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4.3 Myocardial Diseases (Cardiomyopathies) 171
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Fig. 4.3.4 Four-chamber
white-blood cardiac MRI
during diastole ( a ) and
systole ( b ) of a patient
with arrhythmogenic right
ventricular dysplasia
(ARVD) show thinning of
the left ventricle (LV) wall
with hyperintense signal
within the wall representing fi bro-fatty changes
( arrows )
Noncompaction Cardiomyopathy
(Spongy Myocardium)
Signs on MRI
NCCM is a rare, distinct cardiomyopathy characterized by arrest of the left ventricular muscle compaction during embryonal development, causing left
ventricular myocardial trabeculation with deep intertrabecular recesses that makes the left ventricular myocardium looks like sponge.
NCCM commonly affects the LV; however, the right
ventricle can be involved occasionally. The disease has
an incidence of 0.05% in the general population, and
can occur as an isolated case or associated with other
cardiac anomalies. The clinical picture is variable.
Patients may show no symptoms, while others may
show signs of severe heart failure and arrhythmias.
Fig. 4.3.5 Three-chamber
white-blood cardiac MRI
( a ) and short-axis view
( b ) show LV trabeculation
in a patient with
noncompaction cardiomyopathy (NCCM)
( arrowheads )
The left ventricular walls look thickened with prominent
ventricular trabeculations within them (diagnostic feature)
(Fig. 4.3.5 ).
Peripartum Cardiomyopathy
(Cardiomyopathy of Pregnancy)
Peripartum cardiomyopathy is defi ned as heart failure
that occurs during the last 4 weeks of a term pregnancy,
or the fi rst 5 months after delivery.
Peripartum cardiomyopathy is a rare condition with
an incidence of 1:15,000 postpartum women. Exclusion
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4.3
of previous heart disease is essential before making the
diagnosis of peripartum cardiomyopathy. There is a
50% risk of thromboembolic complications associated
with peripartum cardiomyopathy.
For Further Reading
1 . Leon MB et al Hypertrophic cardiomyopathy. Dis Mon.
1981;28:1–87
2 . Burch GE et al Heart muscle disease. Dis Mon. 1968;
14:1–68
3 . Zenovich AG et al Hypertrophic cardiomyopathy with api-
cal aneurysm. Circulations. 2004;110:e450
4 . Isbell DC et al The evolving role of cardiovascular mag-
netic resonance imaging in nonischemic cardiomyopathy.
Semin Ultrasound CT MRI. 2006;27:20–31
5 . Alhabshan F et al Extent of myocardial noncompaction:
comparison between MRI and echocardiographic evaluation. Pediatr Radiol. 2005;35:1147–51
6 . Oduncu V et al Images in cardio-thoracic surgery. Biven-
tricular noncompaction presenting with stroke. Eur J
Cardiothorac Surg. 2008;33:737
7 . Hamamichi Y et al Isolated noncompaction of the ventric-
ular myocardium: Ultrafast computed tomography and
magnetic resonance imaging. Int J Cardiothorac Imaging.
2001;17:305–14
8 . Hedrich O et al Sudden cardiac death in athletes. Curr
Cardiol Rep. 2006;8:316–22
9 . Rochitte CE et al The emerging role of MRI in the diagnosis
and management of cardiomyopathies. Curr Cardiol Rep.
2006;8:44–52
10 . Sparrow P et al Cardiac MRI and CT features of inheritable
and congenital conditions associated with sudden cardiac
death. Eur Radiol. 2008. doi:10.1007/s00330-008-1169-5
11 . Duygu H et al Apical hypertrophic cardiomyopathy might
lead to misdiagnosis of ischemic heart disease. Int J
Cardiovasc Imaging. 2008;24:675–81
12 . Bachou T et al A novel mutation in the G4.5 in a Greek
patient with Barth syndrome. Blood Cells Mol Dis. 2009;
42:262–4
13 . Reardon W et al Consanguinity, cardiac arrest, hearing
impairment, and ECG abnormalities: counselling pitfalls in
the Romano-Ward syndrome. J Med Genet. 1993;30:325–7
14 . Schwartz PJ et al The Jervell and Lange-Nielsen syndrome:
natural history, molecular basis, and clinical outcome.
