Year 2 MRAD lecture by UKM student

1. CHEST 5
Heart: Radio-pathological
correlation
Muhamad Fariz/ Rubeni
Supervisor : Dr Nik Azuan

2. Outline
• Congestive heart failure
• Valvular heart disease
• Pulmonary hypertension – PAH/PVH
• Infarct –CTA/MR Cardiac

3. Congestive heart failure (CHF)

4. Congestive heart failure
• Due to insufficient cardiac output
• Broadly divided into two types:
• LV failure (most common)
• results in decreased cardiac output and increased pulmonary venous pressure.
• lead to dilatation of pulmonary vessels à leakage of fluid into the interstitium and the
pleural space and finally into the alveoli à pulmonary edema.
• RV failure
• Result of long standing LV failure or pulmonary disease
• Causes increased systemic venous pressure
• result in edema in dependent tissues and abdominal viscera.

6. Stage I - Redistribution
• Normal à pulmonary vessels supplying the upper lung fields are
smaller and fewer in number than those supplying the lung bases.
• Equalization of blood flow à redistribution of flow from the lower to
the upper lobes.

7. Artery-to-bronchus ratio
• Vessels in upper lobes à smaller than the accompanying bronchus
with a ratio of 0.85
• At hilum à equal
• Lower lobes à arteries are larger with a ratio of 1.35.
• Redistribution à an increased artery-to-bronchus ratio in the upper
and middle lobes.
• Best visible in perihilar region.

9. Stage II - Interstitial edema
• Increased pressure in the capillaries à fluid leakage into
interlobular and peribronchial interstitium
• Peripheral interlobular septa à Kerley B or septal lines.
• Peribronchovascular interstitiumà thickening of bronchial walls
(peribronchial cuffing) and loss of definition of these vessels
(perihilar haze).

12. Normal CHF stage II

14. Stage III - Alveolar edema
• Continued fluid leakage into interstitium (which cannot be
compensated by lymphatic drainage)
• Eventually à fluid leakage in the alveoli (alveolar edema) and into
pleural space (pleural effusion).
• The distribution of alveolar edema influenced by:
• Gravity
• Obstructive lung disease

20. 1. Cardiothoracic ratio
• Increased CTR
• Almost always due to à cardiomegaly
• Occasionally:
• pericardial effusion
• Fat deposition
• Considered too large when CTR > 50% on a PA chest x-ray
• Sensitivity of 50%, specificity of 75-80% for CHF
• An increase in LV volume of at least 66% is necessary before it is noticeable on a chest x-ray.

21. A patient who recently underwent a valve replacement.

22. 2. Pleural effusion
• In CHF à 70% are bilateral
• Meniscus in the costophrenic angle on a PA image à at least 175 ml
of pleural fluid
• Lateral image à> 75 ml
• Supine film àat least 500 ml

24. 3. Vascular pedicle
• Indicator of the intravascular
volume.
• Width < 60 mm on PA CXR à seen
in 90% of normal chest x-rays.
• Width > 85 mm à pathologic in
80% of cases.
• 5 mm increase in diameter
corresponds to 1 liter increase of
intravascular fluid.
• An increase in width of the vascular
pedicle is accompanied by an
increased width of azygos vein.

25. • 3 main varieties of pulmonary edema
• cardiac, overhydration and increased capillary permeability (ARDS).
• Vascular pedicle width differentiates these:
• Normal VPW: capillary permeability or acute cardiac failure.
• Widened VPW: overhydration/renal failure and chronic cardiac failure.
• Narrowed VPW: capillary permeability.

26. A patient with ARDS

27. 4. Dilatation of azygos vein
• Sign of increased RA pressure
• Usually seen when there is also increase in width of the vascular pedicle.
• Diameter of azygos vein varies according to the positioning.
• Standing position à > 7 mm is most likely abnormal, diameter > 10 mm is definitely
abnormal.
• Supine patient > 15 mm is abnormal.
• An increase of 3 mm in comparison to previous films is suggestive of fluid
overload.
• The difference of the azygos diameter on an inspiration film compared to
an expiration film is only 1mm.
• This means that the diameter of the azygos is a valuable tool whether or not there is
good inspiration.

