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150 Chapter 3 Pulmonology
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Fig. 3.8.5. Posteroanterior
plain chest radiograph ( a ) and
coronal HRCT ( b ) of a
patient with Churg-Strauss
syndrome (CSS) shows
bilateral nodular patchy lung
3.8
infi ltration due to vasculitis
and granulomatosis
Fig. 3.8.6. Sequential axial
HRCT of a patient with
lymphomatoid granulomatosis (LG) shows multiple lung
masses located at the lung
bases in the left lung in ( a )
and bilaterally in ( b )
( arrowheads )
Cardiac Bronchus
Cardiac bronchus is a rare congenital anomaly in which
there is accessory bronchus that arises from the medial
wall of the intermediate bronchus at its proximal third,
but occasionally from the right main bronchus. The
accessory bronchus runs medially and caudally toward
the heart, hence the cardiac appellation.
Cardiac bronchus is not identifi ed on plain chest
radiographs, and usually incidentally found on CT
scans. The anomaly is asymptomatic; however, it may
result in hemoptysis when it is infected.
Signs on CT
The cardiac bronchus is typically identifi ed as a small accessory
bronchus medial to the intermediate bronchus on the right lung
(Fig. 3.8.7 ).
Fig. 3.8.7. Axial HRCT illustration demonstrates the typical
radiographic sign and location of the cardiac bronchus on CT
( arrowhead )
3.8 Hemoptysis 151
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Dieulafoy Disease
Dieulafoy disease is a very rare condition characterized by abnormally dilated submucosal vessels that are
prone to bleed, and classically described in the colon,
small intestine, and the bronchi.
Dieulafoy disease can be seen with cases of chronic
bronchitis. On bronchoscopy, the visualization of
dilated submucosal blood vessels in the presence of
mucosal dilatation should alert the bronchoscopist of
the possibility of Dieulafoy disease. Dieulafoy disease
can be the case of massive upper gastrointestinal bleeding in 1–2% of cases.
For F urther Reading
1 . Furuse M et al Bronchial arteries: CT demonstration with
arteriographic correlation. Radiology. 1987;162:393–8
2 . Cooper C et al CT appearance of the normal inferior pul-
monary ligament. AJR Am J Roentgenol. 1983;141:237–40
3 . Khalil A et al Role of MDCT in identifi cation of the bleed-
ing site and the vessels causing hemoptysis. AJR Am J
Roentgenol. 2007;188:W117–25
4 . van der Werf TS et al Fatal hemorrhage from Dieulafoy’s
disease of the bronchus. Thorax. 1999;54:184–5
5 . Löschhorn C et al Dieulafoy’s disease of the lung: a potential
disaster for the bronchoscopist. Respiration. 2006;73: 562–5
6 . Son JS et al Anomalous systemic arterial supply to the basal
segments of the right lower lobe in neonate. Pediatr Cardiol.
2008;29:1009–10
7 . Temes E et al Young patient with recurrent hemoptysis.
Resp Med (Extra). 2006;2:64–6
8 . Wilson SR et al CT visualization of mediastinal bronchial
artery aneurysm. AJR Am J Roentgenol. 2006;187:W544–5
9 . Ahmed M et al Multislice CT and CT angiography for non-
invasive evaluation of bronchopulmonary sequestration.
Eur Radiol. 2004;14:2141–3
10 . Yoon YC et al Hemoptysis: bronchial and non-bronchial
systemic arteries at 16-detector row CT. Radiology. 2005;
234:292–8
11 . Bentala M et al Cardiac bronchus: a rare cause of hemopty-
sis. Eur J Cardiothoracic Surg. 2002;22:643–5
12 . Katayama K et al Adult case of accessory cardiac bronchus
presenting with bloody sputum. Jpn J Thorac Cardiovasc
Surg. 2005;53:641–4
13 . Chung MJ et al Bronchial and non-bronchial systemic
arteries in patients with hemoptysis: Depiction on MDCT
angiography. AJR Am J Roentgenol 2006;186:649–55
14 . Bruzzi JF et al Multi-detector row CT of hemoptysis.
