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Flashcards in CARDIOVASCULAR Deck (35)
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1
Q

GROSS CARDIOMEGALY ON CXR

A
  1. Ischaemic heart disease—and other cardiomyopathies.
  2. Pericardial effusion—globular (supine radiograph) or flask-shaped
    heart (erect radiograph), crisp cardiac outline (as the effusion
    masks ventricular wall motion).
  3. Multivalve disease—particularly regurgitation.
  4. Congenital heart disease—ASD is the most common to present
    in adults. Eisenmenger’s syndrome may develop in longstanding
    untreated ASD, resulting in chronic pulmonary hypertension, shunt
    reversal and gross cardiomegaly
2
Q

RIGHT ATRIAL ENLARGEMENT

A

Volume loading
1. Tricuspid regurgitation.
2. ASD or AVSD.
3. Chronic atrial fibrillation (AF).
4. Anomalous pulmonary venous return—partial type if presents in
adulthood.
5. Ebstein’s anomaly—congenitally abnormal tricuspid valve, which
is displaced into the RV, resulting in a large RA and a small RV ±
6110 Aids to Radiological Differential Diagnosis
tricuspid regurgitation. Usually presents in childhood. May be
associated with other congenital heart defects, particularly ASD.
Pressure loading
1. Tricuspid stenosis.
2. Constrictive pericarditis or restrictive cardiomyopathy—both
usually cause biatrial enlargement with small/normal ventricles. In
constrictive pericarditis there is usually pericardial calcification/
thickening >3 mm and often a diastolic septal ‘bounce’ on MRI. In
restrictive cardiomyopathy these features are absent and there may
be myocardial thickening/LGE on MRI depending on the cause
(e.g. amyloidosis, HCM, systemic sclerosis).
3. Tricuspid valve obstruction—by tumour or thrombus

3
Q

RIGHT VENTRICULAR ENLARGEMENT

A

Volume loading
1. Tricuspid or pulmonary regurgitation.
2. ASD, VSD or AVSD.
3. Anomalous pulmonary venous return—partial type if presents in
adulthood.
4. Cardiomyopathy—ARVC (fibrofatty replacement of the RV
myocardium + dilatation + hypokinesis ± small RV aneurysms ±
LGE, usually presents in young adults) or Uhl’s anomaly (absence
of the RV myocardium resulting in a paper-thin RV wall but no
intramural fat, usually presents in infancy).
Pressure loading (which may lead to increased
RV volume)
1. Pulmonary hypertension—see Section 6.21.
2. Pulmonary stenosis—including Tetralogy of Fallot.
3. Acute PE—right heart strain.

4
Q

LEFT ATRIAL ENLARGEMENT

A

Volume loading
1. Mitral regurgitation.
2. Chronic atrial fibrillation.
3. VSD or PDA.
Pressure loading
1. Left ventricular failure.
2. Mitral stenosis.
3. Hypertrophic cardiomyopathy—via LV diastolic dysfunction,
outflow obstruction and mitral regurgitation.
4. Constrictive pericarditis or restrictive cardiomyopathy—both
usually cause biatrial enlargement (see Section 6.2).
5. Mitral valve obstruction due to tumour—e.g. myxoma

5
Q

LEFT VENTRICULAR ENLARGEMENT

A

Myocardial disease
1. Ischaemic heart disease—evidence of significant coronary artery
disease on CT. Old myocardial infarcts are seen on MRI as focal
areas of subendocardial/transmural LGE ± wall thinning/
calcification/fat deposition conforming to a vascular territory.
2. Cardiomyopathy
(a) DCM—dilated LV + systolic dysfunction without evidence of
IHD/valve disease. Linear midwall/subepicardial LGE is
common and a poor prognostic indicator. Many different
causes, though idiopathic is most common and often shows
LGE in the septum. Some causes have suggestive features
on MRI:
(i) Haemochromatosis—diffusely reduced T2/T2 signal
throughout the myocardium (as well as the liver).
(ii) Sarcoidosis—patchy areas of myocardial thinning and
midwall/subepicardial LGE ± aneurysms. Lung and nodal
involvement is usually also present.
(iii) Chagas disease
—focal myocardial thinning typically
involving the apex and inferolateral wall with midwall/
subepicardial LGE ± apical aneurysm.
(b) ARVC—can be biventricular; LV-dominant forms also exist.
Diagnosis is based on task force criteria; MRI cannot make the
diagnosis alone. Intramural fat may be present.
3. LV aneurysm/pseudoaneurysm—focal thin-walled saccular
dilatation ± mural thrombus ± calcification. True aneurysms usually
develop weeks to months after myocardial infarction (MI) and
typically arise from the apex/anterolateral wall, with a broad neck
and a low risk of rupture. Pseudoaneurysms usually represent a
contained LV rupture (developing soon after a transmural MI) and
typically arise from the basal inferolateral wall, with a narrow neck
and a high risk of rupture. Cardiac surgery/trauma are less
common causes. If visible on CXR (due to calcification), true
aneurysms are best seen on the frontal view, whereas
pseudoaneurysms are best seen on the lateral view (arising from
the posterior margin of the cardiac shadow). A congenital LV
diverticulum may mimic an aneurysm on MRI, but is usually found
in younger patients and often demonstrates contractility.
Volume loading
1. Aortic or mitral regurgitation.
2. PDA—the pulmonary arteries and ascending aorta are also usually
dilated.
3. VSD—this shunts blood directly into the right ventricular outflow
tract (RVOT) leading to LV dilatation even in large defects.
4. Athlete’s heart—depending on the type of athletic activity, can
lead to increased LV/RV volumes and/or LV hypertrophy (which Cardiovascular system 113
6
rarely exceeds 15 mm in thickness). Mild LA dilatation may also be
seen. Cardiac function is normal.
5. High-output cardiac failure—e.g. due to severe anaemia (e.g.
sickle cell), hyperthyroidism, systemic arteriovenous shunting.
Pressure loading (usually causes diffuse concentric
hypertrophy but may increase LV volume)
1. Hypertension.
2. Aortic stenosis