29. Right ventricular failure
• Radiographic features:
• Increased VPW due to dilatation of the
superior vena cava
• Dilatation of azygos vein
• Dilatation of the right atrium
• In many cases there will be both signs of
RV and LV failure
• Sonographic signs of RV failure:
• Dilatation of the inferior vena cava (IVC)
and hepatic veins
• Hepatomegaly
• Ascites

30. Valvulopathies

31. Valvulopathies
• Mitral valvulopathies
• Aortic valvulopathies
• Pulmonary valvulopathies
• Tricuspid valvulopathies
• Mixed valvulopathies

34. Mitral valvulopathies
Mitral stenosis
Mitral regurgitation

35. Mitral stenosis: Etiology
• Rheumatic heart disease
• Mitral annular calcification with leaflet involvement (age
related)
• Congenital mitral stenosis
• Infective endocarditis
• Cor triatriatum
• Connective tissue disorders
• Radiation-induced heart disease

36. Mitral regurgitation- Etiology
• Acute MR
• MI with papillary muscle rupture
• Infective endocarditis
• Chordae tendinae rupture seen in myxomatous degeneration (e.g. due to mitral valve prolapse, Marfan
syndrome, Ehlers-Danlos syndrome, etc.)
• Prosthetic mitral valve dysfunction
• Trauma
• Chronic MR
• Annular calcification
• Myxomatous degeneration (same underlying causes as in acute mitral regurgitation)
• Previous infective/inflammatory illness
• rheumatic heart disease
• infective endocarditis
• connective tissue diseases
• Congenital valvular malformation (e.g. parachute mitral valve in the Shone complex)
• Dilated cardiomyopathy
• Hypertrophic obstructive cardiomyopathy

37. MS/MR: plain radiograph
• Left atrial enlargement
• convexity or straightening of the left atrial appendage just below the main
pulmonary artery (along left heart border)
• double density sign = double right heart border: the right side of the enlarged
left atrium pushes into the adjacent lung and creates an addition contour
superimposed over the right heart
• elevation of the left main bronchus and splaying of the carina
• walking man sign on lateral projections
• Upper zone venous enlargement due to pulmonary venous
hypertension
• Pulmonary edema

44. Tricuspid valvulopathies
Tricuspid stenosis
Tricuspid regurgitation

45. Tricuspid stenosis
• Etiology: most common cause:
sequela of rheumatic fever
• Other causes:
• Congenital tricuspid stenosis
• carcinoid heart disease (always combined
with tricuspid regurgitation)
• nonbacterial thrombotic endocarditis
• infective endocarditis
• fibrosis/adhesions associated with
endocardial pacemaker leads
• Fabry disease
• cardiac amyloidosis
• Whipple disease
Plain radiograph:
• Often subtle, especially due to
presence of signs of
concurrent MS
• RA enlargement
• SVC enlargement
• Features of MS
• Calcifications of tricuspid
valve (rare)
• +/- features of congestive heart
failure

46. Tricuspid regurgitation
• 70-85%: considered 'functional'
(or 'secondary'), where it is caused
by dilatation of the annulus as a
result of increased pulmonary and
right ventricular pressures
• 15–30%: organic (or 'primary’)
• TR in isolation is very rare
• à more often found in association
with other valvular disease,
especially mitral valve disease
Plain radiograph
• Often subtle
• Features:
1. RA enlargement
2. RV enlargement
3. Reduced prominence of
pulmonary vascularity
4. SVC enlargement
5. IVC enlargement
6. Distension of azygos vein
7. +/- features of CHF

49. Aortic valvulopathies
Aortic stenosis
Aortic regurgitation

50. Aortic stenosis
• Supravalvular
• Congenital (William syndrome)
• Acquired (syphilitic aortitis, Takayasu
arteritis)
• Valvular
• Congenital (bicuspid aortic valve,
tricuspid aortic valve, unicuspid aortic
valve)
• Acquired (rheumatic heart disease, senile
calcific aortic stenosis, radiation induced
heart disease)
• Subvalvular
• Congenital (Shone complex, HOCM)
• Plain radiograph
• Variable appearance depending on stage
and severity of disease
• Early à can be entirely normal or
it dilatation of ascending aorta with a
normal heart size
• Late à valvular calcifications (if valvular
aortic stenosis) and/or cardiomegaly with
features of heart failure, such
as pulmonary venous
congestion and pulmonary
interstitial/alveolar edema
• ECHO
• Mild: mean gradient is <20 mmHg
• Moderate: mean gradient 20-40 mmHg
• Severe: mean gradient >40 mmHg

