Cardiac MRI provides high quality images of the heart and great vessels and can evaluate a wide range of cardiac diseases without exposing the patient to ionizing radiation. It has excellent soft tissue contrast and the ability to obtain multiplanar views. Rapid imaging sequences combined with ECG gating and respiratory gating help mitigate the challenges of cardiac motion. Different sequences such as T2-weighted, bright blood, and delayed enhancement are used to evaluate conditions such as myocardial infarction and viability. Cardiac MRI can assess injury extent, microvascular obstruction, hemorrhage, and predict response to therapy in acute MI. It is also useful for evaluating complications like thrombus and characterizing cardiac tumors.

1. Cardiac MRI
Dr Crystal K C
Resident
NAMS , Radiology

2. Cardiac MRI
• Cardiac MRI is indicated for evaluating a wide variety of
congenital and acquired heart diseases, including
cardiac masses, myocardial ischemia or infraction,
cardiomyopathies, valvular disease, coronary artery
disease, pericardial disease, and complex congenital
anomalies .
• The high soft-tissue contrast, availability of a large FOV,
multiplanar acquisition capability, and lack of ionizing
radiation are particularly appealing features of cardiac
MRI.
• However, the main limitation of cardiac MRI compared
with CT is the evaluation of coronary calcifications.

3. Limitations
General contraindications for cardiac MRI
• Iron particles in the globe and intracranial
aneurysm clips .
• Arrhythmia and excess device heating, most
patients with modern pacemakers and other
types of implanted cardiac devices can safely
undergo cardiac MRI.
• Valvular prostheses do not preclude cardiac MRI
but their presence can degrade image quality.

4. Challenges
• Rapid and complex motion of the heart and
pulsatility of the great vessels due to normal
contractility.
• In addition, the effects of respiratory motion
and systolic ventricular blood velocities up to
200 cm/s further complicate cardiac imaging.

5. Mitigations
• Implementation of ECG (cardiac) gating;
navigator echo respiratory gating;
• Breath-hold techniques;
• Rapid, high-performance gradients
• Improved field homogeneity
• Advanced pulse sequences.

6. Prospective gating
• ECG gating can be either prospective or retrospective.
• Prospective gating consists of initiating image
acquisition with R wave triggering.
• The advantage to this approach is that only the
necessary data are collected.
• However, excessive heart rate variability limits the
application of this technique.
• In addition, prospective gating is prone to artifacts that
cause increased initial signal intensity, but increased
signal intensity can be corrected using additional
pulses during the dead time interval.

7. Retrospective gating
• Involves continuous image acquisition throughout the cardiac
cycle and selecting the desired data subsequently during post-
processing.
• Although retrospective gating is less sensitive to heart rate
fluctuations, retrospective gating is more time-consuming
than prospective gating.
• Navigator echo respiratory gating enables image acquisition
during free breathing.
• An excitation pulse at the level of the diaphragm or heart is
used to track patient breathing: Images are acquired only
during end-expiration.

8. Pulse Sequences
• Pulse sequences are software programs that encode the magnitude
and timing of the radiofrequency pulses emitted by the MR scanner,
switching of the magnetic field gradient, and data acquisition.
• The components of a pulse sequence are termed “imaging engines”
and “modifiers”.
• Imaging engines are integral features of a pulse sequence, whereas
modifiers are optional additions.
• Imaging engines include fast spin-echo (FSE), gradient-echo (GRE),
steady-state free precession (SSFP), echo-planar imaging (EPI), and
single-shot versus segmented modes.
• Modifiers include fat suppression, inversion prepulse, saturation
prepulse, velocity-encoded, and parallel imaging

9. Dark Blood Imaging
• Dark blood imaging refers to the low-signal-intensity
appearance of fast-flowing blood and is mainly used to
delineate anatomic structures.
• Traditionally, spin-echo (SE) sequences have been used for
dark blood imaging.
• SE has been supplanted by the newer FSE and turbo spin-echo
(TSE) techniques in cardiac imaging.
• Although these techniques have lower signal-to-noise ratio
than SE, they enable rapid imaging, which minimizes the
effects of respiratory and cardiac motion.

