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Radiología. 2010;52(6):500-512
ISSN: 0033-8338
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UPDATE
Pulmonary hypertension: The contribution of MDCT
to the diagnosis of its different types
M.A. Sánchez Nistal
Servicio de Radiodiagnóstico, Hospital Universitario 12 de Octubre, Madrid, Spain
Received 16 February 2010; accepted 29 May 2010
KEYWORDS
Pulmonary
hypertension;
Multidetector CT;
Magnetic resonance
imaging;
Ultrasonography;
Hemodynamic study;
Ventilation-perfusion
scintigraphy
Abstract
Pulmonary hypertension is characterized by progressive involvement of the pulmonary vessels
that leads to increased vascular resistance and consequently to right ventricular failure. Vascular
lesions are a common factor in a wide spectrum of diseases, and their result, pulmonary
hypertension, is a severe clinical condition with a poor prognosis that worsens the normal course
of the diseases to which it is associated (COPD, collagen disease, sarcoidosis, and congenital or
acquired heart disease).
It is important for pulmonary hypertension to be diagnosed as early as possible because
nowadays drugs can reduce mortality and improve the quality of life; furthermore, some types
of pulmonary hypertension (e.g., chronic thromboembolism and those associated with some
congenital heart diseases like left-to-right shunt) can be treated surgically.
In cases of suspected pulmonary hypertension, imaging methods can confirm the diagnosis,
suggest a cause, help choose the most appropriate treatment, and monitor the response to
treatment. This review describes the approach to pulmonary hypertension using different
imaging techniques; special emphasis is given to the role of multidetector CT (MDCT), which
makes it possible to study all the organs in the thorax in a single acquisition.
We review the radiological signs of pulmonary hypertension and the current (Dana Point)
radiological criteria for classifying the type of hypertension based on alterations in the lung
parenchyma, mediastinum, pleural spaces, and pericardium, as well as on the study of the
chambers of the heart.
© 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.
E-mail: [email protected]
0033-8338/$ - see front matter © 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.
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Pulmonary hypertension: The contribution of MDCT to the diagnosis of its different types
PALABRAS CLAVE
Hipertensión
pulmonar;
TC multidetector;
Resonancia
magnética;
Ecocardiografía;
Estudio
hemodinámico;
Gammagrafía de
ventilación-perfusión
501
Hipertensión pulmonar: aportación de la TCMD al diagnóstico de sus distintos tipos
Resumen
La hipertensión pulmonar (HP) es una enfermedad caracterizada por la progresiva afectación de
los vasos pulmonares, lo que produce aumento de las resistencias vasculares y, como
consecuencia, fallo ventricular derecho. La lesión vascular es el factor común a un amplio
abanico de patologías y su resultado, la HP, un cuadro clínico grave de mal pronóstico, que
agrava el curso normal de las enfermedades a las que se asocia (EPOC, colagenosis, sarcoidosis,
cardiopatías congénitas o adquiridas…).
El interés por diagnosticarla lo más precozmente posible se debe a que, actualmente, se dispone
de fármacos que mejoran la calidad de vida y han disminuido la mortalidad de estos pacientes y
que existen posibilidades quirúrgicas para algunos tipos de hipertensión como la tromboembólica
crónica o la asociada a algunas cardiopatías congénitas con cortocircuitos izquierda-derecha.
Ante una sospecha clínica de HP los métodos de imagen son los que confirman el diagnóstico,
sugieren una causa, ayudan a seleccionar el tratamiento más adecuado y monitorizan la
respuesta. En la actual revisión del tema se presenta la aportación de los diferentes métodos de
imagen para el diagnóstico de la enfermedad, haciendo especial hincapié en la TC multidetector
(TCMD), que ofrece la posibilidad de estudiar con una sola adquisición todos los órganos
torácicos.
Se revisan los signos radiológicos de HP y se establecen los criterios radiológicos actuales para
etiquetar el tipo de hipertensión, según la clasificación de Dana Point, basados en el estudio de
las alteraciones del parénquima pulmonar, mediastino, espacios pleurales y pericardio y en el
estudio de las cámaras cardíacas.
© 2010 SERAM. Publicado por Elsevier España, S.L. Todos los derechos reservados.
Introduction
Histological changes
Pulmonary hypertension (PH) is defined as a group of
diseases characterized by a progressive increase in the
pulmonary vascular resistance leading to right ventricular
(RV) failure and death. Functional capacity of the RV is the
major determinant of prognosis in PH 1,2.
Idiopathic PH is a rare condition, with an incidence of
2.5 to 3.5 cases per million population in Western countries.
It is 2 or 3 times more common in women than in men, at
any age, and peaks in the 4th, 5th and 6th decades of life. PH
associated with other conditions is more common, although
its actual incidence in those cases is unknown 3.