6
Q

CARDIAC CALCIFICATION
Valves (if visible on CXR, suggests clinically
significant stenosis)

A
  1. Aortic valve calcification—bicuspid aortic valve (especially in
    patients <65 years), degenerative aortic sclerosis (usually >65
    years), previous rheumatic fever. A calcified ring with a central bar
    (calcified commissure) suggests a bicuspid valve. Rarer causes
    include previous infective endocarditis, end-stage renal failure,
    Paget’s disease and ochronosis.
  2. Mitral calcification—degenerative annular calcification (involves
    valve annulus only; curvilinear/J-shaped), previous rheumatic fever
    (involves valve leaflets; amorphous/nodular).
  3. Pulmonary valve calcification—rare; pulmonary stenosis, chronic
    pulmonary hypertension, rheumatic fever.
  4. Tricuspid valve calcification—rare; rheumatic fever, previous
    infective endocarditis, ASD. Degenerative annular calcification can
    also occur (curvilinear, C-shaped).
  5. Homograft calcification
7
Q

CARDIAC CALCIFICATION

Intracardiac (intraluminal)

A
  1. Calcified thrombus—e.g. in the LV (post MI) or LA appendage.
    Often thick and laminated.
  2. Papillary muscle calcification—associated with coronary artery
    disease, dilated cardiomyopathy, mitral valve disease and disorders
    of calcium metabolism.
  3. Calcified tumour—mostly myxomas, although rare intracardiac
    tumours such as haemangiomas, paragangliomas and primary
    cardiac osteosarcomas can also calcify.114 Aids to Radiological Differential Diagnosis
  4. Postinfective calcification—valve vegetations, tuberculomas and
    hydatid cysts may all calcify
8
Q

CARDIAC CALCIFICATION

Myocardium

A
  1. Postinfarction—usually involves LV. Myocardial thinning ± fat also
    present on CT/MR.
  2. Previous rheumatic fever—usually involves the posterior LA wall.
    Curvilinear, may be extensive (‘porcelain atrium’—ring shape on
    frontal CXR, C shape on lateral view).
  3. Calcified tumour—cardiac fibromas often contain dystrophic
    calcification. Some metastases can also calcify.
  4. Metastatic calcification—due to chronic renal failure/
    hypercalcaemia/oxalosis. Usually diffuse throughout myocardium.
  5. Severe sepsis/myocarditis—can rarely cause diffuse myocardial
    calcification in the acute setting, which may slowly resolve after
    recovery.
9
Q

CARDIAC CALCIFICATION

Pericardium 6

A
  1. Previous pericarditis—idiopathic, uraemic, viral, TB, pyogenic infection. Calcification related to previous TB is usually thick, irregular and located along the atrioventricular groove.
  2. Following radiotherapy.
  3. Previous trauma—e.g. haemopericardium, cardiac surgery.
  4. Chronic renal failure/hypercalcaemia.
  5. Asbestos-related pleural plaques—overlying the pericardium.
  6. Calcified pericardial mass—e.g. pericardial cyst or teratoma
10
Q

CARDIAC CALCIFICATION

Coronary arteries

A
  1. Atheroma—Agatston score obtained by an unenhanced low-dose
    CT assesses the extent of coronary artery calcification (not
    soft-tissue plaques). It allows for a risk stratification for major
    adverse cardiac events.
  2. Chronic renal failure—often heavy diffuse calcification that is
    partly related to advanced atheroma
11
Q
LV generalized (concentric) myocardial wall 
thickening ≥12 mm (measured at end-diastole)
A
  1. Hypertension—LV wall usually <15 mm. Typically no LGE.
  2. Aortic stenosis—LV wall usually <15 mm. Typically no LGE.
  3. Athlete’s heart—LV wall usually <15 mm. No LGE. Normal cardiac
    function.
  4. Hypertrophic cardiomyopathy (concentric subtype)—LV wall
    usually >15 mm. Patchy midwall areas of LGE, particularly at the
    anterior and posterior insertion points of the RV.
  5. Myocardial infiltration
    (a) Amyloid—usually in older patients. Concentric myocardial
    hypertrophy, diastolic dysfunction and restrictive filling. Global
    subendocardial LGE is pathognomonic. Difficult to achieve
    myocardial nulling on the TI scout. Often involves both
    ventricles and atria; thickening of the RA free wall >6 mm is
    suggestive. Pericardial and pleural effusions are common.
    (b) Fabry disease—younger patients, M>F (X-linked). Concentric
    LV hypertrophy with focal LGE typically in the basal
    inferolateral midwall.
    (c) Danon disease—younger patients, X-linked, rare. Marked
    concentric LV thickening (up to 60 mm) ± RV thickening.
    Subendocardial LGE not conforming to a vascular territory
12
Q

RV generalized myocardial wall thickening

A
  1. Pulmonary hypertension.
  2. RV outflow tract obstruction—e.g. tumour, myocardial infiltration
    or congenital bands.
  3. Pulmonary valve stenosis
13
Q