10. • Basic FSE and TSE sequences consist of radiofrequency pulses
with flip angles (α) of 90°and 180° followed by acquisition of 1
or 2 signals.
• FSE and TSE sequences can be T1- or T2-weighted acquired
over a series of single or double R-R intervals.
• However, real-time nongated black blood sequences with
gadolinium contrast administration have proven to be
effective for evaluating myocardial ischemia

11. Fig. 1—Diagram shows fast spin-echo pulse
sequence. RF = radiofrequency pulse, ADC =
analog-to-digital converter.

12. Bright Blood Imaging
• Bright blood imaging describes the high signal
intensity of fast-flowing blood and is typically used to
evaluate cardiac function.
• The main pulse sequences used for bright blood
imaging include GRE and the more recently
introduced, but related, technique termed “steady-
state free precession” or“SSFP.”

13. • GRE sequences (i.e., spoiled gradient recall [SPGR],
turbo FLASH, turbo field echo, and fast-field echo
[FFE]) are produced by emitting an excitation
radiofrequency pulse that is usually less than 90°,
followed by gradient reversals in at least two
directions, which create an echo signal that can be
detected.
• SSFP sequences (i.e., fast imaging employing steady-
state acquisition [FIESTA], fast imaging with steady-
state precession [FISP], balanced FFE) are similar but
incorporate a short TR with gradient refocusing that is
less vulnerable to T2* effects compared with standard
GRE.

14. Fig. 2—Diagram shows steady-state free precession
pulse sequence. RF = radiofrequency pulse, ADC =
analog-to-digital converter.

15. Modifiers
• Inversion recovery (IR) consists of applying additional
180° pulses.
• Double or triple IR can be used to further null signal
from blood for black blood imaging, thereby improving
contrast between the cardiac tissues and blood pool.
• This sequence is particularly useful for tumor imaging,
delayed enhancement imaging, and coronary
angiography.
• Fat suppression is accomplished in a similar manner, in
which the inversion time of the additional selective
180° pulse is set to match the null time of fat.

16. • Phase-contrast imaging with velocity-encoded
imaging is a noncontrast technique that is
frequently used to estimate pulmonary blood
flow (Qp) and systemic blood flow (Qs) to
calculate the pulmonary-to-systemic flow ratio
(Qp:Qs) to determine shunt fraction.
• A Qp:Qs > 1.5 usually indicates a significant
left to- right shunt that requires surgical or
percutaneous correction.

17. Body planes and Anatomy
• Consists of axial, sagittal, and coronal planes.
• Provides scout images and overview of cardiac morphology.
• The axial plane can depict the four chambers of the heart and the
pericardium simultaneously.
• The sagittal plane can show the great vessels arising in continuity from
the ventricles.
• The coronal plane can be used to assess the left ventricular outflow tract,
the left atrium, and the pulmonary veins.

18. Cardiac planes
• Include short axis, horizontal long axis (four-
chamber view), and vertical long axis (two-
chamber view)

19. • These planes are prescribed along a line extending
from the cardiac apex to the center of the mitral valve
(long axis of the heart) using the axial body plane
images.
• The short-axis plane extends perpendicular to this true
long axis of the heart at the level of the mid left
ventricle.
• The horizontal long axis is generated by selecting the
horizontal plane that is perpendicular to the short axis,
whereas the vertical long axis is prescribed along a
vertical plane orthogonal to the short-axis plane.

23. Fig. 9—Normal cardiac MRI anatomy shown in healthy subject. Ao = aorta, AIVG = anterior interventricular groove,
APM = anterior papillary muscle, AV = aortic valve, CS = coronary sinus, CT = crista terminalis , D = diaphragm, EV =
eustachian valve, FO = fossa ovalis, IAS = interatrial septum, IVC = inferior vena cava, IVS = interventricular septum,
LA = left atrium, LAAP = left atrial appendage, LAD = left anterior descending artery, LCA = left coronary artery, LCCA
= left common carotid artery, LCX = left circumflex artery, LIV = left innominate vein, LMB = left mainstem bronchus,
LPA = left pulmonary artery, LV = left ventricle, LVOT = left ventricular outflow tract, MB = moderator band, MV =
mitral valve, PA = pulmonary artery, PMVL = posterior mitral valve leaflet, PPM = posterior papillary muscle, PUV =
pulmonary valve, RA = right atrium, RAAP = right atrial appendage, RCA = right coronary artery, RMB = right
mainstem bronchus, RPA = right pulmonary artery, RV = right ventricle, RVOT = right ventricular outflow tract, SVC =
superior vena cava, T = trachea, TV = tricuspid valve, PV = pulmonary vein.
A–E, Short-axis (A), horizontal long-axis (B), two-chamber (C), right ventricular outflow tract (D), and left
ventricular outflow tract (E) views.