PH is defined as a mean pulmonary artery (PA) pressure —
assessed by right cardiac catheterization — ≥ 25 mmHg at
rest. In addition to this measurement, the combination of
different hemodynamic parameters including normal or
reduced cardiac output, normal pulmonary capillary wedge
pressure, in other words, normal left atrial pressure
(≤ 15 mmHg) and increased pulmonary vascular resistance
( ≥ 2 4 0 d y n a s / s g / c m - 5 , o r > 3 Wo o d u n i t s ) , a l l o w
differentiation between precapillary PH (clinical groups 1,
3, 4 and 5) and postcapillary PH (group 2) (table 1) 3,4.
Clinical classification is the key to identify the type of PH
and to plan the treatment. The last classification was
adopted during the 4 th Word Symposium on Pulmonary
Hypertension held in February 2008 in Dana Point (table 1).
This classification puts into groups diseases that cause or
may present with PH and that show similarities in their
clinical presentation, their pathophysiology, and in the
therapeutic options 3,5.
All the types of PH show identical pathological obstructive
changes in the pulmonary microcirculation, defined as
hypertensive pulmonary vascular disease. This similarity
suggests a pathobiological process shared by the spectrum
of PH diseases 2,6. The exact process that initiates the
pathological changes is unclear, but it is well known that the
pathobiology is multifactorial and that increased vascular
resistances, typical of this condition, are caused by
vasoconstriction, obstructive remodeling of the vascular
wall, inflammation and thrombosis 1,7.
Proliferative vascular remodeling involves all the wall
layers. The main pathological finding is abnormal and
disorganized cell proliferation causing a marked wall
thickening. Complex vascular lesions develop, including
plexiform lesions that cause obstruction of small arteries
and increased resistances.
It is unclear if the presence of microthrombi in pulmonary
arterioles is the cause or the consequence of PH; however,
there is no doubt that their presence contributes to the
progression of the disease. Microthrombi are present in 50 %
of cases of idiopathic PH 8 and are common in the
Eisenmenger syndrome 9.
Imaging techniques for the diagnosis
and assessment of the disease
In case of clinical suspicion, we should follow a diagnostic
strategy using different technical modalities aimed to
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502
M.A. Sánchez Nistal
Table 1 Updated classification of PH (Dana Point, 2008) 6
1.
2.
3.
4.
5.
6.
7.
8.
9.
Pulmonary arterial hypertension (PAH)
1.1 Idiopathic
1.2 Heritable
1.2.1 BMPR2
1.2.2 ALK-1, endoglin (with or without
hereditary hemorrhagic telangiectasia.)
1.2.3 Unknown
1.3 Drug- and toxin- induced PAH
1.4 PAH associated with:
1.4.1 Connective tissue diseases
1.4.2 HIV infection
1.4.3 Portal hypertension
1.4.4 Congenital cardiac disease
1.4.5 Schistosomiasis
1.4.6 Chronic hemolytic anemia
1.5 Persistent pulmonary hypertension of the
newborn
1’. Pulmonary venoocclusive disease and/or
pulmonary capillary hemangiomatosis
PH owing to left heart disease
2.1 Systolic dysfunction
2.2 Diastolic dysfunction
2.3 Valvular disease
PH owing to lung diseases and/or hypoxia
3.1 Chronic obstructive pulmonary disease
3.2 Interstitial pulmonary disease
3.3 Other pulmonary diseases with mixed restrictive
and obstructive pattern
3.4 Sleep-Disordered breathing
3.5 Alveolar hypoventilation disorder
3.6 Chronic exposure to high altitude
3.7 Developmental abnormalities
Chronic thromboembolic PH
PH with unclear or multifactorial etiologies
Hematologic disorders: myeloproliferative disorders,
splenectomy
Systemic disorders: sarcoidosis, pulmonary
Langerhans cell histiocytosis,
lymphangioleiomyomatosis, neurofibromatosis,
vasculitis
Metabolic disorders: glycogen storage disease,
Gaucher disease, thyroid diseases
Others: tumor obstruction, mediastinal fibrosis,
chronic renal insufficiency on hemodialysis
ALK-1: kinase 1 similar to activin receptor; BMPR2: Bone
morphogenetic protein receptor type II; HIV: Human
immunodeficiency virus.
confirm the diagnosis, identify the type of PH according to
the Dana Point classification in order to finally perform a
functional and therapeutic evaluation of the disease 3,6.
screening of risk groups: first degree relatives, collagenosis
(particularly scleroderma and CREST), congenital heart
diseases and HIV infection. In portal hypertension,
assessment prior to liver transplantation is essential as
transplantation is contraindicated in case of PH in chronic
liver disease 2.
