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4.1 Acute Chest Pain 161
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Aortic Intramural Hematoma
IMH is a condition characterized by rupture of the vasa
vasorum, the network of vessels that supply the aorta
itself, resulting in bleeding within the aortic wall,
mostly within the media layer.
IMH is clinically indistinguishable from aortic dissection. Patients present with signs of acute aortic syndrome consisting of sudden chest pain that is radiating
to the back or chest depending on which part of the
aorta is affected. IMH accounts for 10–30% of cases
of acute aortic syndrome, and it may be caused by
hypertension, blunt trauma, or penetrating atherosclerotic ulcer. In contrast to aortic dissection, no intimal
tear fl ap is identifi ed in this condition. However,
the hematoma can progress into a true dissection if the
aortic wall continues to enlarge in thickness by the
hematoma >5 cm.
Signs on CTA
Fig. 4.1.10 Axial cardiac CTA shows posterior aortic arch focal
area of aortic wall thickening due to intramural hematoma
( arrowheads )
On contrast-enhanced scan, the aortic wall show a crescentic
area of wall thickening that may show high attenuation if the
bleeding is fresh. There is no intimal fl ap (Fig. 4.1.10 ).
Penetrating Atherosclerotic Ulcer
Penetrating atherosclerotic ulcer is a condition that
results from ulceration and break of an aortic atherosclerotic plaque resulting in an intimal defect. This
defect causes bleeding within the aortic wall surrounding the ulcer, which will result in IMH formation or
pseudoarortic aneurysm formation.
Signs on CTA
The scan will show an area of intimal defect within the aorta
with the formation of saccular pseudoaneurysm, IMH, or
periaortic mediastinal hematoma (Fig. 4.1.11 ).
Fig. 4.1.11 Axial cardiac CTA shows an area of aortic wall ulceration of the descending thoracic aorta ( arrowhead ) with a jet of
bleeding into the aortic wall creating a periaortic mediastinal
hematoma ( arrowhead )
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4.1
For Further Reading
1 . Hoffmann U et al Cardiac CT in emergency department
patients with acute chest pain. RadioGraphics. 2006;26:
963–80
2 . Oliver TB et al Spiral CT in acute non-cardiac chest pain.
Clin Radiol. 1999;54:38–45
3 . Jeudy J et al Nontraumatic thoracic injuries. Radiol Clin N
Am. 2006;44:273–93
4 . Birchard KR. Acute aortic syndrome and acute traumatic aortic
injury. Semin Roentgenol. 2009. doi:10.1053/j.ro.2008.10.002
5 . Choe YH et al. Comparison of MDCT and MRI in the detec-
tion and sizing of acute and chronic myocardial infarcts. Eur
J Radiol. 2008;66:292–9
6 . Winter-Muram HT et al Suspected acute pulmonary embo-
lism: evaluation with multi-detector row CT versus digital
subtraction pulmonary arteriography. Radiology. 2004;
233:806–15
7 . Castañer E et al Congenital and acquired pulmonary
anomalies in the adult: radiologic overview. RadioGraphics.
2006;26:349–71
8 . De Becker J et al Marfan and Marfan-like syndromes.
Artery Res. 2009;3:9–16
4.2 Diseases of the Great Vessels 163
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4.2
Diseases of the Great Vessels
The great vessels include the aorta, the superior and
inferior vena cava, the pulmonary artery, and the pulmonary veins. There are multiple medical conditions
affecting the great vessels that require imaging to asses
their complications, establish their diagnosis, or monitor their therapy response. This topic discusses some of
the common medical conditions where radiology plays
an important role in their diagnosis and assessment.
Thoracic Aortic Aneurysm
Thoracic aortic aneurysm (TAA) is a disease characterized by dilatation of the wall of the aorta affecting
its three layers (intima, media, and adventitia). In contrast, pseudo-aortic aneurysm is a condition characterized by saccular dilatation of the outer most layers of
the aortic wall (media and/or adventitia) with an intact
inner wall layer (intima).
The most common cause of TAA is atherosclerosis,
while the most common cause of pseudo-aortic aneurysm is aortic trauma violating the wall integrity. TAA
originates in the ascending aorta (50%), descending
aorta (40%), and the aortic arch (10%). In contrast,
pseudo-aortic aneurysm usually arises at three basic
levels: the aortic root, the aortic isthmus, and the aortic
diaphragm.