24. Myocardial Infarction
• Myocardial infarction (MI) is defined as myocardial
cell death secondary to prolonged ischemia that
results in an inadequate supply of oxygenated blood
to an area of the myocardium, particularly when
ischemia exceeds a critical threshold that
overwhelms cellular repair mechanism.

28. Figure 1. Wavefront phenomenon of myocardial ischemic cell death.
Irreversible injury of ischemic myocardium progresses as a wavefront,
occurring first in the subendocardial myocardium but ultimately
becoming transmural if ischemia persists. Pink = nonischemic, purple =
ischemic, yellow = necrotic. (

30. MR findings in MI
• T2-weighted images
show wall thickening
and myocardial
edema.
• If there is irreversible
damage,
hyperenhancement
can be seen on
delayed-enhancement
images along the
distribution of the
involved epicardial
coronary artery

31. Partial myocardial damage
• Subendocardial
hyperenhancement can be
seen on delayed-enhancement
images
• If the ischemia continues,
necrosis gradually progresses
outward to involve the
epicardium, with ensuing
transmural delayed
hyperenhancement.
• Microvascular obstruction
may be present and can be
seen as a dark nonenhancing
area within the enhancing scar
on delayed-enhancement
images

32. Chronic MI
• Cine images -wall thinning and
regional wall-motion
abnormalities in the affected
territory.
• Edema is not seen on T2-
weighted images.
• Delayed-enhancement images
show wall thinning and
subendocardial or transmural
delayed hyperenhancement in
a vascular distribution.
• Perfusion defects may be seen
on both rest and stress
perfusion images, depending
on the degree of transmurality
of irreversibly damaged
myocardium

35. MR Imaging in Determining Age of
Infarct
• MR imaging can also be used to distinguish acute and chronic
infarcts,
• When a patient has multiple infarcts in various vascular territories
or when an infarct is discovered in the absence of clinical symptoms
• Both acute and chronic infarcts may be associated with wall-motion
abnormalities, perfusion defects, and scarring; these characteristics
are therefore not definitive in differentiating between infarct types.
• Although wall thickening is a feature of acute MI and wall thinning
a feature of chronic MI, these findings are not specific to either
diagnosis.
• Microvascular obstruction is characteristic of acute MI, but is seen
in at most 50% of these cases (7).
• Edema on T2-weighted images is seen only in acute MI.

36. MR Imaging in Risk Stratification and
Prognostic Indicators
• Acute MI
• Reversible versus Irreversible Injury.—Delayed
hyperenhancement of myocardium indicates
irreversible injury for both acute and chronic MI;
myocardial edema on T2-weighted images indicates
acute MI.
• The myocardial salvage index (MSI) (T2-weighted
area − delayed-enhancement area/T2-weighted area)
has a prognostic value with high sensitivity and
specificity.

37. • Transmurality:
There is an inverse relationship between the transmural extent
of MI and the recovery of segmental contractile function after
revascularization: a greater transmural extent is associated
with poorer recovery.
• Microvascular Obstruction.—
Microvascular obstruction or “no-reflow” phenomenon is seen in
acute MI and indicates a failure to reperfuse a portion of
myocardium despite re-establishment of epicardial coronary-
artery patency.

38. Hemorrhage in Core of Infarct
• Hemorrhage is seen in the core of an infarct in
up to 25% of patients with MI, particularly
those with reperfused infarcts.
• This hemorrhage appears on T2-weighted
images as a dark area because of hemosiderin
produced by hemoglobin degradation.
• Hemorrhage within the core has been shown
to be an adverse prognostic indicator.

39. Ischemia
Figure Peri-infarct ischemia. (a, b)
Short-axis delayed-enhancement
images from the midventricle (a) and
base (b) show focal near-transmural
infarction in the inferior wall (arrow in
a) and subendocardial infarction in
the inferior and inferolateral walls
(arrowheads in b). (c, d) Short-axis
stress perfusion images from the
same midventricular (c) and basal (d)
section positions show hypoperfusion
(ischemia) (arrow in c, arrowheads in
d) adjacent to and of greater extent
than the noted myocardial scar seen
on the delayed-enhancement images,
indicative of peri-infarct ischemia.

