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Chapter 5 · Cardiology
Dilated Cardiomyopathy
DCM is characterized by le ventricular or biventricular
dilatation with impaired systolic function.
e most common presentation of DCM is le -sided
heart failure. Causes can be due to alcoholism (50 % of cases),
cocaine abuse, and hyper- and hypothyroidism. Contrastenhanced MRI for DCM study is mainly indicated to di erentiate primary DCM (e.g., without a cause) from secondary
(e.g., postmyocardial infarction) DCM.
5
Signs on Chest Radiographs
The cardiac heart is markedly enlarged with increased
cardiothoracic ratio due to cardiac muscles dilatation
(. Fig. 5.3.2 ).
. Fig. 5.3.3 Four-chamber white blood cardiac MRI shows
left ventricular apical dilatation due to previous myocardial
infarction ( arrowhead )
. Fig. 5.3.2 Anteroposterior chest radiograph of a bedridden
patient shows massively dilated heart due to dilated
cardiomyopathy (DCM)
Signs on MRI
5 There is marked dilatation of the heart ventricles,
often with global wall motion abnormalities on
cine MR images. Focal wall motion abnormalities
are more commonly seen in DCM due to ischemic
heart disease (e.g., postmyocardial infarction)
(. Fig. 5.3.3 ).
5 Secondary DCM usually shows late contrast
enhancement, depending on its primary cause
(e.g., myocardial infarction): the contrast uptake
reflecting areas of degeneration, necrosis, and
fibrosis. In contrast, primary DCM shows no late
contrast enhancement. The contrast enhancement
can be subendocardial or transmural.
5 Intraventricular thrombus may be found.
Restrictive Cardiomyopathy
RCM is a disease characterized by ventricular lling defect.
RCM can be caused by diseases that disturb the myocardial
integrity such as amyloidosis, sarcoidosis, metastasis, and
glycogen storage diseases.
Patients may present with signs of congestive heart failure
because of ventricular contractility restriction in a similar
fashion to constrictive pericarditis. Cardiac MRI in RCM is
used to di erentiate restrictive pericarditis from RCM.
Signs on Chest Radiographs
The heart size is generally enlarged due to atrial dilatation
or due to the development of congestive heart failure.
Signs on MRI
The ventricular chamber dimensions and thickness are
within normal range, with both atria enlarged as a direct
sign of right ventricular and left ventricular lling resistance.
Arrhythmogenic Right Ventricular Dysplasia
ARVD is a rare, progressive disease characterized by in ltration and replacement of the right ventricle free wall myocardium with bro-fatty tissue, which causes contractility
dysfunction and right ventricular dilatation.
ARVD is one of the causes of arrhythmias and sudden
cardiac deaths because this bro-fatty tissue causes electrical
5.3 · Myocardial Diseases (Cardiomyopathies)
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instability of the right ventricular wall. ARVD is familial in
up to 50 % of cases, with an autosomal dominant mode of
inheritance. e disease has a male predominance. Patient is
typically a young male (30years) complaining from arrhythmias initiated by exercise.
Signs on MRI
5 There is right ventricular bulging and dilatation,
thinning of the right ventricle free wall (2–6mm in
thickness), and high signal intensity seen within the
myocardium on T1W images representing fat
in ltration within the myocardium (diagnostic key)
(. Fig. 5.3.4 ). If fatty in ltration cannot be
a
209
demonstrated, right ventricular trabeculation also
ful lls the criteria of ARVD, presuming the clinical
picture also suggests it.
5 Abnormal wall motion is demonstrated on cine
images.
Noncompaction Cardiomyopathy (Spongy
Myocardium)
NCCM is a rare, distinct cardiomyopathy characterized by
arrest of the le ventricular muscle compaction during
embryonal development, causing le ventricular myocardial
trabeculation with deep intertrabecular recesses that makes
the le ventricular myocardium looks like sponge.