Circulation. 2006;113;783–90
15 . Malouf J et al Apical hypertrophic cardiomyopathy in a
father and a daughter. Am J Med Genet. 1985;22:75–80
16 . Zandrino F et al Magnetic resonance imaging of athlete’s
heart: myocardial mass, left ventricular function, and crosssectional area of the coronary arteries. Eur Radiol. 2000;10:
319–25
4.4 Endocarditis 173
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4.4
Endocarditis
Endocarditis is a term used to describe acute or chronic
infl ammation of the cardiac chamber’s interior.
Although the most common cause of endocarditis is
infectious agents, other rare causes of endocarditis can
be encountered uncommonly.
Infective Endocarditis
Infective endocarditis (IE) is a disease that results from
bacterial colonization of the platelet fi brin vegetation
on the surface of the heart endothelium by circulating
microorganisms.
IE can be acute or subacute. Acute IE is caused by
highly virulent bacteria infecting even a healthy valve,
whereas subacute IE occurs in a patient with prosthetic
or defective heart valve with low virulent bacteria. The
bacteria in the acute IE are present in the blood as septicemia, while in the subacute IE, a bacteremia is suffi cient to initiate the disease.
The acute IE embolus initiates abscess and pyemia
in the tissue in which it is deposited because of the
high virulent bacteria within it. In contrast, subacute
emboli cause localized effect within the vessels or the
organs such as mycotic aneurysms and infarction due
to vascular occlusion.
Classically, patients with IE are patients with known
previous injury to their heart valves (e.g., patients with
past history of rheumatic fever) who present with signs
of fever and night sweat, typically weeks after dental
or surgical procedures. Nowadays, intravenous drug
abusers (IVDAs) are the most common population at
risk of developing IE.
The most common infectious organisms causing IE
include: staphylococci , streptococci , Candida albi-
cans , Coxiella burnetii (Q fever), and the HACEK
organisms ( Hemophilus parainfl uenza , Hemophilus
aphrophilus , Actinobacillus [Hemophilus] actinomycetemcomitans , Cardiobacterium hominis , Eikenella
species, and Kingella species).
Patients with IE typically present with fever, anorexia,
weight loss, malaise, night sweat, bacteremia, evidence
of active vasculitis, septic emboli, and immunologic
vascular phenomenon. However, the previous typical
stigmata are not always present and the symptoms may
be nonspecifi c, especially among IVDA patients.
The modifi ed Duke criteria for IE diagnosis :
Diagnosis of IE must fulfi ll two major criteria, 1 major
plus 3 minor, or 5 minor criteria.
Major Criteria
Positive blood culture.
Two separated blood cultures consistent with IE organ-
isms (e.g., Staphylococcus aureus ) in the absence of
the primary focus.
Evidence of endocardial involvement.
Positive echocardiogram for heart valves vegetations.
New partial dehiscence of prosthetic valve.
New valvular regurgitation.
Minor Criteria
Predisposing heart condition (e.g., congenital heart
disease)
F e v e r .
Vascular phenomenon (septic arterial emboli, intracra-
nial or conjunctival hemorrhage, Janeway’s lesions).
Immunologic phenomenon (glomerulonephritis,
Osler’s nodes, Roth’s spots, or rheumatoid factor).
Positive blood culture that does not meet major crite-
ria or serological evidence of infection.
The cardiac complications of IE include valvular heart
defect, mostly affecting the mitral valve followed by
the aortic valve. The valvular disease in the subacute
form is due to stenosis and long-term fi brosis, whereas
in the acute form, the valvular disease or insuffi ciency
arises due to acute valvular destruction. The most
common valves involved are the left-side heart valves,
except in IVDAs, where infection in the right-side
valves is as common as in the left side. Left-sided heart
failure is the end product of mitral or aortic valves
insuffi ciency when the tricuspid or the pulmonary
valves are also involved. Extra-cardiac manifestations
of IE are mostly related to septic vascular emboli, vascular phenomenon, and immunological phenomenon.
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The organs most commonly affected are the central
nervous system, the thorax, the vascular system, the
spleen, the kidneys, and the skin.