The aims of echocardiography in PH are:
• Detection of elevated pulmonary pressure.
• Assessment of the RV function.
• Making a differential diagnosis, since the size of the heart
chambers, valvular function, thickness and functioning of
heart chambers may be assessed. This imaging modality
also allows the study of intracardiac shunts and, with
transesophageal echocardiography, the presence of ductus
or other extracardiac shunts.
Therefore, echocardiography allows the etiological study
of PH in case of congenital and left heart disease2,6, provides
valuable information on the severity and prognosis of PH
and therapeutic outcome monitoring 4,11.
There are several methods for estimating the PA
pressure using echocardiography and, in general, there is
a good correlation with the pulmonary pressure measured
by contrast-enhanced Doppler (in 10 % of cases it cannot
be measured); however, there is no exact correlation with
the values obtained by right cardiac catheterization,
as echocardiography tends to overestimate the
pressures 2,3,4,6.
Hemodynamic study
This is the only method that may establish a definitive
diagnosis of PH, as it measures the PA pressure directly;
for this reason, it is the gold standard in the diagnosis
of the disease and is essential prior to any specific
treatment 3,4,11,12.
The hemodynamic study has three main goals:
• To determine RV and PA hemodynamics, directly measuring
the PA pressure, the pulmonary capillary wedge pressure
and the pulmonary resistance. To measure the cardiac
output and to determine oxygen saturation in the heart
chambers.
• To assess the vasodilatory response to the therapeutic
agents (nitric oxide, epoprostenol).
• To rule out a left-right shunt as well as any significant left
lesion, and to assess the coronary ostium 12.
In case of suspicion of chronic pulmonary thromboembolism
(CPTE), pulmonary arteriography helps determine the
location, extension and size of the thrombus and select
candidates for thromboendarterectomy.
Pulmonary ventilation/perfusion scintigraphy
Echocardiography
Echocardiography is the first diagnostic modality that should
be used in case of suspicion of PH and, at a later stage, to
assess the response to the treatment. It is also used in the
For many years this was the main technique for diagnosis of
acute pulmonary emboli, but now it is frequently used in
the screening for chronic thromboembolic PH (CTEPH), after
anticoagulant therapy, after an acute episode of pulmonary
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Pulmonary hypertension: The contribution of MDCT to the diagnosis of its different types
thromboembolism, to determine the degree of pulmonary
perfusion and to rescue those cases that might progress to
CTEPH 6,16.
A normal ventilation/perfusion scan (V/Q) practically
rules out CTEPH. In contrast, CTEPH is the most likely
diagnosis if the V/Q scan shows multiple bilateral perfusion
defects, segmental or larger, with normal ventilation;
however this finding is not specific of CTEPH and may
occasionally appear in other types of PH such as
venoocclusive disease, or other conditions including
sarcoma or vasculitis of the PA or fibrosing mediastinitis 13,14.
In cases of PH associated with congenital heart disease or
idiopathic PH, perfusion is normal or minimal defects
appear 14,15.
Magnetic resonance (MR)
MR has the advantage of being a morphological and
functional method; for this reason, some authors propose
MR as the gold standard for the assessment of the RV in
PH 2.
Contrast enhanced MR allows visualization of mediastinal
and pulmonary vessels and a functional study of the heart
c h a m b e r s 4,11,15. P l a n i m e t r y u s i n g c i n e M R a l l o w s
measurement of end-systolic and end-diastolic volumes,
ejection fraction, stroke volume, muscular mass and
changes in the movement of the ventricular wall or the
interventricular septum. It may also assess systemic and
pulmonary flow in right-left or left-right shunts and shows
good correlation between the parameters of the curve of
PA blood velocity and the degree of PH and resistances 17.
MR is superior to echocardiography in the assessment of
the remodeling of the RV wall.
The main advantage is that MR involves no ionizing
radiation and makes the ideal technique for young or sick
patients requiring serial assessment. Its major disadvantage
is lower spatial resolution than computed tomography (CT)
and angiography, making difficult the assessment beyond
the segmental level and the pulmonary parenchyma. Other
drawbacks of MR, in comparison with CT, are the low
availability of MR equipments, the duration of the
examination that, along with the enclosed gantry, require
patient collaboration and might hinder the exam due to
claustrophobia 16. As MR is a non-invasive method, it may be
used repeatedly to assess disease progression and treatment
response 2,6.
503
Particularly, in the case of HPTEC, CT angiography (CTA)
provides a reliable road map of localization and extension of
thrombi, intraarterial webs and stenosis. In the assessment
of non-occlusive or calcified mural thrombi, CTA supersedes
angiography. In addition, CTA is an appropriate non invasive
method for assessing the outcome of endarterectomy or
other surgical procedures.