40. Chronic MI
• Scar Size.—The extent
of infarct is inversely
proportional to the
prognosis : the
likelihood of recovery
is lower if ≥50% of
the myocardium is
involved in the
infarcted segment.
• Scarring predicts
adverse LV
remodeling after
infarction.
Figure 11. (a) Short-axis delayed-
enhancement image in a 72-year-old man
shows extensive infarct in all vascular
territories (arrows), which is associated with
poor success after revascularization.

41. MR Imaging in Predicting Response to
Therapy

43. Complications

45. Figure 18. Thrombus in a 63-year-old man. (a) Four-chamber phase-sensitive
inversion-recovery delayed-enhancement image shows a small area of dark
thrombus (curved arrow) adjacent to a scarred segment of apical myocardium
(straight arrow). (b) On a short-axis delayed-enhancement image with a long
inversion time (600 msec), the thrombus stays dark (curved arrow) while the normal
myocardium has turned grayish (straight arrow). This feature allows thrombus to be
distinguished from a cardiac mass (which is vascular and would also turn grayish,
similar to the myocardium).

46. Cardiac Tumors
• To evaluate the signal properties, morphologic
characteristics (location, size, infiltrative
nature, presence of pleural/pericardial
effusions) and contrast enhancement of
cardiac tumors.
• Multiplanar capability.
• Better soft tissue characterization.
• Higher temporal resolution
• No ionizing radiations

51. Figure 5: Left ventricular thrombus in a
55-year-old man with a history of
myocardial infarction. A mass
was seen at transthoracic
echocardiography, which prompted
further evaluation with MR imaging. A,
The mass (arrow) was clearly seen in
the left ventricle at cine imaging and
was adherent to the severely
hypokinetic mid- to apical
anteroseptum (Movie 1 [online]). B,
There was no uptake of contrast agent
in the mass (arrow) at EGE imaging,
which suggested it was avascular. C, D,
LGE images demonstrated
hyperenhancement (arrowheads) in the
mid- to apical anteroseptum consistent
with a left anterior descending territory
myocardial infarction, and the adjacent
mass (arrow) did not enhance. The
combination of an avascular mass
overlying a regional wall motion
abnormality with demonstrable
infarction confirmed the diagnosis of
left ventricular thrombus.

53. MR images in a 45-year-old
man who had a suspected
myxoma at echocardiography
that was
subsequently characterized as
a lipoma (arrow) with MR
imaging. The key diagnostic
finding was, A, homogeneous
high signal intensity (relative to
myocardium) on T1-weighted
image that, B, markedly
suppressed
with the application of
additional fat-saturation
prepulses. Note the similar
signal intensity of surrounding
chest wall fat on T1- and T2-
weighted images (arrowheads).
D, There was no enhancement
with contrast
agent administration.).

54. Figure 10: Fibroma in a 30-year-old
woman who presented with syncope
and had unexplained hypertrophy of
the anterolateral wall at
echocardiography. The mass (arrow)
was, A, intramyocardial, with local
mass effect (Movie 3 [online]), B, C,
isointense (relative to myocardium)
on T1-weighted images and, D,
hypointense on T2-weighted images.
On perfusion images, the mass did
not show any substantial contrast
enhancement with gadolinium-based
contrast agent, suggesting
avascularity (Movie 4 [online]).The
most characteristic feature was
diffuse homogeneous enhancement
of the mass on, E, F, LGE images,
suggestive of a fibroma, which was
confirmed at histologic examination.

55. Figure 11: MR images of sarcoma in a 20-year-old man with cardiac tamponade at presentation
owing to the compressive effects of a large mass (arrow, A) involving the right atrium and the
associated hemorrhagic effusion (arrowheads, A and B ) (Movie 5 [online]). There was
heterogeneous signal intensity on both T1- and T2-weighted images owing to regions of
hemorrhage, ischemia, and necrosis (arrows, C–E ). At first-pass perfusion imaging, the mass in
this example was heterogeneously enhanced, especially in the periphery, consistent with a
degree of tissue vascularity (Movie 6 [online]). Typical of angiosarcomas, LGE image revealed
heterogeneous enhancement with regions of central necrosis (hypoenhancement) and
surrounding fibrosis (hyperenhancement) (arrow, F ). Postoperative histologic examination
confirmed a highly invasive, poorly differentiated angiosarcoma.