Neurological manifestations of IE are the most com-
mon complications, and they involve embolic strokes
4.4
(15–20% of cases). The septic embolic stroke may precede the diagnosis of IE in up to 75% of IE complicated
by strokes. Septic embolic strokes rate increases in
patients with IE when the vegetation is >10 mm in
diameter. Rarely, the septic emboli may result in the
formation of brain abscess, or meningitis. S. aureus is
the most common organism causing embolic strokes.
Mycotic arterial aneurysm involving the cerebral vessels with intracranial hemorrhage is seen in 2–10% of
IE cases. Mycotic aneurysm is formed secondary to
septic emboli injuring the vascular endothelium intima
of the vasa vasorum and implanting infectious focus, or
due to vasculitis. Patients with mycotic aneurysms may
present with headaches and neurological defi cits.
Mortality can reach up to 80% if the mycotic aneurysm
is ruptured. Streptococci are the most common organisms causing mycotic aneurysms.
Thoracic IE complications are seen when IE affects
the right side of the heart. Complications include septic emboli (65–75% of cases) and pulmonary infarction, pneumonia, empyema, abscess formation, and
mycotic aneurysm of the pulmonary arteries. IVDA
patients are affected by pulmonary septic emboli in up
to 75% of cases.
Splenic abscesses are the most common abdominal
extra-cardiac manifestations of IE (55% of cases), and
occur due to septic emboli dissemination. The abscess
formation can be single or multiple. Renal involvement
may occur in up to 66% of patients in the form of glomerulonephritis or renal infarction due to septic emboli.
Musculoskeletal complications of IE include spondylodiscitis (1.8–5% of cases), sacroiliitis, septic
arthritis, and osteomyelitis; all which are explained by
septic emboli dissemination. However, aseptic, selflimiting arthralgia with low back pain may occur in up
to 44% of cases.
Skin manifestations of IE are explained by vasculitis that results from deposition of circulating immune
complexes on various endothelial locations. The most
common skin lesions in IE are Osler’s nodes and
Janeway’s lesions. Osler’s node is a tender, erythema-
tous, non-hemorrhagic lesion with white center
located at the fi ngers pads (Fig. 4.4.1 ), whereas
Janeway’s lesions are non-tender, small hemorrhagic,
Fig. 4.4.1. A hand illustration of a patient with IE shows Osler’s
nodes, Janeway’s lesion, and splinter hemorrhage
and slightly nodular lesions located at the palms and
soles (Fig. 4.4.1 ). Splinter hemorrhage is another
lesion found in IE, which is characterized by extravasation of blood from the longitudinally located vessels of the nail bed (Fig. 4.4.1 ). Splinter hemorrhage
is seen as small areas of bleeding under the nails,
commonly affecting the fi ngernails more than the
toes. Roth’s spots are areas of retinal bleeding within
the globe, which is seen on fundoscopy (Fig. 4.4.2 ).
Clubbing of fi ngers occurs due to chronic toxemia in
the subacute form.
Fig. 4.4.2. A Fundoscopic illustration demonstrating Roth’s
spots as multiple hemorrhages within the vitreous humor
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Signs on Chest Radiographs
Signs of heart failure with enlarged cardio-thoracic ratio
(>55%), and pulmonary edema is seen in up to 65% of cases
in patients with clinical signs of heart failure.
Empyema is detected as a pleural eff usion with thick irregular
meniscus sign that is immobile on decubitus views.
Signs on CT and CTA
On cardiac CT, vegetations are seen as round lesions located at
the heart valves (Fig. 4.4.3 ). Lesions >10 mm in diameter
have a high risk of embolization.
In the brain, embolic strokes are often multiple, and typically
are located at the corticomedullary junction extending to the
gray matter. Up to 90% of septic embolic strokes are in the
middle cerebral artery (MCA) vascular territory.
Cerebral mycotic aneurysms are most commonly seen at the
distal branches of the MCA, and multiple in 29% of cases.
Single or multiple splenic abscesses are seen as hypodense
lesions within the spleen on non-enhanced scan. The lesions
typically show rim-enhancement after contrast injection.