Patients with TAA are typically in their 50s and 70s,
and usually are asymptomatic. Up to 30% of patients
present with complications due to TAA rupture. Pain or
dysphagia due to mass effect over the adjacent mediastinal structure may be seen uncommonly.
TAA expands at a rate of 0.5 cm per year, with an
increased risk of rupture when it is >5 cm in diameter.
Patients with TAA >6 mm may present with spontaneous bleeding resulting in hemomediastinum or periaortic hematoma formation.
Diff erential Diagnoses and Related Diseases
Marfan syndrome is a disease characterized by ocu-
lar, musculoskeletal, central nervous system, and
cardiovascular complications. Marfan syndrome
patients are known to suffer from aortic root dilatation in up to 80% of cases. Patients may suffer also
from mitral valve prolapse, or dissection of the
aorta.
Loeys-Dietz syndrome is a disease characterized by
aortic aneurysm and dissection, with widespread
arterial tortuosity/aneurysms (seen in the thoracic
aorta and neck vessels mainly). The disease has an
autosomal dominant mode of inheritance. The disease is divided into two types: type I Loeys-Dietz
syndrome is characterized by craniosynostosis,
hypertelorism, bifi d uvula, cleft palate, and/or arterial aneurysms and tortuosity; type II lacks the
hypertelorism, craniosynostosis, and cleft palate.
Aortoduodenal syndrome is a very rare disease char-
acterized by obstruction of the duodenum by aneurysmal dilatation of the abdominal aorta. Patients
classically present with abdominal pain, bilious
vomiting, and pulsatile abdominal mass.
Signs on Radiographs
Aortic aneurysm is detected as a marked dilatation of the
aortic knuckle and mediastinal widening (Fig. 4.2.1 ).
Bronchial compression or erosion of the thoracic vertebrae
due to mass eff ect and chronic pressure causing anterior
scalloping may be seen on lateral views.
Aortic wall calcifi cation may be seen.
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4.2
Fig. 4.2.1. Posteroanterior chest radiograph of a patient with
thoracic aortic aneurysm (TAA) shows marked dilatation of the
aortic knuckle and the descending thoracis aorta
Pulmonary Hypertension
Pulmonary hypertension (PHT) is a disease characterized hemodynamically by a mean pulmonary artery
pressure >25 mmHg at rest (normal level, 10 mmHg)
or >30 mmHg during exercise (normal level, 15 mmHg)
with increased pulmonary vascular resistance.
Causes of PHT can be divided into two main groups:
a group with pathology is confi ned to the arterial side
of the pulmonary circulation ( precapillary PHT ), and a
second group with pathology confi ned to the venous
circulation, between the capillary bed and the left
atrium ( postcapillary PHT ). When the cause of the
PHT is unknown, it is called “idiopathic or primary”
PHT, and when the cause of the PHT is known, it called
“secondary” PHT.
Causes of PHT
Signs on CTA
The thoracic aorta is considered dilated when its diameter is
>4 cm (Fig. 4.2.2 ).
Periaortic hematoma is detected as a hypodense mass located
in the mediastinum surrounding the aorta. If the bleeding is
fresh, the hematoma may show high density (Fig. 4.2.3 ).
Aortic wall calcifi cation may be seen.
Fig. 4.2.2. Axial thoracic CTA demonstrates TAA with fresh
blood leak into the mediastinum ( arrowhead )
Precapillary PHT : primary PHT, congenital heart
defects with left-to-right shunt, pulmonary embolism, parasites (e.g., schistosomiasis), and talcosis
(lung disease due to talc crystals inhalation).
Postcapillary PHT : primary veno-occlusive disease,
mitral stenosis, and mediastinal fi brosis.
Primary PHT is an idiopathic condition characterized
by precapillary PHT in the absence of an identifi able
cause. Patients typically present with dyspnea (60%),
fatigue, angina, cor pulmonale, and Raynaud’s phenomenon. Typically, the patient is a young or middleaged female. Risk factors associated with primary PHT
include: portal hypertension, collagen vascular disease,
pregnancy, and women who use contraceptive pills.