NCCM commonly a ects the LV; however, the right ventricle can be involved occasionally. e disease has an incidence of 0.05 % in the general population and can occur as an
isolated case or associated with other cardiac anomalies. e
clinical picture is variable. Patients may show no symptoms,
while others may show signs of severe heart failure and
arrhythmias.
5
Signs on MRI
The left ventricular walls look thickened with prominent
ventricular trabeculations within them (diagnostic
feature) (. Fig. 5.3.5 ).
b
. Fig. 5.3.4 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 bro-fatty changes ( arrows )
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Chapter 5 · Cardiology
ab
5
. Fig. 5.3.5 Three-chamber white blood cardiac MRI ( a ) and short-axis view ( b ) show LV trabeculation in a patient with noncompaction
cardiomyopathy (NCCM) ( arrowheads )
Peripartum Cardiomyopathy
(Cardiomyopathy ofPregnancy)
Peripartum cardiomyopathy is de ned as heart failure that
occurs during the last 4 weeks of a term pregnancy or the rst
5 months a er delivery.
Peripartum cardiomyopathy is a rare condition with an incidence of 1:15,000 postpartum women. Exclusion of previous
heart disease is essential before making the diagnosis of peripartum cardiomyopathy. ere is a 50 % risk of thromboembolic
complications associated with peripartum cardiomyopathy.
Further Reading
Alhabshan F, et al. Extent of myocardial noncompaction:
comparison between MRI and echocardiographic evaluation. Pediatr Radiol. 2005;35:1147–51.
Bachou T, etal. A novel mutation in the G4.5in a Greek patient
with Barth syndrome. Blood Cells Mol Dis. 2009;42:262–4.
Burch GE, etal. Heart muscle disease. Dis Mon. 1968;14:1–68.
Duygu H, etal. Apical hypertrophic cardiomyopathy might
lead to misdiagnosis of ischemic heart disease. Int J
Cardiovasc Imaging. 2008;24:675–81.
Hamamichi Y, etal. Isolated noncompaction of the ventricu-
lar myocardium: Ultrafast computed tomography and
magnetic resonance imaging. Int J Cardiothorac Imaging.
2001;17:305–14.
Hedrich O, et al. Sudden cardiac death in athletes. Curr
Cardiol Rep. 2006;8:316–22.
Isbell DC, etal. e evolving role of cardiovascular magnetic
resonance imaging in nonischemic cardiomyopathy.
Semin Ultrasound CT MRI. 2006;27:20–31.
Leon MB, et al. Hypertrophic cardiomyopathy. Dis Mon.
1981;28:1–87.
Malouf J, etal. Apical hypertrophic cardiomyopathy in a
father and a daughter. Am J Med Genet. 1985;22:75–80.
Oduncu V, et al. Images in cardio-thoracic surgery.
Biventricular noncompaction presenting with stroke. Eur
J Cardiothorac Surg. 2008;33:737.
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.
Rochitte CE, etal. e emerging role of MRI in the diagnosis
and management of cardiomyopathies. Curr Cardiol Rep.
2006;8:44–52.
Schwartz PJ, etal. e Jervell and Lange-Nielsen syndrome:
natural history, molecular basis, and clinical outcome.
Circulation. 2006;113:783–90.
Sparrow P, etal. 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.
Zandrino F, et al. Magnetic resonance imaging of athlete’s
heart: myocardial mass, le ventricular function, and
cross-sectional area of the coronary arteries. Eur Radiol.
2000;10:319–25.
Zenovich AG, etal. Hypertrophic cardiomyopathy with api-
cal aneurysm. Circulation. 2004;110:e450.
5.4 Endocarditis
Endocarditis is a term used to describe acute or chronic
in 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.