Focal myocardial thickening

A
  1. Hypertrophic cardiomyopathy—many subtypes depending on
    region of LV myocardium involved. Thickness usually >15 mm. LGE
    is usually present in a patchy midwall distribution, often involving
    the thickest segments.116 Aids to Radiological Differential Diagnosis
    (a) Classical (asymmetric)—most common (70% of patients).
    Hypertrophy involves the basal anteroseptal and anterior
    segments, which can obstruct the LV outflow tract and cause
    systolic anterior motion of the mitral valve.
    (b) Apical (Yamaguchi syndrome)—more common in East Asian
    patients. ‘Ace of spades’ appearance of LV due to apical
    thickening ± thin-walled apical aneurysm with LGE
    (‘burned-out apex’). RV apex may also be involved.
    (c) Midventricular—thickened mid-third of LV myocardium ±
    apical aneurysm, resulting in a dumbbell configuration. Rare.
    (d) Mass-like—focal myocardial thickening, which may mimic a
    neoplasm, but can be differentiated based on T1/T2 signal
    (isointense to normal myocardium), contractility on myocardial
    tagging sequences and the typical LGE pattern.
    (e) Noncontiguous—separate focal areas of LV wall thickening ±
    patchy LGE.
  2. Sarcoidosis* (acute phase)—focal nodular areas of myocardial
    thickening, most commonly in the basal septum and LV free wall,
    demonstrating increased T2 signal and midwall/transmural LGE,
    representing active granulomatous inflammation.
  3. Eosinophilic myocarditis/endomyocardial fibrosis—both
    conditions have similar and characteristic features on MRI:
    obliteration of the RV and/or LV apex with subendocardial LGE and
    overlying mural thrombus. Differentiation between the two is
    based on the presence of eosinophilia (absent in endomyocardial
    fibrosis). The appearances may mimic apical HCM, but the apical
    obliteration is due to fibrosis rather than true hypertrophy.
  4. Friedreich ataxia—young patients. Focal thickening of LV septum
    and posterior wall. Diagnosis usually known due to earlier onset of
    neurological abnormalities
14
Q

Myocardial thinning

A
  1. Generalized—in LV dilatation due to IHD or DCM. The presence/
    absence of coronary artery disease and pattern of LGE helps
    differentiate the two—subendocardial in IHD, midwall (or no LGE)
    in DCM.
  2. Focal
    (a) Previous infarction—most common cause. May be associated
    with focal fat deposition, calcification and aneurysm/
    pseudoaneurysm formation. Subendocardial or transmural LGE
    on MRI. Conforms to coronary artery territory.
    (b) LV noncompaction—congenital arrest of the normal
    compaction process of LV trabeculae resulting in characteristic
    focal myocardial thinning and hypertrabeculation, most
    commonly involving the midapical myocardium ±
    subendocardial/trabecular LGE ± small mural thrombi. The Cardiovascular system 117
    6
    ratio of noncompacted to compacted myocardium is usually
    >2:1 at end systole on short-axis views.
    (c) Sarcoidosis* (chronic/fibrotic phase)—typically involves the
    basal septum and LV free wall with focal thinning and patchy
    subepicardial/midwall LGE ± aneurysms.
    (d) Myocardial crypt—narrow U/V-shaped clefts within the LV
    myocardium most commonly found in the inferobasal region,
    without evidence of noncompaction. Usually a normal variant
    but can also be associated with HCM mutations.
    (e) Takotsubo cardiomyopathy—transient LV dysfunction caused
    by severe emotional/physical stress, most common in
    postmenopausal women, although it can also rarely be due to
    an underlying phaeochromocytoma. Typically causes
    hypokinesis of the midapical LV with apical ballooning and
    thinning in systole ± myocardial oedema, but characteristically
    no LGE. An ‘inverted’ pattern of hypokinesis involving the
    basal/midventricular myocardium has also been described.
    (f) Burned-out HCM—e.g. at the LV apex in the apical/
    midventricular subtypes.
    (g) Chagas disease* (chronic)—protozoan infection (Trypanosoma
    cruzi) endemic in areas of Central/South America. Causes focal
    thinning, akinesis and fibrosis of the LV myocardium typically
    involving the apex and inferolateral wall with midwall/
    subepicardial LGE. Apical aneurysms are common.
15
Q

Fatty lesions of the myocardium

A
  1. Lipomatous hypertrophy of the interatrial septum—normal
    variant associated with increasing age, obesity and steroid use.
    Typically dumbbell-shaped and spares the fossa ovalis. Often
    demonstrates increased uptake on PET due to brown fat content.
  2. Fatty replacement of an old myocardial infarct—usually linear
    and subendocardial in the LV, with evidence of coronary artery
    disease ± myocardial calcification/thinning.
  3. Lipoma—well-defined purely fatty mass, usually endocardial
    (protruding into lumen) or epicardial (protruding into pericardial
    space).
  4. Fatty infiltration of the RV free wall—typically seen in ARVC, but
    may also be seen incidentally in older patients (usually in the
    RVOT). In ARVC there is also RV enlargement + hypokinesis ± LGE
    ± small aneurysms. The LV is affected less frequently.
  5. Tuberous sclerosis*—unencapsulated fatty deposits (often
    multiple), typically midmyocardial in the septum/LV. Cardiac
    angiomyolipomas have also been reported.
  6. Teratoma—rare, usually intrapericardial, typically presents in
    infancy. Soft-tissue, fluid and calcified components also present.118 Aids to Radiological Differential Diagnosis
  7. Liposarcoma—very rare. Often large, infiltrative + soft-tissue
    component ± metastases
16
Q

Pericardial thickening (>3 mm)

A
  1. Previous pericarditis—idiopathic, infection (viral, TB, pyogenic),
    connective tissue diseases (most commonly seen in SLE and
    rheumatoid arthritis).
  2. Post cardiac surgery or mediastinal radiotherapy.
  3. Previous trauma/haemopericardium.
  4. Malignancy—e.g. metastases (most common by far), pericardial
    mesothelioma, lymphoma, sarcoma, direct invasion from lung/
    oesophageal cancer. Nodular pericardial thickening + enhancement
    ± effusion. Lymphoma and sarcomas may present as a large
    infiltrative pericardial mas
17
Q