CT provides only a morphological study, but recently,
MDCT dynamic study with cardiac synchronization has been
proposed for the functional evaluation of the systolic and
diastolic ventricular volumes, ejection fraction and
ventricular mass 18, and even to assess the severity of PH by
measuring PA distensibility during systole and diastole and
correlating it with the mean PA pressure 19.
MDCT technique
Studies are performed on CT units with panels of 4, 8,
16 and 64 detectors. The examination always requires
breath holding, and is performed either in a craniocaudal
direction, following the entrance direction of the IV
contrast, or caudocranial direction in order to obtain an
early visualization of the distal vessels of the inferior
lobes, where subsegmental emboli are more common. This
fact is more relevant for the study of acute PE than of
HPTEC. The study should include from the supra-aortic
trunks to the drainage site of the hepatic veins into the
inferior vena cava (IVC). Collimation should be the lowest
allowed by the scanner, with ≤ 1 mm reconstructions and
50 % overlap, which enable high-resolution multiplanar
reconstructions. Radiation dose is 100–120 KV and
70-200 mAs with dose modulation and several examination
protocols have been proposed in order to minimize
radiation risks 20.
Intravenous non-ionic contrast agent is used, at
350-370 mg/cc iodine concentration and 4 cc/s injection
rate. Optimal image acquisition time is determine using
the bolus-tracking technique, placing the cursor on the
PA 21 and starting the acquisition after reaching a
150-180 HU threshold. Image analysis is carried out in
the work station with windows for the pulmonary
parenchyma (W1600/ L-600), soft tissues (W500/L 35)
and angiographic (W700/L 100). Multiplanar
r e c on s tr u c tion s ar e ob tain e d u s in g th e M aximum
Intensity Projection (MIP) and the Minimum Intensity
Projection (minIP) techniques, at different thickness,
and also using volume rendering.
Multidetector computed tomography (MDCT)
Diagnosis of PH using MPCT
MDCT allows volume acquisition. Highly reliable multiplanar
reconstructions in all planes may be acquired using < 1mm
collimation. The creation of slabs or slices of variable
thickness with selection of Maximum-Intensity-Projection
points (slab-MIP) is very helpful to: follow very small arteries
including subsegmental vessels or the bronchial or intercostal
arteries, assess the cardiac chambers, ventricular wall, and
pulmonary venous drainage and perform a high-resolution
study of the lung parenchyma. This information provides an
approach to etiological diagnosis of PH and, for this reason,
the new ESC/ERS Guidelines 6 propose a thorax CT from the
moment PH is suspected 2,4.
1. Vascular changes
• Initially, the first radiological sign assessed was the
PA diameter. Main PA diameter should be measured
in its bifurcation, at a right angle to its long axis and
just lateral to the ascending aorta. According to
Kuriyama 22 , a PA diameter ≥ 29 mm has a PPV of
0.97, 87 % sensitivity and 89 % specificity in predicting
PH; for this reason, this value has been used as
indicative of PH 8,9. However, it has been proven that
absolute measures are not completely reliable, as PA
pressure and size depend on the body mass, sex and
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504
•
•
•
•
M.A. Sánchez Nistal
age. It seems to be increased by 6 % in healthy
individuals over the age of 50 and in obese patients.
It also increases with exercising and in athletes 2.
Specificity climbs to 100 % when a PA diameter ≥ 29mm
is accompanied by a segmental artery-to-bronchus
ratio > 1:1 in most lung lobes 8,9.
It is better to compare the main PA with the adjacent
aorta (Ao) and if the PA/Ao ratio is > 1, HP is very
likely, particularly in patients below the age of 50 23
(fig. 1).
Another recent parameter is the assessment of the PA
at the level of the aortic arch (egg —PA— and banana
—Ao— signs) 9, seen in severe PH (fig. 2A).
Within the parenchymal vessels, Sheehan 10 reports the
phenomenon of “neovascularization”, which describes
serpiginous and fine peripheral vessels that frequently
emerge from the centrilobular arterioles, without
following the normal anatomy of the pulmonary
vessels. Originally, Sheehan described these findings in
idiopathic PH and in the Eisenmenger syndrome;
Figure 1 Axial image shows a wider caliber of the PA trunk
than that of the ascending aorta. PA/Ao > 1. Pulmonary
artery > 29mm.
however, they seem to be a manifestation of all-cause
severe PH 9 (fig. 2A).
• Peripheral anastomoses of systemic intercostal vessels
that supply the lung periphery 8,10 (fig. 2B).
2. Cardiac changes
• RV functional changes seem to be the main determinant
of the progression and prognosis of the disease.
Although the pulmonary vascular bed is the leading
cause of the disease, the symptoms and prognosis are
strongly related to the pump function of the RV.