5.4 · Endocarditis
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5
Infective Endocarditis
Infective endocarditis (IE) is a disease that results from bacterial colonization of the platelet 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. e bacteria in the acute IE
are present in the blood as septicemia, while in the subacute
IE, a bacteremia is su cient to initiate the disease.
e 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 e ect 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 a er dental or surgical procedures. Nowadays, intravenous drug abusers (IVDAs) are the
most common population at risk of developing IE.
e most common infectious organisms causing IE
include staphylococci , streptococci , Candida albicans , Coxiella
burnetii (Q fever), and the HACEK organisms ( Haemophilus
parain uenzae , Haemophilus aphrophilus , Actinobacillus
[Haemophilus] 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 nonspeci c, especially among IVDA patients.
e modi ed Duke criteria for IE diagnosis : Diagnosis of
IE must ful ll two major criteria, 1 major plus 3 minor, or 5
minor criteria.
Major Criteria
5 Positive blood culture
5 Two separated blood cultures consistent with IE
organisms (e.g., Staphylococcus aureus ) in the absence of
the primary focus
5 Evidence of endocardial involvement
5 Positive echocardiogram for heart valves vegetations
5 New partial dehiscence of prosthetic valve
5 New valvular regurgitation
Minor Criteria
5 Predisposing heart condition (e.g., congenital heart disease)
5 Fever
5 Vascular phenomenon (septic arterial emboli, intracranial
or conjunctival hemorrhage, Janeway’s lesions)
5 Immunologic phenomenon (glomerulonephritis, Osler’s
nodes, Roth’s spots, or rheumatoid factor)
5 Positive blood culture that does not meet major criteria
or serological evidence of infection
e cardiac complications of IE include valvular heart
defect, mostly a ecting the mitral valve followed by the aortic valve. e valvular disease in the subacute form is due to
stenosis and long-term brosis, whereas in the acute form,
the valvular disease or insu ciency arises due to acute valvular destruction. e most common valves involved are
the le -sided heart valves, except in IVDAs, where infection in the right-sided valves is as common as in the le
side. Le - sided heart failure is the end product of mitral or
aortic valves insu 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. e
organs most commonly a ected are the central nervous system, the thorax, the vascular system, the spleen, the kidneys, and the skin.
Neurological manifestations of IE are the most common
complications, and they involve embolic strokes (15–20 %
of cases). e 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 >10mm 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 de cits. Mortality can
reach up to 80 % if the mycotic aneurysm is ruptured.
Streptococci are the most common organisms causing
mycotic aneurysms.
oracic IE complications are seen when IE a ects 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 a ected by pulmonary septic emboli in up to 75 % of cases.
Splenic abscesses are the most common abdominal extracardiac manifestations of IE (55 % of cases) and occur due to
septic emboli dissemination. e 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, self-limiting 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. e most common skin lesions
in IE are Osler’s nodes and Janeway’s lesions. Osler’s node is a
tender, erythematous, nonhemorrhagic lesion with white
center located at the ngers pads (. Fig. 5.4.1 ), whereas
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Chapter 5 · Cardiology
Osler’s
node
5
Splinter
hemorrhage
Janeway’s
lesion
. Fig. 5.4.1 A hand illustration of a patient with IE shows Osler’s
nodes, Janeway’s lesion, and splinter hemorrhage
Janeway’s lesions are non-tender, small hemorrhagic, and
slightly nodular lesions located at the palms and soles
(. Fig. 5.4.1 ). 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. 5.4.1 ).
Splinter hemorrhage is seen as small areas of bleeding under
the nails, commonly a ecting the ngernails more than the
toes. Roth’s spots are areas of retinal bleeding within the globe,
which is seen on fundoscopy (. Fig. 5.4.2 ). Clubbing of n-
gers occurs due to chronic toxemia in the subacute form.
. Fig. 5.4.2 A fundoscopic illustration demonstrating Roth’s spots as
multiple hemorrhages within the vitreous humor
Signs on CT and CTA
5 On cardiac CT, vegetations are seen as round
lesions located at the heart valves (. Fig. 5.4.3 ).
Lesions >10mm in diameter have a high risk of
embolization.
5 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.
5 Cerebral mycotic aneurysms are most commonly
seen at the distal branches of the MCA and
multiple in 29 % of cases.
5 Single or multiple splenic abscesses are seen as
hypodense lesions within the spleen on
nonenhanced scan. The lesions typically show rim
enhancement after contrast injection.