Pericardial effusio
Globular heart on frontal CXR if effusion is large. ‘Oreo cookie’
sign may be seen on lateral CXR. May cause tamponade if fluid
accumulates quickly—features on MRI include diastolic collapse of
the RA and RV free wall, and IVC dilatation without inspiratory
collapse

A
  1. Transudate—e.g. cardiac failure, hypoalbuminaemia, renal failure.
    No pericardial thickening, enhancement or septations. Fluid
    attenuation close to water (<20 HU).
  2. Exudate—e.g. infection (viral, TB, empyema), uraemic pericarditis,
    collagen vascular diseases (SLE, rheumatoid arthritis, scleroderma),
    malignancy, Dressler syndrome. Smooth pericardial thickening +
    enhancement may be present. Fluid attenuation is often higher
    than in transudate. Septations may be present in empyema.
  3. Haemopericardium—acute aortic dissection, trauma, following
    cardiothoracic surgery, acute MI, tumour (metastases, lymphoma,
    local tumour invasion, primary pericardial malignancy). High
    attenuation fluid on CT, high T1 signal on MRI.
  4. Chylous—e.g. malignancy, cardiothoracic surgery, pericardial
    lymphangioma. Fluid may be of low attenuation
18
Q

CARDIAC MASSES

4

A
  1. Thrombus—most common intracardiac mass, often broad-based/crescent-shaped, may mimic a tumour but does not enhance. Usually occurs in aneurysms or in areas of hypokinesis, e.g. post MI (ventricles) or in AF (LA appendage). Also seen at ventricle apices in endomyocardial fibrosis/eosinophilic myocarditis, and around trabeculae in LV noncompaction. Can occur in RA around indwelling venous catheters with insufficient anticoagulation. May contain calcification if chronic.
  2. Benign tumours—typically well-defined and noninfiltrative.
    (a) Myxoma—most common primary cardiac tumour, typically within the LA arising from the interatrial septum close to the fossa ovalis. Lobular/oval shape, low attenuation on CT, usually pedunculated and mobile (can prolapse through the AV valve), ± calcification. Patchy LGE on MRI. If
    multiple/recurrent, consider a familial syndrome, e.g. Carney complex.

(b) Papillary fibroelastoma—typically small (<15 mm), pedunculated, arising from a valve (usually aortic/mitral). May mimic valve vegetation but can usually be differentiated based on clinical history and presence of other features seen in infective endocarditis, e.g. valve perforation, perivalvular
abscess, pseudoaneurysm.

(c) Lipoma—purely fatty on CT/MRI.
(d) Fibroma—typically located within ventricle myocardium (LV>RV), usually presents in infancy/childhood but occasionally is seen in adults. Homogenous, low attenuation on CT, T2 hypointense on MRI + intense LGE. Dystrophic calcification is common. Associated with Gorlin-Goltz syndrome and Gardner variant FAP.

(e) Rhabdomyoma—most common cardiac neoplasm in children, presents in infancy or prenatally in most cases. Located within the myocardium (LV/RV>atria), often multiple. Strongly associated with tuberous sclerosis,
particularly if multiple. Homogenous, T2 hyperintense on MRI, no LGE or calcification. Most regress spontaneously in childhood.

(f) Haemangioma—can arise from any location. May contain phleboliths. Diffuse high T2 signal on MRI with intense heterogenous first pass and delayed enhancement.
(g) Teratoma—usually in children, typically arises from the pericardium.
(h) Solitary fibrous tumour—rare, typically arises from pericardium. Well-defined, heterogenous enhancement.
(i) Paraganglioma—very rare. Arises from neuroendocrine cells located in the interatrial/AV grooves or root of the great vessels, therefore typically epicardial in location. Very high T2 signal, intense first pass and delayed enhancement.
(j) Cystic tumour of the AV node—very rare. Small (<2 cm), arises from the AV node region at the base of the interatrial septum. High T1/T2 signal + LGE. Causes arrhythmias ±sudden death.
(k) Tumour mimics—caseous calcification of the mitral valve annulus: mass-like variant of mitral annulus calcification, which may be uniformly dense on CT (putty-like) or have a low attenuation centre with a calcified rim. Other tumour mimics include a prominent crista terminalis (lateral RA wall) or Eustachian valve (RA–IVC junction).

  1. Malignant tumours—typically ill-defined, infiltrative, enhance on MRI, often involve >1 chamber and/or pericardium (pericardial effusion suggests malignancy).
    (a) Metastasis—e.g. from lung, breast, lymphoma, melanoma. Much more common than primary tumours. Often multiple; usually seen in the presence of metastases elsewhere. Pericardial > epicardial > myocardial > endocardial. Melanoma metastases are often T1 hyperintense. RCC/HCC may extend into the RA directly via the IVC.
    (b) Primary sarcoma—angiosarcoma is most common; typically arises from the lateral RA wall and often infiltrates the AV groove (± right coronary artery aneurysm) and tricuspid valve. Other sarcomas usually arise from the LA. Calcification suggests osteosarcoma, fat suggests liposarcoma. Pulmonary
    vein invasion suggests leiomyosarcoma. Pericardial involvement and metastases are common in all sarcomas.

(c) Primary lymphoma—typically involves RA/RV and encases the right coronary artery in the AV groove. Often multifocal/diffuse with a homogenous signal on MRI + pericardial effusion. Primary cardiac lymphoma usually occurs in immunocompromised patients, particularly with HIV.

  1. Mass-forming infections
    (a) Tuberculosis*—most commonly involves the pericardium but can rarely involve the myocardium (usually right heart). Tuberculoma may be single or multiple. T1/T2 iso/hypointense, heterogenous LGE.

(b) Hydatid cyst—cardiac involvement is rare but has a characteristic multiloculated cystic appearance due to multiple daughter cysts. May rupture and embolize to other sites.
(c) Cysticercosis*—cardiac involvement is rare, usually in the presence of disseminated disease elsewhere. Multiple small cystic lesions throughout the heart, each containing a focus of low T2 signal representing the scolex.