Congenital heart defects associated with left-toright shunts predispose to PHT. Common defects with
PHT include: atrial septal defects, ventricular septal
defects, and truncus arteriosus. Eisenmenger syndrome
is an advanced stage of PHT associated with congenital heart defects. The disease is characterized by dyspnea, cyanosis, generalized fatigue, and syncope.
Patients with Eisenmenger syndrome may die at a
young age due to cardiac arrhythmias, which are
4.2 Diseases of the Great Vessels 165
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common features of this disease. Patients may also
develop paradoxical embolus passing from the right
side of the heart to the left through a heart defect.
Pulmonary veno-occlusive disease ( PVOD ) is a rare
idiopathic disease characterized by postcapillary PHT, in
the presence of normal left atrial and left ventricular pressures. PVOD is characterized by PHT, congestive heart
failure, and interstitial pulmonary edema with a normal
wedge pressure on cardiac catheterization. The pathological fi ndings in PVOD show extensive and diffuse occlusion of pulmonary veins by fi brous tissue, which may be
loose edematous or dense and sclerotic. Patients present
with dyspnea, fl ue-like symptoms, and hemoptysis. It
commonly affects children (30% of cases), transplant
patients, and pregnant women. The disease may be misdiagnosed initially as interstitial lung disease (Fig. 4.2.3).
a
Signs on Chest Radiograph
The pulmonary vasculature diminishes in caliber as it extends
from the center toward the peripher y (pruning), with a mean
width of the right descending pulmonary artery >24 mm
(normal <17 mm in width).
Dilatation of the right and left main pulmonary arteries
(Fig. 4.2.4 ).
Signs of right ventricular enlargement, right atrial enlarge-
ment, or left atrial enlargement (mitral stenosis).
POVD is suggested radiographically when the radiograph
shows signs of pulmonary PHT associated with pulmonary
interstitial edema, and normal-size left atrium. The interstitial
edema is visualized as a diff use linear interstitial pattern.
Mediastinal hilar lymphadenopathy may be present.
b
Fig. 4.2.3. Axial mediastinal-window ( a ) and lung-window ( b )
HRCT illustrations of a patient with pulmonary veno-occlusive
disease (PVOD) show right-sided heart chambers dilatation with
Fig. 4.2.4. Anteroposterior chest radiograph
( a ) and coronal CTA ( b )
of a patient with primary
pulmonary hypertension
(PHT) shows massively
dilated pulmonary arteries
( arrowheads )
normal left heart chambers size. In ( b ), the lung parenchyma
shows bilateral diffuse linear interstitial lung pattern. Notice
also the small pericardial effusion in ( a ) ( arrowhead )
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Signs on HRCT and CTA
PHT is diagnosed when the mean diameter of the pulmonary
artery is >29 mm, with a segmental artery-to-bronchus
4.2
ration >1:1 in three or four pulmonary lobes (Fig. 4.2.4 ).
The lung parenchyma shows mosaic pattern of lung
attenuation due to variation in parenchymal perfusion.
Arteriography shows symmetric enlargement of the central
arteries with tapering subsegmental vessels toward the
peripheries (pruning).
The right ventricle is considered dilated when the ratio of its
diameter to the diameter of the left ventricle is greater than
1:1, with bowing of the interventricular septum toward the
left ventricle.
Right ventricular hypertrophy is confi rmed when the
myocardial wall thickness is >5 mm (normally <4 mm).
Signs of pericardial thickness with small pericardial eff usion
can be seen in a percentage of patients with PHT without an
obvious reason.
In PVOD , classical CT fi nding show the combination of
diff use linear interstitial lung pattern with or without mosaic
ground glass opacities, dilated pulmonary arteries,
right-sided heart chambers dilatation, mediastinal
lymphadenopathy, pericardial or pleural eff usion, with
normal-sized left atrium and pulmonary veins (Fig. 4.2.3 ).
Coral Reef Aorta
Coral reef aorta is a rare condition characterized by
excessive calcifi cation of the suprarenal and juxtarenal
aorta resembling the growth of hyperplastic bone, in
the absence of abnormalities in serum calcium levels.
Coral reef aorta can cause malignant hypertension
due to signifi cant abdominal aortic lumen stenosis, or
renal artery stenosis when it involves the renal arteries.
Other complications include blue toe syndrome due to
dislodged ulcerated atherosclerotic plaques.
