
of individuals and it courses in the posterior interventricular sulcus.
Anomalous origin of a coronary artery can occur from the pulmonary artery or aorta (Figs. 18-21 and 18-22). Ectopic origin of coronary arteries from the aorta is found in approximately 1% of the population (18).
On occasion, these anomalies are seen incidentally on CT. The most
common anomaly is ectopic origin of the Cx artery from the right
coronary cusp or right coronary artery. When a major coronary artery
such as the left main or LAD passes between the pulmonary artery and
the aorta, the patient can suffer from angina pectoris, myocardial
infarction, or sudden death.
Coronary Artery Calcification
Electron beam or helical multidetector CT of the
coronary arteries is being used increasingly often for the detection
and quantification of calcium deposits. A calcium "score" is computed
and compared with data normalized by sex and age. An elevated score may
be a signal of clinically significant disease. There are several
limitations to this test. Not all calcium deposits in the coronary
arteries mean that there is a blockage, and not all blocked arteries
contain calcium. A high heart rate may interfere with the test. Exactly
how the calcium score relates to the likelihood of experiencing angina,
myocardial infarction, and sudden cardiac death remains uncertain. Men
younger than 35 years of age and women younger than 40 are not likely
to benefit from the test unless there are risk factors such as diabetes
or a strong family history of heart disease. Men older than 65 years
and women older than 70 are not likely to be treated differently as a
result of test findings.
Calcification of the coronary arteries is a frequent incidental finding on chest radiography and routine chest CT (Fig. 18-23). In this setting, the observation should not be considered clinically significant unless the patient is under the age of 40.
Cardiac Postoperative Complications
Coronary artery bypass grafting (CABG) and percutaneous
coronary intervention have long been the definitive aggressive options
for treating patients with coronary artery disease (19).
These treatments, particularly CABG, are associated with a variety of
acute and chronic postoperative complications. Similar complications
are seen after valve replacement, although anticoagulation therapy for
valve replacement results in more problems with bleeding. Acute
complications resulting
from cardiac surgery include atelectasis, edema, hemorrhage, pericardial effusion, and extrapulmonary air collections (e.g., pneumothorax, pneumomediastinum). Chronic complications include postpericardiotomy syndrome (a febrile illness consisting of various combinations of pericarditis, pleuritis, and pneumonitis); constrictive pericarditis; postoperative infection; pseudoaneurysm; and aortic dissection.
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from cardiac surgery include atelectasis, edema, hemorrhage, pericardial effusion, and extrapulmonary air collections (e.g., pneumothorax, pneumomediastinum). Chronic complications include postpericardiotomy syndrome (a febrile illness consisting of various combinations of pericarditis, pleuritis, and pneumonitis); constrictive pericarditis; postoperative infection; pseudoaneurysm; and aortic dissection.
 |
FIGURE 18-19. Cardiac anatomy. A: Electrocardiography-gated multidetector CT shows a normal left main coronary artery (arrow) arising from the left coronary cusp. B: The left anterior descending coronary artery (arrow) arises from the left main coronary artery and courses anteriorly in the interventricular groove. C:
Occasionally, as in this case, the left main coronary artery terminates
in a trifurcation, giving rise to an intermediate coronary artery
(ramus intermedius; solid arrow), left anterior descending coronary artery (coursing anteriorly), and left circumflex coronary artery (dashed arrow). D: The right coronary artery arises from the right coronary cusp (solid arrow). Note the left anterior descending coronary artery (dashed arrow) and circumflex coronary artery (curved arrow). E: The circumflex coronary artery gives rise to marginal branches (arrow). Note the left (L), right (R), and noncoronary (N) cusps. F: Papillary muscles (solid black arrow) are connected to the mitral valve leaflets via the chordae tendineae (dashed black arrows). Note the right coronary artery (curved white arrow). G: Anterior papillary muscles are seen in the left ventricle (arrow). H: The coronary sinus (arrow) drains into the right atrium (RA). I: The posterior descending coronary artery (arrow) arises from the right coronary artery in 85% of individuals and courses in the posterior interventricular sulcus. |
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FIGURE 18-20. Coronary artery stent. A: Lateral chest radiograph of a 46-year-old man shows a right coronary artery stent (arrows). B: CT shows calcification in the left main and left anterior descending arteries (arrow). |
 |
FIGURE 18-21. Anomalous origin of coronary artery. CT shows the right main coronary artery arising from the right coronary cusp (solid arrow). The left main coronary artery also arises from the right coronary cusp and courses posterior to the aorta (dashed arrows).
This is considered a benign anomalous course. (Case courtesy of Cris A.