19
Q

LATE GADOLINIUM ENHANCEMENT ON
CARDIAC MRI
Subendocardial or transmural LGE

A
  1. Myocardial infarction—conforms to a coronary artery territory. In
    the chronic phase there is usually myocardial thinning ± intramural
    fat/calcification.
  2. Amyloidosis*—typically global subendocardial LGE and diffuse
    myocardial thickening in an older patient. LGE may also be diffuse
    throughout the myocardium.
  3. Sarcoidosis*—commonly midwall or subepicardial, but can be
    subendocardial or transmural. Does not conform to a coronary
    artery territory.
  4. Eosinophilic myocarditis/endomyocardial fibrosis—characteristic
    subendocardial LGE at RV/LV apex + overlying mural thrombus.
  5. Danon disease—marked concentric myocardial thickening and
    subendocardial LGE in a young patient.(X-L AD, cardiomyopathy, myopathy, mild intellectual disability)
  6. LV noncompaction—subendocardial LGE can sometimes be seen
    at the LV apex or within the prominent trabeculae
20
Q

Subepicardial or midmyocardial LGE

8

A
  1. Myocarditis—typically subepicardial but may be midmyocardial or
    transmural. Commonly involves inferolateral LV wall but may be
    concentric in severe cases. Associated with myocardial oedema and
    hyperaemia, i.e. increased T2 signal relative to skeletal muscle
    (>1.9x) and increased early gadolinium enhancement relative to
    skeletal muscle (>4×). Usually viral, but can be bacterial,
    tuberculous, inflammatory (e.g. SLE), iatrogenic (drugs,
    radiotherapy) or idiopathic.
  2. Sarcoidosis*—commonly involves the basal septum and LV free
    wall. Associated with myocardial oedema (acute phase) or
    myocardial thinning ± aneurysms (chronic phase).
  3. HCM—typically patchy, most marked at regions of maximal
    myocardial thickening and at RV insertion points.
  4. DCM—typically midmyocardial, particularly in the septum, with LV
    dilatation.
  5. Systemic sclerosis—typically midwall in the septum and RV
    insertion points.
  6. Chagas disease*—typically involves the apex and inferolateral wall
    ± aneurysm.
  7. ARVC—in cases with LV involvement. In LV-dominant forms, LGE is
    seen as a circumferential band in the outer third of the
    myocardium and right side of the interventricular septum. LGE of
    the RV myocardium can be hard to appreciate as the RV wall is
    thin, but tends to appear transmural if present.
  8. Fabry disease—commonly basal inferolateral midwall LGE +
    concentric left ventricular hypertrophy
21
Q

MALIGNANT CORONARY ARTERY

ANOMALIES IN THE ADULT

A
  1. Myocardial bridging—common; possible increased risk of
    ischaemia (controversial). Typically involves the mid-left anterior
    descending artery. The vessel dives into the myocardium over a
    short distance ± narrowing in systole. Depth and length of bridge
    is linked to risk of ischaemia.
  2. Interarterial course of an aberrant coronary artery—increased
    risk of sudden cardiac death due to a combination of a slit-like
    ostium, an acute angle of take-off and an intramural course
    through the ascending aorta.
    (a) Aberrant right coronary artery—arising from the left
    coronary sinus and passing between the aorta and main
    pulmonary artery.
    (b) Aberrant left main coronary artery—arising from the right
    coronary sinus and passing between the aorta and main
    pulmonary artery. Less common than (a), but has a higher risk
    of sudden death.
  3. Anomalous left coronary artery from the pulmonary artery
    (ALCAPA)—rare, can present in infancy or adulthood. Causes
    ischaemia of the left coronary artery territory with dilatation of the
    right coronary artery + multiple collaterals. Eventually results in a
    left-to-right shunt due to reversal of flow in the anomalous left
    coronary artery. ARCAPA is a rarer variant involving the right
    coronary artery.
  4. Coronary artery fistula—rare abnormal communication between
    a coronary artery and another vessel or cardiac chamber
    (commonest being RV or RA). Usually congenital but can rarely
    be traumatic/iatrogenic. The involved coronary artery is dilated
    and tortuous but has a normal origin from its coronary sinus.
22
Q

CAUSES OF A PERFUSION DEFECT ON

CARDIAC STRESS PERFUSION MRI

A
  1. Inducible ischaemia—perfusion defect present on stress but
    absent at rest. No LGE to suggest infarction. Will benefit from
    revascularization.
  2. Infarction—perfusion defect present on both stress and rest
    images (may not be appreciable on rest images due to
    enhancement from residual gadolinium), with associated
    subendocardial/transmural LGE. Unlikely to benefit from
    revascularization if LGE involves >50% of myocardial thickness.
  3. Microvascular disease—tends to be circumferential.
  4. Hibernating myocardium—mild perfusion defect present on both
    stress and rest images (may be hard to appreciate on rest images,
    as above) with an associated wall motion abnormality but no LGE
    to suggest infarction. Indicates chronic ischaemia that will benefit
    from revascularization. Myocardial stunning can have a similar
    appearance, but occurs in the context of an acute transient
    ischaemic event, and perfusion is usually nearly normal.
  5. Susceptibility artefact—appears as a dark rim in the
    subendocardium as the gadolinium bolus arrives in the LV cavity
    and lasts until the bolus leaves the LV cavity.
23
Q