Renal infarction is detected as a peripheral wedge-shaped
area that fails to enhance after contrast injection. The “cortical
rim sign” can be seen in 50% of cases.
L ö ffl er Endocarditis
(Eosinophilic Endomyocardial Disease)
Löffl er’s endocarditis (LE) is a rare disease characterized by eosinophilic vasculitis, infl ammation, and
fi brosis of the myocardium associated with peripheral
systemic eosinophilia. It can be primary (idiopathic
hypereosinophilia) or secondary to some types of
malignancies (e.g., leukemia).
Infi ltration of the myocardium by eosinophils
causes myocarditis, which is transformed later into
myocardial fi brosis and can be superimposed by
thrombus formation within the myocardium (mural
thrombus). The myocardial fi brosis later on results in
restrictive myocardial normal movement similar to the
mechanism of restriction encounter in restrictive cardiomyopathy, which results in heart failure. When the
fi brosis extends to the papillary muscles and chordae
tendineae, disruption of the atrioventricular valves
occurs (mitral or tricuspid valves insuffi ciency).
LE has poor prognosis with high mortality due to
heart failure, sudden death, or thromboembolism.
Systemic eosinophilic vasculitis can cause multiple
infarctions in the brain, kidney, and lungs.
The most characteristic fi nding in LE which should
be indicative is the presence of high eosinophilia in the
routine white blood count (CBC), associated with fever
and signs of cardiac failure.
The eosinophilia can be absent in chronic cases of
LE, where the clinical picture shows the picture of
restrictive endocarditis instead of the acute picture
of the disease, which is characterized by eosinophilia
and cardiac enlargement due to infl ammation.
Fig. 4.4.3. Axial cardiac CTA of a patient with IE shows mitral
valve vegetation ( arrowhead )
Signs on CT
Thickening of the myocardium, commonly seen at the apex
with areas of hypodensity within the myocardium representing edema and infl ammation (Fig. 4.4.4 ).
Localized hypodense mass within the myocardium can be
seen occasionally representing intramyocardial thrombus.
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Fig. 4.4.4. Axial cardiac
CT ( a ) and dark-blood
MRI ( b ) of a patient with
Löffl er’s endocarditis (LE)
showing hypertrophic left
ventricle myocardium with
4.4
subendocardial hypodensities in ( a ) ( arrowheads ),
and hypertrophic left
ventricle myocardium with
subendocardial hyperintensities in ( b ) due to
myocardial infl ammation
and edema
Signs on MRI
Ventricular wall thickening with hypointense signal in T1W
and T2W images representing fi brosis
High signal within the myocardium in T2W images can be
seen representing edema and active myocardial infl ammation
(Fig. 4.4.4 ).
Enhancement of the myocardium after gadolinium injection.
Marantic Endocarditis
(Non-Bacterial Thrombotic Endocarditis)
Non-bacterial thrombotic endocarditis (NBTE) is a
condition characterized by non-bacterial heart valves
vegetation composed of sterile masses of platelets and
fi brin fi bers. The term is partly a misnomer, because
myocardial infl ammation is absent.
NBTE is most commonly associated with end-stage
malignancies like those of the breast, lung, and colon.
Also, NBTE can be seen uncommonly with autoimmune diseases like systemic lupus erythematosus
(SLE) ( Libman-Sacks endocarditis ).
Libman-Sacks vegetations are noninfective verrucous vegetations that develop mainly on the mitral
valves, and maybe the aortic valve. Libman-Sacks vegetations are found in approximately 1 of 10 patients with
SLE. Libman-Sacks endocarditis may be differentiated
from IE by measuring the white blood count (high in IE,
and expected to be low during lupus fl are), the C-reactive
protein (high in IE, and possibly suppressed in SLE),
and the antiphospholipid antibody level (moderate to
high levels in SLE, and unlikely to be high in IE).
The vegetation is believed to be caused by the state
of hypercoagubility secondary to malignancies or autoimmune diseases. The vegetations are usually <3 mm
in diameter, and can present with multiple systemic
embolic attacks involving the cerebral nervous system
or the vascular system (e.g., blue toe syndrome). The
vegetations rarely alter valve function or produce murmurs. Blue toe syndrome is a condition characterized
by sudden onset of acute pain and cyanosis in one or
more toes due to embolic event (Fig.