58. Pericardial Disease
• MRI is ideally suited for evaluation of small or
loculated pericardial effusions, pericardial
inflammation, and functional abnormalities
caused by pericardial constriction and for
characterization of pericardial masses.

59. Pericardial Anatomy
• Outer fibrous layer.
• Inner serous layer.
• The fibrous layer is attached to the diaphragm,
sternum, costal cartilages, and external layer of the
great vessels.
• Serous layer covers heart, the proximal portions of
the ascending aorta, pulmonary artery, left
pulmonary veins, and superior venacava (SVC).

60. Serous Pericardium
• Outer parietal layer and inner visceral layer.
• The parietal layer lines the inner surface of the fibrous
pericardium to which it adheres, whereas the visceral
layer envelops the epicardial surface of the heart,
separated from it only by a layer of epicardial fat that
contains the coronary vessels.
• The pericardial cavity is the space between the parietal
and visceral pericardial layers that typically contains
15–50 mL of clear serous fluid produced by visceral
pericardium, mostly plasma ultrafiltrate and cardiac
lymph, that eventually drains into the thoracic duct and
right lymphatic ducts

61. Pericardial Recesses and Sinuses
• Transverse and Obique sinuses.

63. MRI of Normal Pericardium
• Smooth, curvilinear structure that is surrounded on either
side by high-signal epicardial and mediastinal fat.
• Normal pericardium has intermediate-to-low signal on T1-
and T2-weighted black blood FSE SSFP sequences.
• The two pericardial layers are not separately discerned.
• The presence of fat and fluid makes visualization of
pericardium easier.
• Normal pericardium measures 0.4–1.0 mm thick in autopsy
studies
• Normal pericardium measures 1.2 mm in diastole and 1.7 mm
in systole on MRI studies .

64. Appearance of normal
pericardium on black
blood imaging. Four-
chamber T2-weighted
double– inversion recovery
black blood fast spin-echo
image of 34-year-old woman
shows intermediate-signal
band of pericardium
(straight arrows) situated
between high signal of
epicardial fat (curved
arrows) and mediastinal fat
(arrowheads).

66. Pericardial Effusion
• Accumulation of fluid in the
pericardial sac beyond the
normal physiologic amounts.
Causes
• Cardiac and renal failure.
• Infections.
• Myocardial Infarctions.
• Trauma
• Radiations
• Neoplasms
Type of Fluid
Serous
Fibrinous
Purulent
Hemorrhagic
Earliest site of
collection is the
posterolateral left
ventricular wall or
inferolateral right
ventricular wall.

67. Fig. 2—Pericardial effusion in 28-year-old man.
A, Four-chamber T2-weighted double–inversion recovery black blood
image shows moderate circumferential pericardial effusion (arrows) with
low signal intensity, mostover posterolateral aspect of left ventricle.
B, Four-chamber steady-state free precession image shows moderate
pericardial effusion (arrows) with high signal intensity over lateral aspect
of left ventricle.
C, Phase-sensitive inversion recovery delayed enhancement image shows
effusion (arrows) as dark collection.

68. Differences
Pericardial Effusion
• Signal void on black bood
sequences.
• High signal on SSFP and
gradient echo images.
• Have smooth margins.
• Follow typical distribution
pattern.- changes with
position change.
• Loses myocardial tags with the
cardiac cycle .
• Do not have contrast
enhancement within it.
Pericardial thickening
• Greyish to dark on T1WI, SSFP
and Gradient echo images.
• Irregular or nodular margins.
• Do not follow typical
distribution pattern.- No
changes with position change.
• Myocardial tags persists
throughout cardiac cycle.
• Show enhancement if
inflamed.

69. Pericardial Hematoma
• Typically follows surgery , cardiac truama ,
pericardiocentesis or epicardial injury.
• Signal depends on the age of hematoma.
• No contrast enhancement is seen.
• Differentials include pericardial cyst, neoplasm
or pseudoanurysm.

70. Fig. 4—Hemopericardium in 83-year-old man with history of recent
myocardial infarction.
A, Short-axis T2-weighted black blood image shows heterogeneous fluid
collection with intermediate to high signal (straight arrows) between
thickened layers of pericardium (curved arrow).
B, Two-chamber steady-state free precession image shows heterogeneous
hematoma (straight arrow) between pericardial layers (curved arrow)
caused by rupture of heart.