Chronic pressure overload of the RV leads to changes
in the cardiac morphology and function affecting both
ventricles. Structural changes of the right chambers
include hypertrophy and RV dilatation, right atrium
(RA) enlargement and functional tricuspid
regurgitation, secondary to valvular ring dilatation.
Progressive increase in RV pressure damages the
structure and function of the left ventricle (LV), which
reduces its size and distorts 24.
• The RV/LV size ratio needs to be measured. This may
be done on axial slices, but four-chamber plane
measurements correlate better with echocardiographic
measurements. Under normal conditions, LV diameter
is wider than that of RV (fig. 3).
• Interventricular septum position: As the pressure in
the RV increases, the normal position of the septum
varies and at very high pressures septal inversion
occurs, resulting in LV dysfunction, with reduction of
its volume/minute (output), which is a very serious
condition. Septal inversion is a bad prognostic sign
(fig. 3).
• Increased RV wall thickness. Values > 4 mm 24 are
considered pathological (fig. 3).
• RA enlargement and regurgitation of contrast agent
into the IVC and hepatic veins is indicative of tricuspid
valve insufficiency with 90 % sensitivity and 100 %
Figure 2 Vascular changes (Axial and axial oblique MIP reconstructions). A) In the mediastinum, the pulmonary artery (AP) appears
at the level of the aortic arch (egg and banana sign). Discrepancy in caliber between the central and peripheral vessels. Neovessels
in the lung periphery, which originate at the center of the secondary pulmonary lobule and show a serpiginous and irregular
distribution (black arrows). B) Peripheral vessels with a corkscrew configuration. Anastomosis (arrow) between a peripheral vessel
and a systemic one (intercostal).
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Pulmonary hypertension: The contribution of MDCT to the diagnosis of its different types
505
Along with vascular changes, changes in the bronchial
diameter, such as dilatation of the bronchial lumen
adjacent to the occluded vessel, may also be seen in
CTEPH 33,34 (fig. 4).
Figure 3 Cardiac changes. Four-chamber plane measurements
of the heart chambers: RV larger than LV with thickened wall
(black dash), interventricular septal inversion (black arrow)
and small pericardial effusion (white arrow). These latter are
bad prognostic signs.
specificity. Reflux into the hepatic veins means greater
degree of PH than into the IVC 9,16,24, which can also be
observed in normal individuals when performing
examinations with high contrast injection rate 25.
• Vena cava and azygos vein dilatation is considered a
marker of left-sided hypertension. In addition to this,
Isaacs proposes the assessment of coronary sinus
distension that is easily identifiable on almost all CT
studies. Dilatation > 11mm is associated with increased
PA pressures, confirmed by catheterism 26.
• Pericardial thickening or effusion. It is more common
and earlier visualized in the anterior or aortopulmonary
recess, where it appears in the shape of a “bikini
bottom”. It may be considered an indirect sign of PH,
particularly if associated with increased PA diameter.
It is not necessarily associated with pleural effusion 9,27.
It is also a sign of RV dysfunction and of bad prognosis
(figs. 2, 3 and 5).
Pulmonary nodules
• In some cases, CT demonstrates small or medium size
diffuse nodules without zonal predominance and in varying
number. Nodules typically show a centrilobular distribution
and the histological analysis demonstrates their proximity
to the arteriole/bronchiole. Nodule etiology is diverse:
cholesterol granulomas, accumulation of plexiform lesions
or anastomoses between systemic and pulmonary vessels.
Differential diagnosis with sarcoidosis, hypersensitivity
pneumonitis, bronchiolitis or chronic aspiration caused by
gastroesophageal reflux is also required 28,29.
• Nodules with ground-glass density accompanied by
thickened septa in some slices may be suggestive of
venoocclusive disease or capillary hemangiomatosis.
Mediastinal adenopathies (uncommon in idiopathic PH)
have 100 % specificity in the diagnosis of venoocclusive
disease, as long as CTEPH and congestive cardiac
insufficiency could be ruled out 30 . The presence of
two or three of these signs (nodules, septa and
adenopathies) increases the diagnostic specificity
(fig. 5A and B). These radiological data should be
assessed in conjunction with the clinical data: patients
with venoocclusive disease show lower O 2 saturation,
greater desaturation during the 6-minute walk test,
changes in CO diffusion and hemorrhagic rests in the
bronchoalveolar lavage.
Venoocclusive disease and capillary hemangiomatosis
rarely cause HP. They are included into group 1’ in the
new clinical classification 5 (table 1). Since they were first
described, there are doubts on whether they are two
separate diseases or manifestations of the same
condition 30-32. They are clinically indistinguishable from
Contribution of MDCT to the etiological diagnosis
of PH
In addition to suggest the diagnosis, based on the signs
already discussed, MDCT is the most complete tool for the
differential diagnosis of PH groups, according to the
classification of Dana Point 2008 (table 1).