RadioGraphics. 2006;26:3–22
15 . Frazier AA et al Pulmonary angiitis and granulomatosis:
Radiologic-pathologic correlation. RadioGraphics. 1998;18:
687–710
16 . Do KH et al Systemic arterial supply to the lung in adults:
Spiral CT fi ndings. RadioGraphics. 2001;21:387–402
17 . Bolca N et al Bronchopulmonary sequestration: Radiological
fi ndings. Eur J Radiol. 2004;52:185–91
Chapter 4
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Cardiology
CONTENTS
4.1 Acute Chest Pain 154
4.2 Diseases of the Great Vessels 163
4.3 Myocardial Diseases (Cardiomyopathies) 168
4.4 Endocarditis 173
4.5 Pericardial Diseases 178
J. A. Al-Tubaikh: Internal Medicine – An Illustrated Radiological Guide
DOI: 10.1007/978-3-642-03709-2_4, © Springer-Verlag Berlin Heidelberg 2010
153
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4.1
4.1
Acute Chest Pain
Acute chest pain is one of the most common complaints
encountered in medical emergency departments. Chest
pain is divided into cardiac and noncardiac chest pain.
Causes of cardiac chest pain include angina pectoris
(stable and unstable), myocardial infarction (MI)
(ST-segment elevation and non-ST-segment elevation),
myocarditis, etc. Noncardiac chest pain includes diseases of the great vessels, esophagitis, pneumonia, etc.
This topic discusses the use of radiology in detecting
acute chest pain and how the radiologist can contribute
in assessing causes of acute chest pain in emergency
departments.
Acute Coronary Syndrome
Acute coronary syndrome (CAS) is a term used to
describe symptoms and manifestations of myocardial
ischemia induced by coronary artery disease.
The most important components of CAS are angina
pectoris and its severe complication MI. Angina pecto-
ris is a term used to describe transient myocardial ischemia in the absence of myocardial cell death. In
contrast, MI is a term used to describe myocardial cell
death and necrosis due to ischemia.
Patients with angina pectoris classically present
with retrosternal chest pain, which radiates to the neck
and the left shoulder, accompanied by a sensation of
numbness in the fi ngers. Associated symptoms include
tachycardia, dyspnea, and possibly arrhythmia. The
chest pain in angina pectoris typically lasts <10 min in
duration. Patients with MI classically present with the
symptoms of angina pectoris in a severe fashion. The
retrosternal chest pain is severe and associated with
autonomic nervous system hyperactivity, causing profound sweating and at times loss of consciousness. The
chest pain typically may last up to 30 min in duration.
MI can be transmural involving the whole thickness
of the myocardial wall due to complete occlusion of
the coronary artery. MI can also be subendocardial,
which is classically seen in coronary arterial spasm
and hypertension due to hypoperfusion. The vascular
supply of the endocardium is the part of the heart wall
that is most sensitive to hypoperfusion.
Cardiac CT is used in patients with acute chest pain
to rule out three main conditions (triple rule-out): acute
MI, pulmonary embolism (PE), and aortic dissection.
Cardiac CT can also be used to detect calcium plaques
within the coronary arteries in a technique known as
“calcium scoring.”
Calcium scoring is a method that quantifi es the atherosclerotic plaques within the coronary vessels. The
calcium score is used to assess the risk of heart events,
not to detect coronary stenosis. The basic idea of calcium scoring is to perform a noncontrast CT of the
heart to detect calcifi ed plaques (Fig. 4.1.1 ). Once a cal-
cifi ed plaque is identifi ed in the coronary arteries, the
examiner encircles the plaque by a cursor and a special
program will measure the plaque attenuation and
express it as a number in Hounsfi eld units as a score
(Agatston score). Each coronary branch is measured
separately, and then the numbers added to give a total
calcium burden score. The score predicts the probability of heart attacks in the next 5–10 years on the current
status of the patient without treatment modifi cations.
Uncalcifi ed atherosclerotic plaques take up to 15 years
before they are calcifi ed and visualized in a calcium scoring study or noncontrast CT study. The uncalcifi ed (vulnerable) plaque appears inhomogeneous or with low
density on CT scan (25 ± 15 HU). Uncalcifi ed and
Fig. 4.1.1 Axial non-enhanced cardiac CT examination for calcium scoring shows calcifi ed plaque in the right coronary artery
4.1 Acute Chest Pain 155
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partially calcifi ed plaques are more associated with ACS
than are calcifi ed plaques, because they are unstable and
can be dislodged, initiating a coronary embolic attack.
Cardiac MRI in CAS patients is mainly used to
study myocardial wall motion ( myocardial function
study ), perfusion (same as the thallium perfusion study ),
viability, and ejection fraction measurement like cardiac Doppler study ( phase-contrast fl ow quantifi ca-
tion ). The role of cardiac MRI postinfarction is to
identify viable (salvageable) myocardium, which is
mainly detected by the ( myocardial viability study ).