5 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.
Signs on Chest Radiographs
5 Signs of heart failure with enlarged cardiothoracic
ratio (>55 %), and pulmonary edema is seen in up
to 65 % of cases in patients with clinical signs of
heart failure.
5 Empyema is detected as a pleural effusion with
thick irregular meniscus sign that is immobile on
decubitus views.
5.4 · Endocarditis
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213
5
. Fig. 5.4.3 Axial cardiac CTA of a patient with IE shows
mitral valve vegetation ( arrowhead )
L ö er’s Endocarditis (Eosinophilic
Endomyocardial Disease)
Lö er’s endocarditis (LE) is a rare disease characterized by
eosinophilic vasculitis, in ammation, and 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).
Infiltration of the myocardium by eosinophils causes
myocarditis, which is transformed later into myocardial
fibrosis and can be superimposed by thrombus formation
within the myocardium (mural thrombus). The myocardial fibrosis 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 fibrosis extends to the papillary
muscles and chordae tendineae, disruption of the atrioventricular valves occurs (mitral or tricuspid valves insufficiency).
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.
e most characteristic 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.
e 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
in ammation.
Signs on CT
5 Thickening of the myocardium, commonly seen at the
apex with areas of hypodensity within the myocardium
representing edema and in ammation (. Fig. 5.4.4 ).
5 Localized hypodense mass within the myocardium
can be seen occasionally representing
intramyocardial thrombus.
a
b
. Fig. 5.4.4 Axial cardiac CT ( a ) and dark-blood MRI ( b ) of a
patient with Lö er’s endocarditis (LE) showing hypertrophic left
ventricle myocardium with subendocardial hypodensities in ( a )
( arrowheads ) and hypertrophic left ventricle myocardium with
subendocardial hyperintensities in ( b ) due to myocardial
in ammation and edema
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Chapter 5 · Cardiology
Signs on MRI
5 Ventricular wall thickening with hypointense
signal in T1W and T2W images representing
fibrosis.
5 High signal within the myocardium in T2W images
can be seen representing edema and active
myocardial inflammation (. Fig. 5.4.4 ).
5 Enhancement of the myocardium after gadolinium
injection.
5
Marantic Endocarditis (Nonbacterial
Thrombotic Endocarditis)
Nonbacterial thrombotic endocarditis (NBTE) is a condition
characterized by nonbacterial heart valves vegetation composed of sterile masses of platelets and brin bers. e term
is partly a misnomer, because myocardial in 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 di erentiated from IE by measuring the white blood count (high in IE and expected to be
low during lupus 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).
e vegetation is believed to be caused by the state of
hypercoagulability secondary to malignancies or autoimmune diseases. e vegetations are usually <3mm in diameter and can present with multiple systemic embolic attacks
involving the cerebral nervous system or the vascular system (e.g., blue toe syndrome). e 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. 5.4.5 ).
A blood culture is considered negative a er three or
more sets of blood cultures incubated for a week fail to demonstrate growth. e 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. 5.4.5 An illustration demonstrating the gross appearance of
blue toe syndrome
Further Reading
Bayer AS, et al. Diagnosis and management of infective
endocarditis and its complications. Circulation.
1998;98:2936–48.
Colen TW, etal. Radiologic manifestations of extra-cardiac
complications of infective endocarditis. Eur Radiol.
2008;18:2433–45.
Fanale MA, etal. Some unusual complications of malignan-
cies. Case 2. Marantic endocarditis in advanced cancer. J
Clin Oncol. 2002;20:4108–14.
Farrior JB, etal. A consideration of the di erence between a
Janeway’s lesion and an Osler’s node in infectious endocarditis. Chest. 1976;70:239–43.
Fellah L, etal. 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.
Files MD, etal. A child with eosinophilia, Loe er endocardi-
tis, and acute lymphoblastic leukemia. Pediatr Cardiol.
2009;30:530–2.
Freedman LR.Endocarditis updated. Dis Mon. 1979;26:1–
51.