4.4.5 ).
A blood culture is considered negative after three or
more sets of blood cultures incubated for a week fail to
demonstrate growth. The most common causes of culture negative endocarditis are antibiotic therapy prior to
the blood cultures and infection due to fastidious organisms. NBTE should be considered when a patient with
suspected IE fails to demonstrate positive blood culture
and fails to respond to antibiotic therapy, or in a patient
with multiple cerebral strokes due to unknown cause.
Early recognition of NBTE will lead to early detection
of occult malignancy or autoimmune disease.
Fig. 4.4.5. An illustration demonstrating the gross appearance
of blue toe syndrome
4.4 Endocarditis 177
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For Further Reading
1 . Colen TW et al Radiologic manifestations of extra-cardiac
complications of infective endocarditis. Eur Radiol.
2008;18:2433–45
2 . Bayer AS et al Diagnosis and management of infective endo-
carditis and its complications. Circulation. 1998;98: 2936–48
3 . Friday BB et al Systemic complications of infective endo-
carditis. Circulation. 2005;112:e324
4 . Fellah L et al Combined assessment of tricuspid valve endo-
carditis and pulmonary septic embolism with ECG-gated
40-MDCT of the whole chest. AJR. 2007;189:W228–30
5 . Mahlab K et al Diagnosis of Candida endocarditis by com-
puted tomography scanning. IMAJ. 2006;8:442–4
6 . Lawrence R. Freedman. Endocarditis updated. Dis Mon.
1979;26:1–51
7 . Farrior JB et al A consideration of the difference between a
Janeway’s lesion and an Osler’s node in infectious endocarditis. Chest. 1976;70:239–43
8 . Saladi RN et al Idiopathic splinter hemorrhages. J Am Acad
Dermatol. 2004;50:289–92
9 . Hirschmann JV et al Blue (or purple) toe syndrome. J Am
Acad Dermatol. 2009;60:1–20
10 . Kleinfeldt T et al Hypereosinophilic syndrome: a rare case
of Loeffl er’s endocarditis documented in cardiac MRI. Int J
Cardiol. 2009. doi:10.1016/j.ijxard.2009.03.059
11 . Files MD et al A child with eosinophilia, Loeffl er endo-
carditis, and acute lymphoblastic leukemia. Pediatr Cardiol.
2009. 30:530–532
1 3 . L o fi ego C et al Ventricular remodeling in Loeffl er endo-
carditis: implications for therapeutic decision making. Eur
J Heart Fail. 2005;7:1023–6
14 . Yalonetsky S et al Mitral valve destruction by Hodgkin’s
lymphoma-associated Loefl er endocarditis. Pediatr Cardiol.
2008. doi:10.1007/s00246-007-9135-6
15 . Joshi SB et al Marantic endocarditis presenting as recur-
rent arterial embolization. Int J Cardiol. 2009;132:e14–16
16 . Fanale MA et al Some unusual complications of malignan-
cies. Case 2. Marantic endocarditis in advanced cancer.
J Clin Oncol. 2002;20:4108–14
17 . Singh V et al Marantic endocarditis (NBTE) with systemic
emboli and paraneoplastic cerebellar degeneration:
uncommon presentation of ovarian cancer. J Neurooncol.
2007;83:81–3
18 . Moyssakis I et al Libman-Sacks endocarditis in systemic
lupus erythematosus: prevalence, associations, and evolution. Am J Med. 2007;120:636–42
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4.5
4.5
Pericardial Diseases
The pericardium is a double-walled sac that encloses
the heart. The outer sac is called the “fi brous pericardium,” and the inner sac is called the “serous pericardium.” The serous pericardium is composed of an outer
(parietal) layer, and an inner (visceral) layer separated
by potential space (pericardial cavity). Both the fi brous
and the serous layers are continuous with the adventitia of the great vessels.
The anterior aspect of the fi brous pericardium is
attached to the left half of the sternum and to the fourth,
fi fth, and sixth left costal cartilages. Inferiorly, it is
attached to the central tendon of the diaphragm. Only
the fi brous pericardium below the fi fth or sixth intercostal space is sensitive to pain, while the remaining
fi brous and entire serous pericardium is insensitive.