Signs on CT
On non-enhanced images, the aorta shows hard, irregular, and
gritty intra-aortic mass of calcifi cation. In contrast to the typical
appearance of atherosclerosis of the great vessels, which follows
the curve of the vessel wall, the calcifi cation in coral reef aorta is
irregular and protrudes into the lumen (Fig. 4.2.5 ).
Fig. 4.2.5. Axial abdominal CT illustration demonstrates coral
reef aorta seen as diffusely calcifi ed arterial wall with projection
of the calcifi ed plaques into the aortic lumen ( arrowhead )
Superior Vena Cava Syndrome
Superior vena cava syndrome (SVCS) is a disease characterized by a triad of edema of the upper torso, venous
distension of the neck, and chylothorax. SVCS arises
due to extrinsic or intrinsic SVC obstruction, causing
disturbance of the venous backfl ow from the head and
neck region and formation of venous collaterals.
Extrinsic causes of SVCS include bronchogenic
carcinoma or lymphoma compressing the SVC (80%
of cases). Intrinsic causes of SVCS are mostly due to
thrombosis, most commonly due to intravenous catheters use. Other causes of intrinsic SVCS include
thrombus propagation from the subclavian veins to the
SVC due to thoracic outlet syndrome.
Patients with SVCS typically present with marked
cyanosis and swelling involving the head and neck
region and the upper extremities, with development of
superfi cial collateral circulation. Complications include
pulmonary embolism (5–35% of cases), thrombophlebitis, sepsis, and thrombus propagation into intracranial sinuses or veins. In some patients, blood may be
“sucked” into the thorax during inspiration, but because
of the limited ventricular fi lling, the neck veins may
become further distended (Kussmaul’s sign).
In infants, SVCS has been linked with the formation
of hydrocephalus, called “ extraventricular obstructive
hydrocephalus ” (EVOH). The mechanism of hydrocephalus is believed to be caused by decrease in cerebrospinal fl uid absorption at the level of the arachnoid
4.2 Diseases of the Great Vessels 167
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granulation secondary to the elevated venous pressure.
EVOH can be seen in up to 91% in infants with SVCS.
Complications of EVOH include hemorrhagic infarction and seizures.
Signs on Chest Radiographs
Pleura eff usion (chylothorax).
The chest may show the cause of SVCS if the reason was
obstruction from a mediastinal tumor.
Rib notching may present with long-standing SVC
obstruction.
Signs on Superior Vena Cavography
There is partial or complete SVC fi lling defect with formation of
numerous venous collaterals (Fig. 4.2.6 ).
Fig. 4.2.6. Superior vena cava venography shows occlusion of
the superior vena cava (SVC) due to thrombosis ( arrowhead )
Signs on Chest CT
Mediastinal masses (e.g., bronchogenic carcinoma)
can be found in cases of extrinsic SVC obstruction.
After contrast injection, partial or complete fi lling
defects representing SVC thrombosis can be seen in
cases of intrinsic SVC obstruction.
Signs on Brain CT
In infants with EVOH, brain CT may be normal in early stages, or
show signs of ventricular dilatation due to hydrocephalus.
For Further Reading
1 . Gotway MB et al Thoracic aorta imaging with multislice CT.
Radiol Clin N Am. 2003;41:521–43
2 . Schulte K-M et al Coral reef aorta: a long-term study of 21
patients. Ann Vasc Surg. 2000;14:626–33
3 . Rosenberg GD et al Blue toe syndrome from a “coral reef”
aorta. Ann Vasc Surg. 1995;9:561–4
4 . Rosenberger A et al Superior vena cava syndrome: a new
radiologic approach to diagnosis. Cardiovasc Intervent
Radiol. 1980;3:127–30
5 . Karmazyn N et al Neuroimaging fi ndings in neonates and
infants from superior vena cava obstruction after cardiac
operation. Pediatr Radiol. 2002;32:806–10
6 . Frazier AA et al Pulmonary vasculature: hypertension and
infarction. RadioGraphics. 2000;20:491–524
7 . Beghetti M et al Eisenmenger syndrome. A clinical per-
spective in a new therapeutic era of pulmonary arterial
hypertension. JACC. 2009;53:733–40
8 . Akpinar E et al PVOD suggested by MDCT and clinical
fi ndings in a pregnant woman. Emerg Radiol. 2008;15:
193–5
9 . Johnson PT et al Loeyz-Dietz syndrome: MDCT angiogra-
phy fi ndings. AJR. 2007;189:W29–35
10 . Deitch JS et al Abdominal aortic aneurysm causing duode-
nal obstruction: two case reports and review of the literature.