Friday BB, etal. Systemic complications of infective endocar-
ditis. Circulation. 2005;112:e324.
Hirschmann JV, etal. Blue (or purple) toe syndrome. J Am
Acad Dermatol. 2009;60:1–20.
Joshi SB, etal. Marantic endocarditis presenting as recurrent
arterial embolization. Int J Cardiol. 2009;132:e14–6.
Kleinfeldt T, etal. Hypereosinophilic syndrome: a rare case of
Loe er’s endocarditis documented in cardiac MRI.Int J
Cardiol. 2009. doi:10.1016/j.ijxard.2009.03.059.
L o ego C, etal. Ventricular remodeling in Loe er endocar-
ditis: implications for therapeutic decision making. Eur J
Heart Fail. 2005;7:1023–6.
Mahlab K, etal. Diagnosis of Candida endocarditis by com-
puted tomography scanning. IMAJ. 2006;8:442–4.
Moyssakis I, etal. Libman-Sacks endocarditis in systemic
lupus erythematosus: prevalence, associations, and evolution. Am J Med. 2007;120:636–42.
5.5 · Pericardial Diseases
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5
Saladi RN, etal. Idiopathic splinter hemorrhages. J Am Acad
Dermatol. 2004;50:289–92.
Singh V, etal. Marantic endocarditis (NBTE) with systemic
emboli and paraneoplastic cerebellar degeneration:
uncommon presentation of ovarian cancer. J Neurooncol.
2007;83:81–3.
Yalonetsky S, et al. Mitral valve destruction by Hodgkin’s
lymphoma-associated Loe er endocarditis. Pediatr
Cardiol. 2008. doi:10.1007/s00246-007-9135-6.
5.5 Pericardial Diseases
e pericardium is a double-walled sac that encloses the
heart. e outer sac is called the “ brous pericardium,” and
the inner sac is called the “serous pericardium.” e serous
pericardium is composed of an outer (parietal) layer and an
inner (visceral) layer separated by potential space (pericardial cavity). Both the brous and the serous layers are continuous with the adventitia of the great vessels.
e anterior aspect of the brous pericardium is attached
to the le half of the sternum and to the fourth, h, and
sixth le costal cartilages. Inferiorly, it is attached to the central tendon of the diaphragm. Only the brous pericardium
below the h or sixth intercostal space is sensitive to pain,
while the remaining 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 h cervical segments.
e pericardial cavity contains normally 20–50mL of
serous uid, although the sac has a potential space of
80–100mL. e pericardial uid is absorbed by the lymphatics found near the base of the heart. e blood supply of the
pericardium comes from the internal thoracic artery via the
pericardiophrenic artery.
Pericardial e usion is a disease characterized by excess
uid within the pericardial cavity that exceeds 50mL.Like
pleural e usion, this uid can be classi ed into transudative
or exudative based on the protein content. e pericardial
uid can be edematous (e.g., in uremia) and 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 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
250mL of uid must be present within the pericardial cavity
to cause a cardiac tamponade.
Pericarditis is a condition characterized by in ammation
of the pericardium, which can be acute or chronic. Pericarditis
can arise due to infections, autoimmune diseases, and granulomatous diseases. Patients with pericarditis o en present
with symptoms due to in ammation, pericardial e usion or
tamponade, or constriction and/or restriction due to 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. e 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 in 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 repre-
senting 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 e usion may accompany pericarditis in all
stages of the disease (>50 % of cases). In patients with large
pericardial e usion, 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). is
sign is explained by the fact that large pericardial e usion
forces the heart and the great vessels backward, thereby compressing the lung and the bronchi.
Chronic pericarditis, like any chronic in ammation, is
characterized by calci cation and brosis. Pericardial brosis
due to chronic in ammation with pericardial space limitation is called constrictive pericarditis . Constrictive pericardi-
tis can occur due to tuberculosis, radiation, and previous
pericardiotomy, and up to 49 % are idiopathic. Patients with
constrictive pericarditis o en present with signs of rightsided heart failure and atrial 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 during heart beat cycle due to
friction of the brous pericardium layers. Pericardial rub is a
diagnostic clinical sign of pericarditis.