When this pain-sensitive area is stimulated by a disease, pericardial pain is perceived as pain in the neck
and trapezius muscle via the phrenic nerve, which
enters the spinal cord at the fourth and fi fth cervical
segments.
The pericardial cavity contains normally 20–50 mL
of serous fl uid, although the sac has a potential space
of 80–100 mL. The pericardial fl uid is absorbed by the
lymphatics found near the base of the heart. The blood
supply of the pericardium comes from the internal thoracic artery via the pericardiophrenic artery.
Pericardial effusion is a disease characterized by
excess fl uid within the pericardial cavity that exceeds
50 mL. Like pleural effusion, this fl uid can be classifi ed into transudative or exudative based on the protein
content. The pericardial fl uid can be edematous (e.g.,
in uremia), hemorrhagic (e.g., in trauma), contain pus
(e.g., infective endocarditis), or contain lymph (e.g.,
due to rupture of the thoracic duct). When the pericardial fl uid is severe enough to compromise the heart
contractility, the condition is called “ pericardial tam-
ponade ,” and it is a medical emergency. Between 150
and 250 mL of fl uid must be present within the pericardial cavity to cause a cardiac tamponade.
Pericarditis is a condition characterized by infl am-
mation of the pericardium, which can be acute or
chronic. Pericarditis can arise due to infections, autoimmune diseases, and granulomatous diseases.
Patients with pericarditis often present with symptoms due to infl ammation, pericardial effusion or
tamponade, or constriction and/or restriction due to
fi brosis.
Symptoms of pericarditis include acute sudden
neck or upper arm pain that is exaggerated by body
movements, respiration, swallowing, and rarely by
heart beat. The pain may be relieved by leaning forward, which will stabilize the pericardial sac and
reduce the movement of the pain-sensitive area. When
the peripheral diaphragmatic pleura are infl amed, epigastric pain is felt, which can be seen in up to 50% of
patients with acute idiopathic pericarditis. Moreover,
dull abdominal pain in the right upper quadrant may be
felt due to congestion of the abdominal viscera in cases
of tamponade and pericardial constriction. Other
symptoms include fever, dyspnea, and paroxysmal
nocturnal dyspnea in complicated cases. Paradoxical
pulse is a normal pulse variation representing the fact
that the systolic pressure is less during inspiration than
during expiration in a normal person. An accentuation
of this normal respiratory variation may be found in
patients with pericarditis with tamponade. Also, in
patients with tamponade, an alternation of a weak
pulse and a strong pulse in the presence of a regular
rhythm may be found ( pulsus alternans ).
A pleural effusion may accompany pericarditis in
all stages of the disease (>50% of cases). In patients
with large pericardial effusion, an area of dullness of
variable size can be found in the region of the inferior
angle of the scapula where there is normally bronchial
breathing (Ewart’s sign). This sign is explained by the
fact that large pericardial effusion forces the heart and
the great vessels backward, thereby compressing the
lung and the bronchi.
Chronic pericarditis, like any chronic infl ammation,
is characterized by calcifi cation and fi brosis. Pericardial
fi brosis due to chronic infl ammation with pericardial
space limitation is called “ constrictive pericarditis .”
Constrictive pericarditis can occur due to tuberculosis,
radiation, previous pericardiotomy, and up to 49% are
idiopathic. Patients with constrictive pericarditis often
present with signs of right-sided heart failure, and
atrial fi brillation in up to 40% of cases. Clinical signs
of liver enlargement, ascites, and peripheral edema
may be seen in patients with constrictive pericarditis
due to congestive heart failure. On auscultation,
patients with acute and constrictive pericarditis have
pericardial friction rub, in which a sound is heard
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during heart beat cycle due to friction of the fi brous
pericardium layers. Pericardial rub is a diagnostic clinical sign of pericarditis.
Pneumopericardium is a rare condition character-
ized by the presence of air within the pericardial cavity. Pneumopericardium can occur as a complication
of pneumomediastinum, pneumothorax, or pericardial
fl uid aspiration.