By carefully assessing the thoracic organs (lung
parenchyma, mediastinum and heart chambers), we can
not only differentiate between types of PH, but also
assess their complications or postsurgical outcomes
(thromboendarterectomy and shunt correction).
Parenchymal lung changes
Asymmetry of the vascular diameter
It is typical of CTEPH and does not appear in other types
of PH. The marked regional variation in the size of
segmental vessels helps differentiate CTEPH with the
rest of causes of PH presenting a more diffuse pattern 3.
Figure 4 Asymmetry in the caliber of vessels in the different
pulmonary lobes. Mosaic pattern image with areas of high
attenuation in LIL containing larger caliber vessels. Note the
subsegmental bronchial dilatations in the LSL with low
attenuation (arrows). Mosaic pattern image cannot be used for
differential diagnosis of PH types. Additional presence of
vessels with different caliber and changes in the airway suggest
CTEPH.
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506
M.A. Sánchez Nistal
Figure 5 Parenchymal nodules. A) Ground-glass millimetric nodules with centrilobular distribution (broken arrows), thickened
interlobular septa (black arrow) and small pericardial effusion (thick arrow). B) Thickened interlobular septa, mediastinal
adenopathy (broken arrow), right pleural effusion and pericardial effusion at the anterior superior recess (arrow). Figures A and B
show the radiological signs of venoocclusive PH. C) Coronal oblique MIP reconstruction shows an arteriovenous fistula in a patient
with PH: Rendu-Osler disease.
idiopathic PH, at least initially. Histologically, there is
involvement of septal venules. The diseases have a very
poor prognosis and are characterized by rapid clinical
deterioration despite vasodilator therapy; for this reason,
patients are placed on the waiting list for lung or
heart-lung transplantation early. One of the reasons why
the new Guides for clinical practice recommend a CT prior
to the treatment is to rule out this type of PH. This
condition is described as associated with an ever-growing
number of diseases: collagenosis, Hashimoto’s thyroiditis,
sarcoidosis, bone marrow transplantation, HIV infection,
chemo- and radio-therapy and myeloproliferative
diseases.
• Subpleural nodules and parenchymal bands suggest
infarctions in different stages and are significantly more
common in CTEPH 33,34.
• Arteriovenous fistulas show a characteristic morphology,
with an afferent nutrient and an efferent drainage vessel,
and suggest Rendu-Osler-Weber disease and the feasibility
of percutaneous embolization as part of its treatment
(fig. 5C).
Mosaic pattern
Mosaic pattern, seen in all types of PH, is a finding suggestive
of small vessel changes or regional variation in perfusion. It
was first described in CTEPH, but appears frequently in
idiopathic PH and Eisenmenger syndrome. Despite being
more common in CTEPH, mosaic pattern is not useful in the
differential diagnosis with other types of PH. In CTEPH, the
areas of high attenuation contain larger caliber vessels
(fig. 4).
Diffuse parenchymal disease
High-resolution slices obtained for the study of PH show
parenchymal changes secondary to usual interstitial
pneumonia (UIP) or collagenosis, (Group 1.4.1) (table 1),
which are the second more common cause of PH, after
idiopathic PH 3. Clinically, they have worse overall prognosis
and detecting signs of PH has therapeutic implications if
lung transplantation is being considered as part of the
treatment. In these cases, PH is not caused by destruction
of the vascular bed, but to plexiform lesions. There is no
correlation between PA diameter and mean pressure in the
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Pulmonary hypertension: The contribution of MDCT to the diagnosis of its different types
507
PA, and the artery/segmental bronchus ratio is difficult to
assess due to presence of traction bronchiectasis.
Assessment of the PA/Ao ratio is recommended 9,35, which is
easily identified in serial studies of diffuse pulmonary
disease, and may become our radiological contribution to
PH screening.
This assessment is also recommended for patients with
COPD, sarcoidosis or histiocytosis X eligible for lung
transplantation or in CT follow-up, since the presence of PH
in all these cases worsens the prognosis significantly and
may be a contraindication to lung transplantation 36.
Mediastinal changes
Adenopathies
Adenopathies may be seen in CTEPH and in venoocclusive
disease but are rare in idiopathic PH. They should be
assessed in conjunction with the rest of the findings in order
to determine a diagnosis between the former two diseases 30,31
(fig. 5B).