The basic concept of the myocardial viability study
is to detect how much viable (alive and contractile)
myocardium is left after MI. The technique depends
upon the fact that gadolinium diffuses into the myocardial interstitial spaces after its injection into the body.
As long as the myocardial membrane (sarcolemma) is
intact, the gadolinium is pumped out of the intracellular
compartment and concentrated in the extracellular
compartment until it is washed out 10 min after its
injection. This scenario occurs with normal and viable
myocardium. If the myocardium is diseased or infarcted,
the gadolinium will diffuse inside the extra- and intracellular compartments, which makes its clearance take
longer time than 10 min. Myocardial contrast enhancement that exceeds 10 min from gadolinium injection is
called “late gadolinium enhancement,” which is considered pathological and the test is considered positive
for nonviable myocardium.
Loss of cardiac wall motion, which is assessed in the
myocardial function study, is another important sign of
nonviable myocardium. However, there are two situations where the myocardium is viable but is not contracting: myocardial stunning and hibernating myocardium.
Myocardial stunning is a situation where the cardiac
muscles are viable but they do not contract as a transient
phenomenon after MI (like penumbra after stroke).
Hibernating myocardium is a situation where the car-
diac muscles are viable but are not contracting after
reestablishing coronary perfusion due to a long period of
chronic perfusion abnormalities. This situation is typically seen in patients with long-standing, compromised
coronary perfusion who have undergone coronary artery
bypass surgery (CABG). Although the perfusion is normally established after a long period of hypoperfusion,
the muscles are not contracting due to a long period of
cardiac muscle ischemia and hypofunction.
Signs on Chest Radiographs
Indirect signs of CAS include aortic calcifi cation of aorta or
coronary arteries calcifi cation.
If the MI is complicated by heart failure, signs of pulmonary
edema may be detected such as upper lobe vessel cephalization and enlarged cardiac silhouette (Fig. 4.1.2 ).
Signs on Cardiac CT
In a patient with acute chest pain, detection of calcifi ed
plaques on the nonenhanced coronary vessels with absence of
signs of aortic dissection or embolism confi rms the diagnosis
of CAS. However, absence of the coronary calcifi ed plaques
does not rule out CAS because uncalcifi ed plaques can be
present. Up to 50% of patients with sudden cardiac arrests
show calcifi ed lesions in their coronary arteries (Fig. 4.1.1 ).
MI may be seen as a subendocardial ventricular hypodense
area depending upon the blocked coronary artery and its
vascular territory.
Post myocardial infarction calcifi cation and ventricular
dilatation may occur (Fig. 4.1.3 ).
Fig. 4.1.2 Anteroposterior chest radiograph of a bedridden
patient with myocardial infarction (MI) shows congested hilar
vessels and beginning of pulmonary edema
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Fig. 4.1.3 Posteroanterior
chest radiograph ( a ) and
thorax CT ( b ) shows
focal apical left ventricular dilatation with
calcifi ed rim due to old
4.1
MI of this region
( arrowheads )
Signs of MI on MRI
Wall motion abnormalities (akinesia or hypokinesia) on
Cine-MRI.
Contrast enhancement on delayed images (>10 min). There
are four patterns of late contrast enhancement of MI: First
pattern is subendocardial enhancement with sparing of the
subepicardial region (Fig. 4.1.4a ). Second pattern is full
thickness myocardial wall enhancement (Fig. 4.1.4b ). Third
pattern is full thickness myocardial wall enhancement, with
subendocardial hypointense area, representing a severe
edema compressing the intramural vessels (Fig. 4.1.4c ).
Fourth pattern is seen as a dark hypointense area that
represents the infracted area surrounded by a rim enhancement (Fig. 4.1.4d ). The fourth pattern is seen in extensive MI
with less viable myocardium.
Stunned and hibernating myocardium is visualized as wall
motion abnormalities (akinesia or hypokinesia) in Cine-MRI
with no contrast enhancement on delayed images (>10 min).
Why does atherosclerosis not develop in the veins
and is only seen in the arteries, although the cholesterol circulates in the blood in both veins and
arteries?
This occurs because the arterial pulsation assists in
the deposition of the cholesterol molecules within the
intima. Normally, the pulmonary arteries do not pulsate, but when pulmonary hypertension develops, the
high pressure blood within the arteries evokes the
arterial wall to pulsate, resulting in developing atherosclerosis within the pulmonary arteries.
Acute Pulmonary Embolism
Acute pulmonary embolism (PE) is an emergency
situation characterized by closure of a pulmonary
artery by an embolus causing pulmonary ventilationperfusion mismatch, or in a worse scenario, pulmonary infarction.