Diff erential Diagnoses
and Related Diseases
Dressler’s syndrome , also known as “ post-myocardial
infarction syndrome ,” is a disease seen as early as 10
days and as late as 2 years following myocardial
infarction characterized by fever, pericarditis or pleuritis with hemorrhagic effusion, and pneumonia with
gross hemoptysis. The disease has a tendency for
recurrence.
CACP syndrome is an uncommon disease character-
ized by C amptodactyly, noninfl ammatory A rthropathy,
C oxa vara, and P ericarditis. The disease is related to a
group of diseases known as “ familial arthropathy dis-
eases .” The disease arises due to hypertrophies synovium in the absence of synovitis (in contrast to
rheumatoid arthritis or its juvenile form), which is
typically detected by synovial biopsy. Patients affected
present with arthropathy usually since childhood.
Camptodactyly is a congenital or acquired nontraumatic fl exion deformity of the proximal interphalangeal (PIP) joint of one or several fi ngers, which is
usually bilateral in CACP syndrome. Noninfl ammatory
arthropathy involves large joints such as elbows, knees,
and ankles. Coxa vara is a horizontally oriented femoral neck. Mild noninfl ammatory pericarditis with pericardial effusion occurs in 30% of cases. The condition
may be mild or self-limited. MRI studies classically
show hypertrophied synovium with rim-like enhancement of the fl uid-fi lled bursae, a feature that distinguishes CACP syndrome from rheumatoid arthritis,
which shows synovial hypertrophy, signs of soft tissue
hyperemia, and diffuse contrast enhancement.
Signs on Chest Radiographs
Pericardial eff usion is detected as increased heart enlarge-
ment on serial radiographs. The pericardial eff usion starts to
show radiographic abnormalities when the pericardial fl uid
exceeds 250 mL in adults (Fig. 4.5.1 ).
Constrictive pericarditis can be detected when calcifi cation of
the pericardium occurs (Fig. 4.5.2 ). Calcifi ed pericardium is
visualized as a wide area of calcifi cation that follows the heart
silhouette.
Pneumopericardium is visualized as an air surrounding the
heart contour (Fig. 4.5.3 ).
Fig. 4.5.1 Posteroanterior chest radiograph ( a ) and axial chest
CT of two different patients with pericardial tamponade show
massive heart enlargement in ( a ) due to pericardial effusion, and
hypodense material is seen surrounding the heart due to marked
pericardial effusion in ( b ). Also, bilateral pleural effusion can be
seen in ( b )
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Fig. 4.5.2 Lateral chest
radiograph ( a ) and axial
chest CT of two different
patients with constrictive
pericarditis show calcifi ed
pericardium ( arrowheads )
4.5
Fig. 4.5.3 Posteroanterior
chest radiograph ( a ) and
axial chest CT of two
different patients with
pneumopericardium show
air surrounding the heart
in ( a ) and ( b )
( arrowheads )
Signs on CT and MRI
Pericardial eff usion and tamponade are seen as fl uid signal
intensity material located within the pericardial space
(Fig. 4.5.1 ). The normal pericardial space should not exceed 4
mm in width. On CT, the fl uid can have high density if it is
hemorrhagic (e.g., >80 HU). On MRI, the signal intensity of
the fl uid is variable according to the content of the fl uid (e.g.,
high T1 and T2 signal intensities if it is hemorrhagic).
The normal pericardium is visualized on MRI as a thin
hypointense line surrounding the heart outlined by the
high-intensity pericardial fat, which normally should not
exceed 3 mm in thickness. Acute pericarditis on CT and
MRI is diagnosed when the pericardium is >3 mm in
thickness and enhances after contrast injection
(Fig. 4.5.4 ).
Constrictive pericarditis shows diff use thickening and
irregularities of the pericardium with or without calcifi cation. Pericardial calcifi cation is a diagnostic sign of
constrictive pericarditis (Fig. 4.5.2 ). Normal or near normal
thickening of the pericardium does not rule out constrictive
pericarditis.
Pneumopericardium is seen as an air that surrounds the heart
within the pericardial space (Fig. 4.5.3 ).
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