J Vasc Surg. 2004;40:543–7
11 . Takagi H et al Aortoduodenal syndrome. J Vasc Surg. 2006;
43:851
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4.3
4.3
Myocardial Diseases (Cardiomyopathies)
Cardiomyopathies are a group of diseases with different etiologies, all characterized by cardiac muscles
dysfunction. Cardiomyopathies are an important cause
of arrhythmias and sudden cardiac death in young
patients. Three types of cardiomyopathies have been
described by the World Health Organization (WHO):
Hypertrophic cardiomyopathy ( HCM ) is character-
ized by inappropriate left ventricular hypertrophy,
with preservation of the myocardium contractility.
Dilated cardiomyopathy ( DCM ) is characterized by
ventricular dilatation with contractility dysfunction.
Most secondary causes of cardiomyopathies are
related to this type.
Restrictive cardiomyopathy ( RCM ) is characterized
by diastolic dysfunction and restricted contractility.
Other uncommon forms of cardiomyopathies include:
athlete’s heart, arrhythmogenic right ventricular dysplasia (ARVD), noncompaction cardiomyopathy (NCCM),
and peripartum cardiomyopathy. Each of the classic
three forms and the uncommon forms of cardiomyopathies are discussed below.
Hypertrophic Cardiomyopathy
Primary HCM is a disease characterized by inappropriate myocardial hypertrophy in the absence of a
cause (e.g., hypertension). In contrast, secondary HCM
can be seen due to diseases of protein deposition (e.g.,
amyloidosis).
Cardiac muscles hypertrophy in HCM is described
as “concentric” or “eccentric.” Concentric heart hyper-
trophy means increased heart muscle bulk and wall
thickness, and it is best assessed on cardiac MRI by
looking at the heart thickness in the short axis view.
Eccentric heart hypertrophy means general increase in
the heart muscles with preservation of the normal cardiac wall thickness (isometric).
Patients with HCM often present with symptoms
that include ischemic cardiac pain and arrhythmias,
although most patients may be asymptomatic. HCM is
the most common cause of sudden cardiac death in
athletes. Up to 25% of HCM patients have left ventricle outfl ow tract (LVOT) obstruction due to the thickened interventricular septum. “ Venturi effect ” is a term
used to describe LVOT obstruction by hypertrophic
interventricular septum during systole, which causes
retrograde jet fl ow toward the mitral valve, causing
anterior mitral valve leafl et regurgitation.
Athlete’s heart is a physiological cardiac hypertrophy.
Sports are divided into endurance sports (e.g., weight
lifting) and dynamic sports (e.g., running). Endurance
sports cause concentric cardiac hypertrophy (<12 mm)
thickness, while dynamic sports cause eccentric cardiac
hypertrophy that may reach (13 mm) in thickness.
Differentiation between athlete heart and HCM can
be diffi cult by imaging alone. However, evidence of
bizarre electrocardiogram (ECG) patterns, female sex,
abnormal left ventricular fi lling, and marked left ventricular enlargement, all favor HCM. Moreover, athlete
heart shows reduction in the heart muscle wall thickness from 2 to 5 mm after a 3-month period of athletic
abstaining, a feature that is not seen in true HCM.
Diff erential Diagnoses and Related Diseases
Yamaguchi syndrome , also known as apical HCM , is
a disease characterized by HCM that is confi ned to,
or located primarily in, the left ventricle (LV) apical
region. Up to 40% of patients are asymptomatic.
ECG leads show characteristic deeply inverted T
wave, which might be mistaken for coronary ischemic disease.
Barth syndrome is an x-linked recessive disorder
characterized by HCM, neutropenia, skeletal myopathy, growth delay, hypocholesterolemia, and urinary
excretion of 3-methylglutarate, 3-methylglutaconate,
and 2-ethyldracrylate.
Romano-Ward syndrome is an autosomal dominant
disease characterized by long ECG QT interval, cardiac arrhythmia, and occasional incidence of HCM.