The bronchial circulation only supplies nutrients
and does not participate in gas exchange in normal
situations. However, in PE, the bronchial circulation
responds with enlargement and hypertrophy, and participates in blood oxygenation due to decreased pulmonary fl ow and ischemia.
PE is categorized according to severity into two
main types: acute sub-massive and acute massive PE.
Acute sub-massive PE is characterized by <50% occlusion of the pulmonary vascular bed, whereas acute
massive PE is characterized by >50% occlusion of the
pulmonary vascular bed.
Patients with acute PE often describe acute sudden
chest “gunshot-like” pain with progressive dyspnea,
tachycardia, and cyanosis. Many patients have a history of deep venous thrombosis (DVT), varicose veins,
immobilization, or recent pelvic surgery. A dislodged
part of the initial thrombus, mostly from the lower
limbs, travel through the venous circulation until it
blocks an arterial pulmonary vessel in the chest as an
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Fig. 4.1.4 Short-axis
dark-blood T1W
postcontrast cardiac MR
illustrations show
different pattern of
myocardial enhancement
after MI: ( a ) subendocar-
dial enhancement
with sparing of the
subepicardial region,
( b ) full-thickness
myocardial wall
enhancement,
( c ) full-thickness
myocardial wall
enhancement, with
subendocardial hypointense area, and ( d ) dark
hypointense area
represents the infarction
surrounded by a rim
enhancement
embolus, causing pulmonary vascular congestion. If
this congestion persists, pulmonary infarction occurs.
In small percentage of patients, the unresolved
thrombus after treatment can be incorporated into the
vessel wall and covered by a layer of epithelium. This
thrombus organization causes intravascular stenosis of
the affected lumen, resulting in the development of
pulmonary hypertension and cor pulmonale.
Acute PE is best diagnosed by V/Q scan (ventilation/perfusion nuclear scan study) in circulatory stabilized patient. The scan typically shows pulmonary
ventilation-perfusion mismatch. In unstable acute PE
patients, CT pulmonary angiography is the initial
examination of choice.
Signs on Chest Radiograph
Radiographs are normal in 12% of cases.
Pulmonary infarction can appear as a patchy radio-opaque shadow
on chest radiograph, which cannot be diff erentiated from patchy
pneumonia or pulmonary contusions. Therefore, the radiographic
signs have to be correlated with the history and the clinical data.
Hampton’s Hump : is a wedge-shaped radio-opaque patch that is
round-shaped, located at the lung periphery, and directed from
peripheral toward the hilum (Fig. 4.1.5 ). This patch represents
wedge-shaped infarction of the peripheral lung parenchyma.
PE can be accompanied by Hemorrhagic pleural eff usion.
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Fig. 4.1.5 Posteroanterior
chest radiograph ( a ) and
chest HRCT in two
different patients with
pulmonary infarction
show Hampton’s hump in
4.1
( a ) ( arrowhead ), and basal
area of pulmonary
parenchymal consolidation
due to infarction in ( b )
Fig. 4.1.6 Sagittal, Doppler sonography ( a ) and Duplex ( b ) images of a patient with DVT show hypoechoic material within the
external iliac vein with free labile edge
Signs on Doppler Sonography
Doppler sonography should be performed for patients with PE
or patients with high risk of DVT who show signs of
respiratory distress (e.g., bedridden patients).
DVT is diagnosed on Doppler sonography when an intrave-
nous echogenic material is detected (e.g., thrombus), the vein
is distended and noncompressible (most specifi c and
diagnostic sign), and there is loss of color duplex signal within
the vein. The thrombus should be followed by the probe to
detect its free edge, and an observation of labile, freelymoving edge on real-time sonography should be reported. A
labile, free edge thrombus has a high risk of embolization
(Fig. 4.1.6 ).
Signs on CTA
PE is detected as complete fi lling defect with failure to
enhance the entire lumen (complete thrombosis). The
thrombosed vessel may be enlarged, and the thrombus may
appear hyperdense on non contrast-enhanced images.
Partial fi lling defect of a pulmonary vessel surrounded by
areas of contrast material enhancement (Fig. 4.1.7 ) may be
seen.
Pulmonary infarction is visualized as a wedge-shaped area of
lung parenchyma with high density located in the periphery
of the lung, with the base lying along the pleura (Fig. 4.1.5 ).
Areas of lobar atelectasis in PE may show contrast
enhancement.