Hypertrophy of systemic arteries
The bronchial arteries arise from the thoracic aorta. Their
diameter at origin may reach up to 1.4 mm and they form
anastomoses with the pulmonary arterial tree through
multiple microvascular connections. These anastomoses
occur not only through the major bronchi, but also beyond
the pulmonary lobe, on the alveolar walls. Bronchial
circulation responds to the reduced pulmonary flow with an
increase, hypertrophy and proliferation of vessels along
this tangle of anastomotic channels 10,37. Hypertrophy may
be seen in idiopathic PH, although this finding is more
common in CTEPH. Enlargement may be found in other
systemic arteries in addition to the bronchial systemic
arteries, including the pulmonary ligament, pleural,
intercostal, subclavian branches, axillary and phrenic
arteries, and this finding is almost exclusive of CTEPH 37
(fig. 6).
Vascular changes
Changes in the wall and caliber of vessels
• Idiopathic PH involves the entire arterial tree, increasing
the central arterial caliber and causing a progressive and
fast change in the peripheral arterial caliber that may
show a corkscrew configuration (fig. 2A and B). The
number of arterial branches is reduced, but the arterial
walls are smooth (fig. 7).
• In CTEPH, the arterial wall morphology is completely
diverse. Chronic thrombi seen in this condition adhere to
the vessel wall resulting in a scalloped contour when
observed on its longitudinal axis, or forming an obtuse
angle with the arterial walls when observed on its
transversal axis. Incomplete recanalization of thrombi
results in images of intraarterial webs and, distal to
them, post-stenotic dilatations. Thrombi that do not
reabsorb or recanalize result in a complete stenosis of
the branches with a cul-de-sac image. Eventually, the
arterial tree shows arteries with multiple calibre
changes, typical of this type of PH. CTEPH is generally
bilateral affecting both the main and lobar and segmental
branches. Diagnosis of CTEPH allow us to assess the
Figure 6 Systemic circulation towards the pulmonary
parenchyma. Coronal MIP reconstruction. Hypertrophy of the
right bronchial artery and right vertebro-costal trunk (with
origin in the thoracic aorta) (red arrows) in an almost complete
obstruction of the right PA. Note the lack of contrast in the
right inferior pulmonary vein (white arrow). Wall calcification
of the left PA, a sign of severe PH.
Figure 7 Vessel morphology in idiopathic PH. The typical
aspect of the intrapulmonary vessels in idiopathic PH or in PH
associated with congenital heart diseases is vessels with smooth
walls and rapid tapering, and poor branches.
feasibility of thromboendarterectomy in these
patients 33,34,38-40 (fig. 8A and B).
In case of arterial obstruction, the main role of CT is to
rule out other causes of scintigraphic abnormalities similar
to CTEPH, including venoocclusive disease, PA sarcoma,
large-vessel vasculitis, extrinsic compression by a
mediastinal carcinoma, lymphadenopathy, mediastinal
fibrosis or pulmonary venous thrombosis 38 (fig. 9A–C).
Complications of PH
As with systemic pulmonary arterial hypertension, the
complications of PH are arterial wall calcification, thrombus
formation, aneurysms and dissection.
• In long-standing PH, early atherosclerosis of the muscular
and elastic central arteries is not an unusual finding 8
(figs. 6 and 11).
• An uncommon complication of chronic PH are aneurysms
in the main branches of the PA (diameter > 4 cm) 8. Most of
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508
these aneurysms occur in the presence of other risk
co-factors, such as congenital heart disease or vasculitis,
and patients presenting PH only are rare 41 . Central
aneurysms (trunk and two main branches) may cause
Figure 8 Vessel morphology in CTEPH. A) Mural thrombus with
a scalloped outline from a longitudinal view (right PA) and a
crescent image with obtuse angles from an axial view in the
branch of the LIL (Reproduced with permission Ref. 34 ).
B) Coronal MIP reconstruction shows thrombi recanalization
with intraarterial webs (dotted arrows), post-stenotic
dilatations (asterisk), cul-de-sac vascular obstructions (thick
arrows) and longitudinal stenosis (arrowhead).
M.A. Sánchez Nistal
clinical symptoms due to bronchial compression (fig. 10A),
angina associated with compression of the left coronary
artery by the PA trunk 42,43, PA dissection and/or rupture or
intraarterial thrombus; aneurysms in the peripheral or
intrapulmonary branches are less common. The number of
cases with central or peripheral aneurysms is increasing
due to the higher survival rates of patients with PH. The
fact that these patients have reservoir catheters placed in
has to be taken into account, since they may cause
mycotic aneurysms, which clinically manifest as
hemoptysis 44,45.
• In situ thrombi, in the course of PH, may appear in the
trunk and branches of the main artery. These thrombi
are not hemodynamically signifi cant and do not show
any signs on perfusion scintigraphy 46 . In case of a
thrombus, it is important to make the differential
diagnosis with CTEPH, based on the absence of signs of
chronic lobar or segmental thrombi, lack of parenchymal
signs such as subpleural nodules, bands or mosaic,
adenopathies or bronchial circulation. Up until now,
scintigraphy was key to the differential diagnosis 46,47,
but now, the vascular study using CT can show the
arterial morphology.