71. Cardiac Tamponade
• Acute accumulation of the fluid, air or solid tissue
resulting increase in intra-pericardial pressure
and decrease in the left ventricular filling.
• Common causes pericarditis , ruptured ventricles
, aortic aneurysm dissection , blunt chest trauma
or coronary artery bypass surgery.
• Depends upon the rate of accumulation and
stiffness of the pericardium.
• Becks triad jugular venous distention,hypotension
and muffles heart sounds.

72. Fig. 5—Focal cardiac tamponade. Four-chamber
steady-state free precession image of 63-year-
oldwoman obtained after aortic valve
replacement shows two loculated effusions
(arrows) having high signal intensity adjacent to
right atrium and left ventricle.In addition, there
is collapse of right atrial wall during diastole
(arrowhead), which is indicative of focal cardiac
tamponade.
•The anterior surface of the heart is
flat with diminished anteroposterior
diameter (i.e., “flattened heart”
sign).
•In severe cases, there is diastolic
inversion—that is, collapse of the
right ventricle free wall in early
diastole and collapse of the right
atrium free wall during late diastole
and early systole
•In severe cases, the cardiac
chambers are compressed, along with
compression of the coronary sinus,
pulmonary trunk, or IVC.
•Septal rocking, sigmoid
interventricular septum (convexity to
the left ventricle)

73. Pericarditis
Acute
• Presence of vascularized
granulation tissue , fibrin
and fluid.
• MRI pericardial thickening
and effusion.
• Immediate or delayed
contrast enhancement is
due to inflammation.
Chronic inflammatory
• Accumulation of the
fibroblast and collagen and
less fibrin
• MRI – thickened
pericardium with mild
effusion and variable
contrast enhancement.
Chronic fibrosing pericarditis: presence of fibroblasts and collagen with
calcific and non compliant pericardium.

74. Fig. 6—Diffuse acute pericarditis in 42-
year-old woman with systemic lupus
erythematosus. Shortaxis phase-sensitive
inversion recovery image shows diffuse
enhancement of thickened parietal
(straight white arrows) and visceral
(straight black arrows) pericardium
enclosing dark pericardial effusion (curved
arrow); these findings are consistent with
acute pericarditis.
Fig. 9—Chronic inflammatory pericarditis
in 45-yearold man with chest pain.
A, Vertical long-axis T2-weighted double–
inversionrecovery black blood image
shows diffuse circumferential pericardial
thickening (arrows) without any effusion.
B, Vertical long-axis phase-sensitive
inversion recovery image shows marked
diffuse circumferential enhancement of
pericardium (arrows) consistent with
chronic inflammation.

75. Pericardial constriction
• Caused by thickened, fibrotic or calcified,
nonelastic pericardium that impairs left
ventricle diastolic filling and results in elevated
systemic venous pressures and low cardiac
output.
• Although it typically affects the parietal
pericardium, pericardial constriction can
occasionally involve only the visceral layer.

76. Role of MRI
• To diagnose pericaridal constriction.
• To differentiate from the similar condition restrictive
pericarditis.
• To rule out other causes of right heart failure eg,
right ventricular infarction or dysplsia , pulmonary
hypertension or shunts.
• To evaluate whether the patient will benefit from
pericardial stripping.

77. Findings
• Pericardial thickening more than 4mm.
• More common on the right side, right ventricle and atrioventricular
groove.
Other features
• Diastolic interventricular septal flatenning.
• increased pressure produces septal flattening or even transient
inversion to the left side (“diastolic septal bounce”) in early diastolic
filing.
• Biatrial enlargement
• Narrow atrioventricular groove
• Dilated SVC, IVC, and hepatic veins
• Pleural effusion
• Ascites

78. Fig. 11—Secondary features of pericardial constriction. A, Four-chamber T2-weighted
black blood image of 71-year-old man shows tubular deformity of left ventricle
(LV) and conical deformity of right ventricle (RV). In addition, there is severe biatrial (right
atrium [RA], and left atrium [LA]) enlargement.
B, Axial steady-state free precession image of 72-year-old man shows enlargement of
right atrium (RA) and left atrium (LA). There are also bilateral moderate pleural effusions
(arrows). RV = right ventricle, LV = left ventricle.