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Fig. 4.1.7 Axial
pulmonary CTA of two
different patients with
pulmonary embolism
(PE) shows saddle
thrombus in ( a ) ( arrow-
head ), and distal complete
thrombosis of the right
pulmonary artery with
partial thrombosis of the
distal part of the left
pulmonary artery
( arrows )
Chronic PE is visualized as a peripheral intra-arterial wall
fi lling defect. Calcifi cation of the organized thrombus may be
seen.
Saddle thrombus : is a term used to describe a big thrombus
that abuts over the bifurcation of the main pulmonary arteries
(Fig. 4.1.7 ).
Signs of right ventricular enlargement might be seen in CT
with displacement of the ventricular septum toward the left
ventricle, as a sign pulmonary hypertension.
Areas of mosaic lung parenchyma pattern with pruning of the
pulmonary vessels may be seen (Fig. 4.1.8 ).
Aortic Dissection
The term “ acute aortic syndrome ” is applied to multiple
acute chest pain presentations that are caused by thoracic
aortic diseases, including aortic dissection, aortic intramural hematoma (IMH), and penetrating atherosclerotic ulcer.
Aortic dissection is a condition characterized by
separation of the aortic intima with presence of blood
in a false lumen between the intima and the medial layers of the aortic wall.
The intima is the innermost layer of the aortic wall.
Aortic wall intimal tear starts typically at sites of highest intramural pressure and wall tension. After intimal
tear, the blood fl ow inside the tear dissects its way
between the intima and the media layer, creating a false
lumen. The structure between the true and the false
lumen is called “intimal fl ap,” which is the key diagnosis of aortic dissection on radiological examinations.
Fig. 4.1.8 Axial chest HRCT lung-window illustration shows
mosaic pulmonary parenchymal pattern ( arrowheads ) and prun-
ing of the pulmonary arteries ( yellow circle )
The most common predisposing factors of aortic
dissection are systemic hypertension, bicuspid aortic
valve, aortic coarctation, and Marfan’s syndrome.
Patients typically present with sudden acute chest pain
that is described as “tearing” sensation, and classically
radiation to the back.
Aortic Dissection Is Classifi ed According
to the Stanford and Debakey Classifi cations
Stanford Classifi cation
Type A : this type involves the ascending aorta, and it is
managed surgically. This type carries the risk of spontaneous rupture into the pericardium resulting in pericardial tamponade, or it can continue dissection to
involve the coronary arteries (right coronary more than
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4.1
the left). Patients with this type can also develop aortic
regurgitation (50% of cases).
Type B : this type involves the descending aorta only.
The site of dissection is typically just distal to the subclavian artery, near the insertion of the ligamentum
arteriosum. When the dissection involves both the
descending and the ascending aorta, it is classifi ed as
type A. This type is managed medically; however, in
the current era, even type B is managed with endovascular stent across the origin of the dissection.
Debakey Classifi cation
Type I : involves ascending aorta only
Type II : involves the ascending and the descending
aorta.
Type III : involves the descending aorta only.
Diff erential Diagnoses and Related Diseases
Vascular Ehlers-Danlos syndrome is a disease charac-
terized by joint hypermobility, skin abnormalities (e.g.,
easy bruising), fragility of intestinal and genitourinary
organs, and vascular fragility leading to dissection or
rupture of medium to large muscular arteries. The disease has an autosomal dominant mode of inheritance,
and caused by mutation in collagen type 3 gene
(COL3A1). The dissection arises in vascular EhlersDanlos syndrome that occurs typically without preceding aneurysm.
Signs on Radiographs
There is mediastinal widening with obliteration of the aortic
knuckle on plain radiographs.
Signs on CTA
The key diagnostic fi nding in aortic dissection is identifi cation
of the intimal fl ap, which appears as a thin “line” of soft tissue
within the aortic lumen separating the false lumen from the
true lumen (Fig 4.1.9 ).
The true lumen shows higher enhancement than the false
lumen, because fi lling of the false lumen is slower than the
true lumen. Moreover, the false lumen may show signs of
intravascular thrombosis.
In the ascending aorta, the false lumen is typically the more
anterior lumen, while in the descending aorta, it is typically
the more posterior lumen.
Coronary artery dissection can be suspected when the intimal
fl ap is detected at or near the site of a coronary ostium. When
this sign is identifi ed, coronary CTA should be performed to
detect the extension of the dissection.
Pericardial hemorrhagic eff usion may be detected as highly
attenuated fl uid within the pericardial space (40–50 HU).
Fig. 4.1.9 Axial cardiac
CTA of two different
patients with aortic
dissection Stanford type
A ( a ) and Stanford type B
( b ) shows the classic
intimal fl ap ( arrowheads )
separating the true from
the false lumen
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