ACUTE AORTIC SYNDROMES

A
  1. Aortic dissection—on CXR, medial displacement of intimal
    calcification may be seen. CT demonstrates the dissection flap with
    flow in the true ± false lumen. The dissection flap may extend into
    (and occlude) branches of the aorta ± end-organ infarction. A
    chronic dissection with a thrombosed false lumen may mimic an
    aortic aneurysm with mural thrombus, but the location of intimal
    calcification helps differentiate the two—along the inner margin of
    the thrombus in dissection, along the outer margin of the
    thrombus in an aneurysm.
  2. Intramural haematoma—blood collects in the media of the aortic
    wall due to rupture of the vasa vasorum (usually no visible intimal
    tear). Tends to occur in hypertensive patients or in blunt trauma.
    Characteristic crescentic hyperattenuation within the aortic wall on
    unenhanced CT, which does not fill with contrast, although
    sometimes contrast-filled ulcer-like projections (communicating
    with lumen) or intramural blood pools (not communicating with
    lumen) may be seen. May resolve or progress to dissection,
    rupture or aneurysm—higher risk of progression if ulcer-like
    projections are present.
  3. Penetrating aortic ulcer—focal deep ulceration of the aortic wall
    at a site of intimal atherosclerosis, usually in descending aorta. May
    be hard to differentiate from an ulcerated plaque, but a
    penetrating ulcer should extend beyond the expected margin of
    the aortic wall ± adjacent stranding/haemorrhage. May progress to
    intramural haematoma, dissection, rupture or pseudoaneurysm.
    Mycotic pseudoaneurysm should be considered in the differential if
    there are clinical features of infection and no atherosclerosis.
  4. Traumatic aortic injury—usually due to rapid deceleration injury.
    Typically occurs at the aortic isthmus due to tethering by the
    ligamentum arteriosum. May be subtle on CT (best seen on
    sagittal reformats), particularly in minimal aortic injury where there
    is only intimal irregularity ± a small (<1 cm) intimal flap ± an
    adherent intraluminal thrombus ± intramural haematoma, with an
    otherwise normal aortic contour and no mediastinal haemorrhage.
    More severe injuries will demonstrate an irregular aortic
    pseudoaneurysm ± mediastinal haemorrhage. The differential
    diagnosis includes a chronic traumatic pseudoaneurysm (nearly 126 Aids to Radiological Differential Diagnosis
    always rim-calcified) and a congenital ductus diverticulum (usually
    smooth with obtuse margins).
24
Q

Isolated sinus of Valsalva aneurysm

A
  1. Mycotic—usually due to infective endocarditis of the aortic valve
    (perivalvular pseudoaneurysm), but can rarely be due to TB or
    tertiary syphilis. Irregular shape, often also involves aortic
    annulus with valve thickening/vegetations. High risk of rupture/
    fistulation.
  2. Congenital—smooth contour, usually involves the right coronary
    sinus, may be associated with VSD. May rupture into RV
25
Q

Annuloaortic ectasia

3

A
  1. Marfan syndrome*—classically linked to this aneurysm type.
  2. Other genetic disorders—e.g. Ehlers-Danlos syndrome,
    Loeys-Dietz syndrome, homocystinuria, osteogenesis imperfecta,
    Shprintzen-Goldberg syndrome.
  3. Bicuspid aortic valve—aneurysm formation can occur regardless
    of aortic stenosis.
26
Q

Ascending aortic aneurysm

A
  1. Poststenotic dilatation from aortic stenosis.
  2. Previous aortic dissection—fusiform aneurysm + chronic
    dissection flap.
  3. Atherosclerosis/hypertension—descending > arch > ascending
    aorta. Usually in older patients, fusiform morphology in most
    cases, but can be saccular.Cardiovascular system 127
    6
  4. Aortitis—e.g. Takayasu arteritis, giant cell arteritis, rheumatoid
    arthritis, seronegative spondyloarthropathies, relapsing
    polychondritis, SLE, Behçet’s disease, Cogan syndrome.
  5. Congenital heart disease—as well as PDA and aortic coarctation.
  6. Mycotic pseudoaneurysm—usually due to Staphylococcus aureus
    or Salmonella spp. Irregular, lobulated, noncalcified saccular
    aneurysm + adjacent fat stranding/abscess, can occur at any site
    but descending > ascending aorta. Rapidly progressive, high risk of
    rupture. In TB, pseudoaneurysms are usually due to extrinsic
    erosion of the aorta from an adjacent involved lymph node. HIV is
    also associated with aortitis and fusiform aneurysms.
  7. Tertiary syphilis*—rare, usually causes saccular aneurysms of the
    ascending aorta. Associated with extensive confluent ‘tree-bark’
    calcification of the aortic wall
27
Q

Descending aortic aneurysm

A
  1. Atherosclerosis/hypertension—often together with an AAA.
  2. Previous aortic dissection or penetrating ulcer—postdissection
    aneurysms are usually fusiform, whereas penetrating ulcers
    progress to saccular aneurysms.
  3. Previous trauma with missed rupture—focal saccular
    pseudoaneurysm at the anterior margin of the isthmus. Look for
    other signs of old trauma, e.g. healed rib fractures.
  4. Mycotic pseudoaneurysm—see above. More common in
    descending aorta, including TB.
  5. Kommerell diverticulum—saccular bulge at the origin of an
    aberrant subclavian artery.
28
Q

INCREASED AORTIC WALL THICKNESS

A

. Intramural haematoma—characteristic crescentic
hyperattenuation within the wall on unenhanced CT, which does
not fill with contrast.
2. Vasculitis—particularly Takayasu arteritis (<50 years) and giant cell
arteritis (>50 years). Circumferential wall thickening ± mild
periaortic stranding. Can involve both thoracic and abdominal
aorta ± major branches. Increased uptake on PET. Takayasu arteritis
typically causes stenoses/occlusions. Other vasculitides (see Section
6.14) can also occasionally cause aortitis, but are usually limited to
the ascending aorta.
3. IgG4-related disease—can manifest as periaortitis, inflammatory
AAA or RPF (ill-defined periaortic soft-tissue thickening ± IVC
involvement/narrowing ± ureteric tethering/obstruction). Typically 128 Aids to Radiological Differential Diagnosis
does not extend posterior to the aorta (cf. malignancy and
Erdheim-Chester disease). Treated lymphoma can mimic RPF.
4. Infectious aortitis—usually associated with mycotic
pseudoaneurysm, periaortic fat stranding ± abscess. Infection may
be related to an indwelling stent/graft or could have spread from
an adjacent source, e.g. discitis.
5. Erdheim-Chester disease
—ill-defined periaortic soft-tissue
thickening sparing IVC and not displacing ureters. If perirenal
soft-tissue thickening is also present this is almost pathognomonic