Pneumopericardium is a rare condition characterized by
the presence of air within the pericardial cavity.
Pneumopericardium can occur as a complication of pneumomediastinum, pneumothorax, or pericardial uid aspiration.
D i erential Diagnoses andRelated Diseases
5 Dressler’s syndrome , also known as “ postmyocardial
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 e usion, and pneumonia with gross
hemoptysis. e disease has a tendency for recurrence.
5 CACP syndrome is an uncommon disease characterized
by c amptodactyly, nonin ammatory a rthropathy, c oxa
vara, and p ericarditis. e disease is related to a group of
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Chapter 5 · Cardiology
diseases known as familial arthropathy diseases . e
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 a ected present with
arthropathy usually since childhood. Camptodactyly is a
congenital or acquired nontraumatic exion deformity of
the proximal interphalangeal (PIP) joint of one or several
ngers, which is usually bilateral in CACP syndrome.
Nonin ammatory arthropathy involves large joints such
as the elbows, knees, and ankles. Coxa vara is a
horizontally oriented femoral neck. Mild
nonin ammatory pericarditis with pericardial e usion
occurs in 30 % of cases. e condition may be mild or
self-limited. MRI studies classically show hypertrophied
synovium with rim-like enhancement of the uid- lled
bursae, a feature that distinguishes CACP syndrome
from rheumatoid arthritis, which shows synovial
hypertrophy, signs of so tissue hyperemia, and di use
contrast enhancement.
5
Signs on Chest Radiographs
5 Pericardial effusion is detected as increased heart
enlargement on serial radiographs. The pericardial
effusion starts to show radiographic abnormalities
when the pericardial fluid exceeds 250mL in adults
(. Fig. 5.5.1 ).
a
5 Constrictive pericarditis can be detected when
calcification of the pericardium occurs (. Fig. 5.5.2 ).
Calcified pericardium is visualized as a wide area of
calcification that follows the heart silhouette.
5 Pneumopericardium is visualized as an air
surrounding the heart contour (. Fig. 5.5.3 ).
b
. Fig. 5.5.1 Posteroanterior chest radiograph ( a ) and axial chest CT of two di erent patients with pericardial tamponade show massive
heart enlargement in ( a ) due to pericardial e usion, and hypodense material is seen surrounding the heart due to marked pericardial
e usion in ( b ). Also, bilateral pleural e usion can be seen in ( b )
5.5 · Pericardial Diseases
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a b
. Fig. 5.5.2 Lateral chest radiograph ( a ) and axial chest CT of two di erent patients with constrictive pericarditis show calci ed
pericardium ( arrowheads )
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5
ab
. Fig. 5.5.3 Posteroanterior chest radiograph ( a ) and axial chest CT of two di erent patients with pneumopericardium show air
surrounding the heart in ( a ) and ( b ) ( arrowheads )
Signs on CT and MRI
5 Pericardial effusion and tamponade are seen as
fluid signal intensity material located within the
pericardial space (. Fig. 5.5.1 ). The normal
pericardial space should not exceed 4mm in
width. On CT, the fluid can have high density if it is
hemorrhagic (e.g., >80 HU). On MRI, the signal
intensity of the fluid is variable according to the
content of the fluid (e.g., high T1 and T2 signal
intensities if it is hemorrhagic).
5 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 3mm in
thickness. Acute pericarditis on CT and MRI is
diagnosed when the pericardium is >3mm in
thickness and enhances after contrast injection
(. Fig. 5.5.4 ).
5 Constrictive pericarditis shows diffuse thickening
and irregularities of the pericardium with or
without calcification. Pericardial calcification is a
diagnostic sign of constrictive pericarditis
(. Fig. 5.5.2 ). Normal or near normal thickening of
the pericardium does not rule out constrictive
pericarditis.
5 Pneumopericardium is seen as an air that
surrounds the heart within the pericardial space
(. Fig. 5.5.3 ) .
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