Acute or chronic thrombi may be found in 50 % of cases of
idiopathic PH (fig. 10B) and the role of thrombosis in both
idiopathic and associated PH remains controversial 47.
Figure 9 Usefulness of MDCT in the differential diagnosis of arterial obstruction. A) PA sarcoma with calcified parenchymal
metastases and pleural effusion. The tumor extends beyond the vessel limits into the mediastinum showing heterogeneous
enhancement of contrast agent and calcified areas. B) Fibrosing mediastinitis. Fibrosis involves the right pulmonary artery, superior
vena cava, mediastinal and anterior pleura and the middle lobe bronchus. C) Takayasu’s arteritis. Complete obstruction of the
arteries of both inferior lobes and post-stenotic dilatations in the superior lobes. Patent endograft in the branch of the RSL
(Reproduced with permission Ref. 34).
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Pulmonary hypertension: The contribution of MDCT to the diagnosis of its different types
January 2008
509
June 2008
Figure 10 PH complications. A) and B) PA aneurysm in a case of idiopathic PH that develops a thrombus during its progression.
A severe cough led us to perform a new study. Note the compression caused by the aneurysm on the intermediary bronchus.
(Reproduced with permission Ref. 34). C) Left PA dissection that extends into the inferior lobar branch in a patient previously
diagnosed with PH.
According to Auger and Fedullo, central thrombi may be
found in conditions other than CPTE including idiopathic
PH, Eisenmenger syndrome and COPD 38. It is unknown if
the presence of microthrombi in the pulmonary arterioles
is the cause or the consequence of PH, but there is no
doubt that their presence contributes to the progression
of the disease.
• PA dissection is a rare and fatal condition. In addition to
PH, other rare causes of dissection are chronic arterial
inflammation, right-heart endocarditis, amyloidosis,
trauma and severe atherosclerosis. Dissection seems more
frequent in PH associated with congenital heart diseases
than in idiopathic PH 48,49. CT allows determination of the
localization, size and extent of the aneurysm and of the
dissection 50 (fig. 10C). Dissection is very seldom diagnosed
in living patients and it is usually found at autopsy
studies 48 . The affected site is generally from the
pulmonary valve onward or the two main branches, and
only one publication has described dissection at a
segmental level 48.
Cardiac changes
Although patients are referred to us for a CT exam after
echocardiography, MDCT is an adequate tool for the
morphological study of the heart chambers and interatrial
and interventricular septa51,53. It is very important to include
in all our reports a systematic assessment of the size and
morphology of the heart chambers, septa, wall thickness
and the arterial and venous anastomoses.
Regarding the left chambers, enlarged atrium and
pulmonary veins or pathological LV wall may be indicative of
PH associated with left-heart disease; in some centers this
is the most common cause of PH.
Despite a negative echocargiography, the study of the
site of drainage of the pulmonary veins is essential in order
to rule out partial anomalous venous drainages, either
isolated or in conjunction with interatrial septum defects
(fig. 11A). It has to be taken into account that a sinus
venosus atrial septal defect and partial anomalous venous
drainage might be missed on transthoracic
echocardiography 53.
A PH report should include the thoracic aorta, since the
presence of ductus is not an uncommon finding that can be
easily diagnosed but that may go unnoticed in transthoracic
echocardiography (fig. 11B).
In case of complex heart diseases, CT shows the heart
anatomy and also enables joint assessment of other findings
(pulmonary, pleural or mediastinal) that may be relevant for
the surgical planning 18,52,53 (fig. 11C).
Conflict of interest
The author declares no conflict of interest.
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510
M.A. Sánchez Nistal
Figure 11 Usefulness of MDTC in the study of congenital cardiovascular malformations that present with HP. Axial, sagittal and
coronal MIP reconstructions. A) Anomalous venous drainage of the right superior pulmonary vein into to superior vena cava.
B) Aorto-pulmonary ductus in a patient previously diagnosed with idiopathic PH. C) Complex heart disease with interventricular
communication, common aorto-pulmonary trunk and left PA agenesis. Right PA calcification and left calcified pachypleuritis. This
patient presented also an extensive systemic circulation on the left side (not showed); all these data have an influence on the
surgical assessment of the patient.
Acknowledgement
I would particularly like to express my gratitude to Dr. P.
Escribano Subías and Dr. C. Jiménez López-Guarch from the
Pulmonary Hypertension Unit of the Cardiology Department
of Hospital Universitario Doce de Octubre for their
collaboration in the assessment of the cases and their
constant effort to set up and maintain a multidisciplinary
Unit, where each and every specialist feels encouraged.
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