29
Q

FOCAL NARROWING OF THE AORTA

A

. Atherosclerosis—lumen narrowed by calcified and/or noncalcified
plaque. In severe cases can lead to occlusion of the infrarenal aorta
(aortoiliac occlusive disease).
2. Coarctation—in adults, usually just distal to the aortic isthmus +
multiple collaterals. May be visible on CXR as a ‘figure 3’ aortic
knuckle with inferior rib notching. Beware of pseudocoarctation,
which is kinking of the aorta at the isthmus without true stenosis
or collateral formation.
3. Takayasu arteritis—typically causes multifocal arterial stenoses. In
the aorta the arch is the commonest site of stenosis. Aortitis and
aneurysms may also be present.
4. Narrowing due to mass lesion or retroperitoneal fibrosis.
5. Midaortic syndrome—young patients, relatively long smooth
narrowing of the suprarenal abdominal aorta ± involvement of
renal arteries, SMA or coeliac axis ± multiple collaterals. Associated
with NF1, Williams syndrome and Alagille syndrome.
6. Supravalvular aortic stenosis—focal smooth stenosis of the
ascending aorta just distal to the sinuses of Valsalva, characteristic
of Williams syndrome

30
Q

SYSTEMIC DISORDERS ASSOCIATED WITH

NONAORTIC ANEURYSMS

A
  1. Vasculitis
    (a) Kawasaki disease—characteristically produces coronary artery
    aneurysms ± stenoses.
    (b) Behçet’s disease/Hughes-Stovin syndrome—both cause
    pulmonary artery aneurysms.
    (c) Takayasu arteritis—more commonly causes multifocal
    stenoses, but aneurysms of the arch vessels can also occur.
    (d) Polyarteritis nodosa
    —classically causes multiple
    microaneurysms of the renal, hepatic and/or mesenteric
    arteries ± occlusions/infarcts. Best seen on angiography, may
    be occult on CT. A similar appearance may also be seen in
    SLE, Wegener’s granulomatosis and IV drug abuse-related
    necrotizing vasculitis.
  2. Connective tissue disorders—Marfan syndrome, Ehlers-Danlos
    syndrome type 4 and Loeys-Dietz syndrome can all cause arterial
    aneurysms at any location, although the ascending aorta is most
    commonly involved. Loeys-Dietz syndrome classically also causes
    marked arterial tortuosity.
  3. Fibromuscular dysplasia/segmental arterial mediolysis—both
    conditions are noninflammatory, nonatherosclerotic arteriopathies
    causing a characteristic ‘string of beads’ appearance in involved
    arteries due to alternating aneurysms and stenoses. FMD usually
    occurs in adults <50 years and most commonly involves the renal
    and carotid arteries. SAM usually occurs in adults >50 years and
    most commonly involves the mesenteric arteries, coeliac axis
    and branches. Dissection and haemorrhage is more common
    in SAM.
  4. Neurofibromatosis*—can rarely cause arterial stenoses and
    aneurysms involving the aorta, arch vessels, renal arteries,
    intracranial arteries and visceral arteries
31
Q

INTRAVASCULAR LESIONS 8

A
  1. Atheroma—in arteries only, may be noncalcified or calcified.
    Noncalcified atheroma is irregular in shape and of low attenuation
    on CT. Aortic occlusion/stenosis caused by a large endoluminal
    calcification is known as a ‘coral reef aorta’.
  2. Thrombus/embolus—thrombus is much more common in veins
    (e.g. DVT or superficial thrombophlebitis), but can occur in
    abnormal arteries, e.g. at sites of atherosclerosis or intimal damage
    (e.g. aortic injury), in aneurysms (crescentic mural thrombus) and
    in vasculitis. Emboli are found almost exclusively in arteries (and
    occasionally in hepatic portal veins), usually lodging at branching
    points ± signs of end-organ ischaemia. Acute thrombus is often
    hyperattenuating on unenhanced CT. MRI signal varies widely:
    acute thrombus (<7 days) is usually T1 isointense and T2
    hypointense, subacute thrombus (7–14 days) is usually T1 and T2
    hyperintense and chronic thrombus is usually T1 isointense and
    T2 hyperintense. Acute and subacute thrombus often shows
    high signal on DWI and low signal on T2*. Thrombus does not
    enhance on CT/MRI and does not show internal flow on Doppler
    US—any enhancement or internal vascularity suggests tumour
    thrombus.
  3. Tumour thrombus—direct intravenous extension of a tumour,
    most commonly from RCC or HCC, but can also be seen with
    adrenal carcinoma, pancreatic NET and leiomyosarcoma. Tumour
    thrombus usually shows internal flow on Doppler US, enhances on
    CT/MRI and often expands the vein. Rarely, intravenous extension
    can occur from uterine fibroids (intravenous leiomyomatosis)—this
    usually involves the pelvic veins and IVC, but can extend into the
    right heart.
  4. Nonthrombotic pulmonary emboli.
  5. Cystic adventitial disease—rare, typically presents in young
    adult males as a benign multiloculated cystic mass arising from
    the adventitia of the popliteal artery causing luminal narrowing.
    Can occasionally involve other arteries (and rarely veins)

adjacent to joints.
6. Intravascular lipoma—rare. Most commonly arises from the IVC;
characteristic fatty appearance on CT/MRI.