Meyer, MD, and Rhonda Strunk, RT, R(CT), University of Cincinnati 3D
Post Processing Lab, University of Cincinnati Medical Center,
Cincinnati, OH.) |
CT is helpful in evaluating poststernotomy
complications. Expected postoperative changes, which can persist for 2
to 3 weeks, include minimal presternal and retrosternal soft tissue
infiltration with edema and blood, focal retrosternal air and fluid,
localized hematoma, postincisional bone defects, minor sternal
irregularities or offset, and minimal pericardial thickening (20). After this period of time, these changes should prompt
consideration of infection, especially when focal collections of presternal or retrosternal air and fluid are seen (Figs. 18-24 and 18-25). Noninfected mediastinal fluid collections can also be seen at this time, and only bacteriological analysis can differentiate bland from infected fluid collections.
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consideration of infection, especially when focal collections of presternal or retrosternal air and fluid are seen (Figs. 18-24 and 18-25). Noninfected mediastinal fluid collections can also be seen at this time, and only bacteriological analysis can differentiate bland from infected fluid collections.
 |
FIGURE 18-22. Anomalous origin of coronary artery. CT shows the right main coronary artery arising from the right coronary cusp (solid arrow).
The left main coronary artery also arises from the right coronary cusp.
The left anterior descending coronary artery courses anterior to the
pulmonary artery, a benign course (dashed arrow). The circumflex coronary artery (angled arrow) courses posteriorly, between the aorta and pulmonary artery (PA).
This anomaly can result in angina pectoris or myocardial infarction.
(Case courtesy of Cris A. Meyer, MD, and Rhonda Strunk, RT, R(CT),
University of Cincinnati 3D Post Processing Lab, University of
Cincinnati Medical Center, Cincinnati, OH.) |
 |
FIGURE 18-23. Coronary artery calcification. A: CT of a 66-year-old man shows dense calcification in the left anterior descending coronary artery (arrow). B: CT at a level inferior to (B) shows dense calcification of the circumflex coronary artery (dashed arrow) and a stent in the right coronary artery (solid arrow). |
 |
FIGURE 18-24. Poststernotomy infection. A:
CT of a 47-year-old woman who underwent coronary artery bypass grafting
shows fluid in the presternal and retrosternal areas and an air–fluid
level in the presternal area (arrow). B: CT at a level inferior to (A) shows abnormal air and fluid in the retrosternal area (arrow). |
Aneurysms of saphenous vein grafts to coronary arteries
are unusual complications of CABG surgery, with only 50 cases reported
since 1975 (21). True aneurysms are
atherosclerotic in nature and appear as a late postoperative
complication more than 5 years after CABG. Pseudoaneurysms may occur
early as well as late after initial surgery, at the anastomotic site in
most cases. Whenever a new mediastinal mass is seen on chest
radiography in a patient who has undergone CABG, a graft aneurysm
should be considered, and CT or MRI with intravenous contrast should be
obtained. CT shows a round mass adjacent to a graft site with variable
degrees of luminal enhancement or thrombus (Fig. 18-26).
 |
FIGURE 18-25. Poststernotomy infection. A: CT performed 13 days after coronary artery bypass grafting shows air in the presternal area (solid arrow) and fluid in the retrosternal area (dashed arrow). B: CT at a level inferior to (A) shows a focal fluid collection with an enhancing rim (arrow) encasing the right coronary artery. |
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FIGURE 18-26. Coronary artery bypass graft aneurysm. A:
PA chest radiograph of a 70-year-old woman with a history of coronary
artery bypass grafting shows an abnormal left mediastinal contour (arrow). B: CT shows a round mass with peripheral calcification (arrows) at a graft site. C: MRI shows the graft aneurysm (arrows) adjacent to the main pulmonary artery (P). Note the ascending aorta (A), superior vena cava (SVC), and descending aorta (D). |
More and more patients are undergoing percutaneous
stenting of diseased coronary arteries as an alternative to CABG. These
stents can be visualized on routine chest radiography and CT (Figs. 18-20 and 18-23).
Complications After Myocardial Infarction
Ischemic myocardial disease may be associated with a
normal chest radiograph, or the radiograph may show nonspecific signs
of cardiac failure. Ventricular aneurysm formation can complicate
previous myocardial infarction in up to 10% of cases, occurring between
2 weeks and 2 years after ischemic myocardial necrosis and being
located most often on the anterior wall of the left ventricle or at the
cardiac apex (17) (Fig. 18-27).
An abnormal bulge to the lower left heart border on a frontal chest
radiograph may be seen. CT can show thinning of the involved
myocardium, hypodensity in the abnormal ventricular wall that
approaches that of fat, myocardial calcification, or local endoluminal
thrombus. True ventricular aneurysms arising from previous myocardial
infarction with associated scar formation and thinning of the
myocardium should be differentiated from ventricular pseudoaneurysms,
which are characterized by actual rupture of the myocardium and
containment of the aneurysm by only the thin pericardium and which are
at high risk of fatal rupture (17).