79. Variants
• Focal pericardial constriction.
• Constriction with normal pericardial thickness.
• Effusive constrictive pericarditis.
• Inflammatory constrictive form.
• Occult constrictive pericarditis
• Radiation pericarditis.

80. Fig. 12—Focal constriction in 49-year-old man. Four-chamber T2-weighted double–
inversion recovery prepared black blood image shows focal thickening of pericardium
(arrows) overlying right atrium (RA) and right ventricle (RV).
Note the tubular deformity of ventricles.

81. Pericardial Neoplasms
• The following findings indicate aggressive
disease:
– Disrupted pericardium
– Hemorrhagic effusion
– Invasion into epicardial fat, myocardium, or
cardiac chambers
– Associated mediastinal or pericardial
lymphadenopathy

82. Pericardial metastasis
• Primary sites
• Cancers of the lung, breast,
esophagus, and kidney and
those with melanoma,
leukemia, multiple myeloma,
lymphoma, and thymoma.
• Spread to the pericardium can
occur hematogenously or
through lymphatics or by direct
invasio from adjacent
structures.
• At MRI, pericardial metastasis is
seen as a large hemorrhagic
pericardial effusion, irregular or
nodular pericardial thickening,
nodules, or masses
Image of 57-year-old woman with history of breast
cancer shows diffuse circumferential intermediate-signal-
intensity mass (arrows) is encasing ventricles. B, Two-
chamber T2-weighted black blood image of
homogeneous intermediate-signal-intensity metastatic
mass (arrow) in pericardium. Mass is indenting
underlying anterior wall of left ventricle. Note mild
pericardial thickening.

83. Primary benign pericardial neoplasms
• Lipoma
• Teratoma
• Fibroma
• Hemangioma
• Lymphangioma
• Neurofibroma
• Paraganglioma
• Granular cell myoblastoma.

84. Primary pericardial malignant
neoplasms
• Malignant pericardial neoplasms include
mesothelioma, sarcoma, lymphoma,
malignant teratoma, and
hemangioendothelioma.
• Mesothelioma accounts for 50% of primary
pericardial malignancies, secondary to
asbestos exposure.
• Seen as nodules, masses, diffuse plaque, or
hemorrhagic pericardial effusion.

85. Fig. 15—Pericardial hemangioma in 46-year-old woman.
A, Axial four-chamber T2-weighted black blood image shows homogeneous
intermediate-signal-intensity mass in right atrioventricular groove (arrow) encasing
right coronary artery (arrowhead).
B, Coronal T2 STIR image shows lobulated high signal- intensity mass in right
atrioventricular groove (arrows).

86. Fig. 16—Pericardial paraganglioma in 37-year-old woman.
A, Axial four-chamber T2-weighted black blood image shows homogeneous
intermediate-signal-intensity mass (arrow) in right interatrial groove with small
areas of flow void within it (arrowheads).
B, Axial T2 STIR image shows intensely high-signal-intensity mass (arrow) in right
interatrial groove.
C, Sagittal phase-contrast inversion recovery gradient-echo sequence shows intense
contrast enhancement within mass (arrows

87. Pericardial Cyst
• A pericardial cyst is a developmental abnormality
that is caused by pinching-off of a blindly ending
parietal pericardial recess.
• The right cardiophrenic angle is the most common
location.
• At MRI, a pericardial cyst is seen as a well-defined
and sharply marginated, homogeneous unilocular
cyst with low signal T1-weighted images and high
signal on T2- weighted images (Fig. 17A) with no
contrast enhancement.

88. Fig. 17—Pericardial cyst.
A, Axial T2-weighted STIR image of 44-year-old woman shows well-defined lesion
with high signal intensity (arrows) in right cardiophrenic angle.
B, Axial T2-weighted STIR image of 54-year-old woman shows lobulated cystic
lesion with high signal intensity (arrows), which is atypical appearance for
pericardial cyst.

89. References
• Cardiac Imaging: Part 1, MR Pulse Sequences,
Imaging Planes, and Basic Anatomy Daniel T.
Ginat;AJR 2011; 197:808–815.
• Cardiac MRI: Part 2, Pericardial Diseases Prabhakar
Rajiah; AJR:197, October 2011.
• MR Imaging of Myocardial Infarction Prabhakar
Rajiah et al., RadioGraphics 2013; 33:1383–1412.

90. •THANK YOU