  1. Intravenous lobular capillary haemangioma—rare. Most
    commonly arises from veins in the neck/arms. Hypervascular on
    Doppler US, enhances on CT/MRI.
  2. Primary vascular sarcomas—rare. Typically involve large veins or,
    less commonly, large arteries. Usually demonstrate internal flow on
    Doppler US and enhancement on CT/MRI ± extravascular invasion.
    Pulmonary artery sarcomas may mimic pulmonary emboli. Arterial
    sarcomas may mimic focal atheroma, particularly on CT where
    internal enhancement may be difficult to appreciate. Venous
    sarcomas often cause vessel expansion and associated thrombosis.
    Leiomyosarcoma is the most common subtype (most arising from
    the IVC); other subtypes include intimal sarcoma (most arising
    from the descending aorta or central pulmonary arteries),
    angiosarcoma, synovial sarcoma and epithelioid
    haemangioendothelioma
32
Q

ENDOLEAK APPEARANCES ON
MULTIPHASIC CT FOLLOWING
ENDOVASCULAR ANEURYSM REPAIR

A
  1. Type I—from the graft attachment site. Type Ia proximal. Type Ib
    distal. Contrast present in sac, usually on arterial phase. High
    pressure, high risk; requires treatment.
  2. Type II—retrograde sac filling from collateral vessels (inferior
    mesenteric and lumbar arteries). Most common type; best
    depicted on delayed phase. 50% spontaneously resolve. Serial
    surveillance and treatment if sac expands.
  3. Type III—structural failure of stent graft, including junctional
    separations, fractures or perforations of the graft. High pressure,
    high risk; requires treatment.
  4. Type IV—sac filling through graft fabric due to graft porosity
    after placement. By definition not detected on follow-up
    imaging.
  5. Type V—endotension; sac expansion without visible endoleak.
    Controversial, usually occult Type I–IV endoleak or ultrafiltration of
    blood.
33
Q

Diffuse MPA enlargement (MPA > adjacent

ascending aorta)

A
  1. Pulmonary hypertension—dilated MPA and bilateral central PAs
    with peripheral pruning. See Section 6.21.
  2. Left-to-right shunt—dilated MPA, central and peripheral PAs
    (plethora).
  3. Pulmonary valve stenosis—dilated MPA only (± left PA).
  4. Marfan syndrome*—can rarely cause MPA root dilatation.
34
Q

Focal pulmonary artery aneurysm

A
  1. Vasculitis—typically in Behçet’s disease, but consider
    Hughes-Stovin syndrome if there are no oral/genital ulcers. Often
    multiple ± thrombosis ± pulmonary infarcts. High risk of rupture.
  2. Chronic pulmonary hypertension—particularly in left-to-right
    shunts, e.g. PDA, due to shear stresses. Associated mural
    thrombus/calcification is common. Aneurysms may be very large.
  3. Mycotic pseudoaneurysm—e.g. due to lung abscess, septic
    emboli, TB (Rasmussen aneurysm), invasive fungal infection or
    tertiary syphilis.
  4. Traumatic pseudoaneurysm—most commonly due to Swan-Ganz
    catheters.
  5. Malignancy—a lung tumour/metastasis may erode into an
    adjacent pulmonary artery, causing a pseudoaneurysm. Primary
    sarcoma of the pulmonary artery can also cause focal aneurysmal
    dilatation with an intraluminal mass ± extraluminal extension.
  6. AVM—look for dilated feeding pulmonary artery and draining vein
35
Q

PULMONARY HYPERTENSION

A

Pulmonary venous hypertension—due to left heart failure (e.g.
LVF, mitral valve disease). Pulmonary oedema and pleural effusions
may be present.
2. Chronic lung disease—e.g. emphysema, interstitial lung disease,
cystic fibrosis, LCH, LAM, hypoventilation.
3. Chronic thromboembolic pulmonary hypertension (CTEPH)—
signs on CT include laminar thrombus (usually seen in larger
arteries), intraluminal webs, pulmonary artery stenoses/occlusions
(may be very subtle in smaller vessels—look for bronchi without
accompanying arteries), peripheral lung scarring due to previous
infarcts, dilated bronchial arteries (due to collateralization) and
mosaic attenuation in the lungs with smaller pulmonary arteries in
the more lucent areas.
4. Chronic left-to-right shunt—e.g. ASD, VSD, PDA, partial
anomalous pulmonary venous return (PAPVR).
5. Vasculitis—Takayasu arteritis often involves the pulmonary arteries,
causing multifocal stenoses/occlusions, which can mimic CTEPH.
Behçet’s disease and Hughes-Stovin syndrome can also cause Cardiovascular system 133
6
pulmonary artery stenoses/occlusions due to thrombosis/emboli in
addition to the characteristic PA aneurysms. Small vessel
vasculitides can also cause pulmonary hypertension ± areas of
pulmonary haemorrhage ± nodules/cavities, but the pulmonary
arteries visible on CT typically appear normal.
6. Pulmonary venoocclusive disease—usually young adults. HRCT
features are similar to LVF with interlobular septal thickening,
pleural effusions and ground-glass opacities, but with a normal left
heart. Centrilobular nodules are usually absent (cf. below).
7. Pulmonary capillary haemangiomatosis—usually young adults.
Widespread ill-defined centrilobular nodules on HRCT. Interlobular
septal thickening is rare. Normal left heart.
8. Idiopathic pulmonary arterial hypertension—typically young
adult women. Usually no other imaging features apart from those
of pulmonary hypertension.
9. Other causes—sarcoidosis, connective tissue diseases (e.g.
scleroderma), fibrosing mediastinitis, portal hypertension, NF1, HIV,
schistosomiasis, drugs/toxins and others.