Pseudoaneurysms are typically inferior in location and have a more
discrete, narrower neck than true aneurysms. CT is helpful in
distinguishing aneurysm from pseudoaneurysm by demonstrating a narrow
orifice or "neck" leading from the ventricular chamber to a
pseudoaneurysm.
Pericardial Disease
The pericardium is outlined by epicardial and
pericardial fat, and the two layers of the pericardium together
normally measure no more than 3 mm in thickness. It is important to
understand the anatomy of the pericardial recesses and not mistake them
for enlarged lymph nodes or other masses, especially in the right
paratracheal region (Fig. 18-28), in the aortopulmonary window, in the subcarinal region, and around the insertion of the pulmonary veins (Fig. 18-29). When visible, pericardial recesses can usually be recognized as having fluid attenuation on CT.
The more common causes of pericardial effusion are listed in Table 18-2 (8). Cardiac tamponade is a low cardiac output state caused by excess fluid in the pericardial space that compresses the heart (Fig. 18-30).
This can occur when as little as 150 to 250 mL of fluid accumulate
acutely. In chronic or recurrent pericarditis, pericardial fluid may
accumulate slowly, so that several liters may be present without
tamponade occurring. Enlargement of the cardiac silhouette on the chest
radiograph usually is not apparent until 250 mL of fluid are in the
pericardial space. A typical chest radiograph of a patient with a
pericardial effusion shows a wide cardiac silhouette with little
abnormality in the lungs. The classic appearance is that of a “water
bottle–shaped heart,” in which both sides of the
heart appear rounded and displaced laterally. The epicardial "fat pad" sign is produced when the pericardial layers and fluid widen the space between the anterior epicardial fat and substernal fat stripes by more than 4 mm. This is best appreciated on the lateral chest radiograph. Pulmonary edema is rarely seen in cardiac tamponade unless another disease, such as left ventricular failure from myocardial infarction, is also present. Diagnostic mimics of large pericardial effusions include pan-chamber cardiac enlargement and a large anterior mediastinal tumor in front of the heart.
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heart appear rounded and displaced laterally. The epicardial "fat pad" sign is produced when the pericardial layers and fluid widen the space between the anterior epicardial fat and substernal fat stripes by more than 4 mm. This is best appreciated on the lateral chest radiograph. Pulmonary edema is rarely seen in cardiac tamponade unless another disease, such as left ventricular failure from myocardial infarction, is also present. Diagnostic mimics of large pericardial effusions include pan-chamber cardiac enlargement and a large anterior mediastinal tumor in front of the heart.
 |
FIGURE 18-27. Left ventricular aneurysm. A:
Lateral CT scout image of a 78-year-old man with ischemic
cardiomyopathy and previous anteroseptal and apical septal myocardial
infarction shows a curvilinear area of calcification overlying the
heart (arrow). B: CT shows a focal outpouching of the left ventricular apex with a densely calcified rim (arrow). Note the relatively wide aneurysmal neck, which is typical of true aneurysms and distinguishes this from a pseudoaneurysm. |
 |
FIGURE 18-28. Right paratracheal pericardial recess. A: CT shows a mass of fluid attenuation in the right paratracheal area (arrow). This fluid collection should not be mistaken for paratracheal lymphadenopathy. B: CT at a level inferior to (A) shows pericardial recess fluid (R) posterior to the ascending aorta. |
In chronic constrictive pericarditis, ventricular
filling is impeded by loss of compliance. The cardiac chambers are
constricted by the thickened pericardium, and diastolic pressures are
elevated. In constrictive pericarditis, the thickness of the
pericardial layers typically exceeds 4 mm. The pericardium is calcified
on the chest radiograph in about 50% of patients with constrictive
pericarditis and presents as a curvilinear opacity conforming to the
anatomy of the pericardial sac (Fig. 18-31).
When the calcifications are thin and linear, the etiology is usually viral or uremic pericarditis. Other causes include collagen vascular disease, trauma (including postsurgery), and radiation. When shaggy, thick, and amorphous, the calcification has historically been attributed to tuberculosis. Asbestos can also affect the pericardium, creating thick plaques similar to those occurring in asbestos-related pleural disease. MRI does not show calcification but demonstrates pericardial thickening and sometimes can be used to show impaired diastolic function. Because CT will detect minute amounts of calcium and MRI can miss significant deposits, some have advocated the use of MRI for the diagnosis of constrictive pericarditis only in those patients who have contraindications to iodinated contrast material (22). Additional findings seen with constrictive pericarditis include distorted contours of the ventricles (tubular-shaped ventricles), hepatic venous congestion, ascites, pleural effusions, and occasionally pericardial effusion. Often the atria, coronary sinus, inferior vena cava, and hepatic veins are dilated, reflecting elevated central venous pressure. Patients with constrictive pericarditis and restrictive cardiomyopathy can have similar clinical and physiologic findings. The presence of pericardial thickening or other signs of constriction suggests that the abnormality is pericardial in origin. A normal pericardium with thickening of the myocardium suggests cardiomyopathy as the diagnosis.