Jervell and Lange-Nielsen syndrome is an autosomal
recessive disease characterized by long ECG QT
interval, cardiac arrhythmia, sensorineural hearing
loss, syncopal attacks evoked by emotional stress,
and occasional HCM.
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Signs on Chest Radiographs
The heart size can be enlarged with signs of left ventricular
dilatation.
Signs on MRI
Normal LV end-diastolic septal wall thickness is 8.5–9.0 mm.
In athletes, the LV end-diastolic septal wall thickness should
not exceed >13 mm in males, and >11 mm in females. LV
end-diastolic septal wall thickness >15 mm is defi nitely
abnormal.
Disproportional ventricular wall hypertrophy with end-
diastolic septal wall thickness >15 mm. The interventricular
septum is aff ected in >70% of patients (Fig. 4.3.1 ).
Abnormal, late (>10 min) patchy contrast enhancement of
the hypertrophic muscles is found in 79% of patients of HCM,
probably due to small-vessel disease and ischemia.
Venturi eff ect is seen as an area of signal void and mitral valve
regurgitation with LVOT obstruction on Cine-images during
systole.
Yamaguchi syndrome shows hypertrophic left
ventricular apex, causing the left ventricular cavity to exhibit
characteristic “spade-like” confi guration.
Athlete heart is visualized as mild increase in the left
ventricular myocardial wall thickness that does not exceed 13
mm in thickness on short-axis views. There is no abnormal
wall enhancement after contrast injection.
Dilated Cardiomyopathy
DCM is characterized by left ventricular or biventricular dilatation with impaired systolic function.
The most common presentation of DCM is left-sided
heart failure. Causes can be due to alcoholism (50% of
cases), cocaine abuse, and hyper- and hypothyroidism.
Contrast-enhanced MRI for DCM study is mainly indicated to differentiate primary DCM (e.g., without a cause)
from secondary (e.g., postmyocardial infarction) DCM.
Signs on Chest Radiographs
The cardiac heart is markedly enlarged with increased
cardio-thoracic ratio due to cardiac muscles dilatation (Fig. 4.3.2 ).
Signs on MRI
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. 4.3.3 ).
Secondary DCM usually shows late contrast enhancement,
depending on its primary cause (e.g., myocardial infarction):
the contrast uptake refl ecting areas of degeneration, necrosis,
and fi brosis. In contrast, primary DCM shows no late contrast
enhancement. The contrast enhancement can be subendocardial or transmural.
Intraventricular thrombus may be found.
Fig. 4.3.1 Four-chamber
white-blood cardiac MRI
( a ) and two-chamber view
( b ) show concentric
hypertrophic cardiomyopathy (HCM). Notice the
thickened chorda tendinae
in ( a )
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4.3
Fig. 4.3.2 Anteroposterior chest radiograph of a bedridden
patient shows massively dilated heart due to dilated cardiomyopathy (DCM)
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 differentiate 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 fi lling resistance.
Fig. 4.3.3 Four-chamber white-blood cardiac MRI shows left
ventricular apical dilatation due to previous myocardial infarction ( arrowhead )
Restrictive Cardiomyopathy
RCM is a disease characterized by ventricular fi lling
defect. RCM can be caused by diseases that disturb the
myocardial integrity such as: amyloidosis, sarcoidosis,
metastasis, and glycogen storage diseases.
Arrhythmogenic
Right Ventricular Dysplasia
ARVD is a rare, progressive disease characterized by
infi ltration and replacement of the right ventricle free
wall myocardium with fi 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 fi bro-fatty tissue causes electrical instability of the right ventricular wall. ARVD is
familial in up to 50% of cases, with an autosomal dominant mode of inheritance. The disease has a male predominance. Patient is typically a young male (30 years)
complaining from arrhythmias initiated by exercise.
Signs on MRI
There is right ventricular bulging and dilatation, thinning of
the right ventricle free wall (2–6 mm in thickness), and
high signal intensity seen within the myocardium on T1W
images representing fat infi ltration within the myocardium
(diagnostic key) (Fig. 4.3.4 ). If fatty infi ltration cannot be
demonstrated, right ventricular trabeculation also fulfi lls
the criteria of ARVD, presuming the clinical picture also
suggests it.
Abnormal wall motion is demonstrated on Cine images.
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