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When the calcifications are thin and linear, the etiology is usually viral or uremic pericarditis. Other causes include collagen vascular disease, trauma (including postsurgery), and radiation. When shaggy, thick, and amorphous, the calcification has historically been attributed to tuberculosis. Asbestos can also affect the pericardium, creating thick plaques similar to those occurring in asbestos-related pleural disease. MRI does not show calcification but demonstrates pericardial thickening and sometimes can be used to show impaired diastolic function. Because CT will detect minute amounts of calcium and MRI can miss significant deposits, some have advocated the use of MRI for the diagnosis of constrictive pericarditis only in those patients who have contraindications to iodinated contrast material (22). Additional findings seen with constrictive pericarditis include distorted contours of the ventricles (tubular-shaped ventricles), hepatic venous congestion, ascites, pleural effusions, and occasionally pericardial effusion. Often the atria, coronary sinus, inferior vena cava, and hepatic veins are dilated, reflecting elevated central venous pressure. Patients with constrictive pericarditis and restrictive cardiomyopathy can have similar clinical and physiologic findings. The presence of pericardial thickening or other signs of constriction suggests that the abnormality is pericardial in origin. A normal pericardium with thickening of the myocardium suggests cardiomyopathy as the diagnosis.
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FIGURE 18-29. Right pulmonary vein pericardial recess. CT shows a focal fluid collection (arrow) adjacent to the right inferior pulmonary vein. This should not be mistaken for lymphadenopathy or other masses. |
 |
FIGURE 18-30. Acute infectious pericarditis. A: PA chest radiograph of a 26-year-old man with a neck abscess shows an enlarged cardiac silhouette. B: CT shows high-density pericardial fluid and thickening and enhancement of the pericardium (arrows). C: CT at a level inferior to (B) shows a focal pericardial fluid collection (solid arrow) compressing the superior vena cava (dashed arrow) and left atrium. The patient had clinical symptoms of pericardial tamponade. |
TABLE 18-2 COMMON CAUSES OF PERICARDIAL EFFUSION | |
|---|---|
|
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FIGURE 18-31. Constrictive pericarditis. PA (A) and lateral (B) chest radiographs show curvilinear calcification conforming to the anatomy of the pericardial sac (arrows). |
 |
FIGURE 18-32. Uremic pericarditis. A:
PA chest radiograph of a 33-year-old woman with acute chest pain and a
history of human immunodeficiency virus infection–related nephropathy
shows a "water bottle"–shaped heart. B: After drainage of exudative pericardial fluid, the chest radiograph shows air outlining the pericardial sac (arrows). C: CT shows pneumopericardium (solid arrow), including air in the pericardial recess (dashed arrow). |
 |
FIGURE 18-33. Purulent pericarditis. A: PA chest radiograph of a 61-year-old man with acute chest pain shows pneumopericardium (arrows). The air in the pericardial sac does not extend above the aortic arch. B: CT shows air confined to the pericardial sac (P). One hundred forty milliliters of gas and pus were drained via pericardiocentesis. |
Numerous congenital abnormalities of the pericardium can occur. Pericardial cysts are discussed in Chapter 6.
Absence of the pericardium can be complete but is more often partial,
with the defects more often left-sided. When most of the pericardium is
absent, the heart axis will usually shift to the left and posteriorly.
Partial absence of the left pericardium can result in a
prominent-appearing left atrial appendage or pulmonary artery segment.
Herniation of the heart through a congenital, traumatic, or surgical
pericardial defect is rare but life threatening.
Pneumopericardium is gas in the pericardial sac and can
rarely be idiopathic but more commonly results from trauma; infection
with a gas-forming organism; increased intrathoracic pressure (e.g.,
asthma, barotrauma, Valsalva maneuver); adjacent lung cancer or
infection; esophageal rupture; forceful coughing; cocaine abuse;
gastric perforation; liver abscess; pancreatic pseudocyst; or
pregnancy. When a large amount of air collects in the pericardial sac
acutely, the patient can suffer from cardiac tamponade. On chest
radiography, pneumopericardium presents as lucency confined to the
pericardial sac that does not extend above the aortic arch (Fig. 18-32). CT clearly shows air confined to the pericardial sac, distinguishing it from pneumomediastinum (Fig. 18-33).
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