51. Aortic regurgitation
• Etiology à Due to:
• Root disease
• hypertension, congenital bicuspid
aortic valve, connective tissue
disorders (e.g. Marfan
syndrome, Ehlers-Danlos
syndrome, osteogenesis imperfecta,
etc.), aortic dissection, Takayasu
arteritis, syphilitic aortitis, etc.
• Valvular
• rheumatic heart disease, calcific aortic
valve disease (i.e. calcific aortic
stenosis), bacterial infective
endocarditis, prolapse, quadricuspid
aortic valve, ankylosing
spondylitis, syphilitic aortitis, radiation-
induced heart disease
• Plain radiograph
• Variable depending on stage and
severity
• ECHO
• Mild: central jet has a width <25% of
the left ventricular outflow tract
(LVOT)
• Moderate: worse than mild aortic
regurgitation but do not meet criteria
for severe aortic regurgitation
• Severe: central jet has a width ≥65%
of the LVOT

52. A patient with
limited exercise
tolerance with mild
shortness of breath
on exertion.

54. Pulmonary valvulopathies
Pulmonary stenosis
Pulmonary regurgitation

55. Pulmonary stenosis
• Etiology
• Congenital (95%)
• Acquired (5%)
• Carcinoid heart disease
• Rheumatic heart disease
• Non bacterial thrombotic endocarditis
• Infective endocarditis
• Plain radiograph:
• right ventricular enlargement
• right atrial enlargement
• prominent pulmonary trunk
• Chen sign: vascular fullness at the left
lung base more-so than the right lung
base due to preferential flow of turbulent
jet into the left pulmonary artery
• rarely, calcifications of the pulmonary
valve may be seen
• features of congestive heart failure may
also be present
• ECHO
• Mild: peak gradient <36 mmHg
• Moderate: peak gradient 36-64 mmHg
• Severe: peak gradient >64 mmHg

57. Pulmonary regurgitation
• Etiology
• Secondary (functional) more common than
primary (valvular pathology)
• Primary causes
• iatrogenic (most common primary cause) (surgical
treatment of congenital pulmonary stenosis, tetralogy
of Fallot)
• infective endocarditis
• carcinoid heart disease (often alongside pulmonary
stenosis)
• rheumatic heart disease
• congenital pulmonary regurgitation
• Secondary causes
• any cause of pulmonary arterial hypertension (see
individual article for an in-depth discussion)
• pulmonary artery dilation
• pulmonary artery aneurysm
• tertiary syphilis
• Behçet disease
• Plain radiograph
• Often subtle
• right ventricular enlargement
• prominent pulmonary trunk
• features of tricuspid regurgitation may also be present
• features of congestive heart failure may also be present

58. Valvular calcifications
• Causes:
• 1. Mitral calcification:
Rheumatic fever, degenerative annular calcification
• 2. Aortic calcification:
Bicuspid aortic valve, degenerative aortic sclerosis, previous rheumatic fever
• 3. Pulmonary calcification:
Pulmonary stenosis, rheumatic fever
• 4. Tricuspid calcification:
Rare, rheumatic fever, endocarditis, ASD

59. 72 year old male presented with breathlessness and
cardiac chest pain. Hypertensive with a history of
ischaemic and valvular heart disease.

60. Pulmonary hypertension

63. Pulmonary hypertension: resting mean pulmonary arterial pressure of 25 mmHg or more at catheterization of the right
side of the heart
20 mmHg or less à normal
21–24 mmHg àabnormal
PVH: pulmonary capillary wedge pressure (PCWP) > 12 to 14 mmHg.

65. Plain radiograph
• By the time the diagnosis of pulmonary arterial hypertension is made,
90% of patients have an abnormal chest radiograph although
sensitivity and specificity are low .
• Features include:
• elevated cardiac apex due to right ventricular hypertrophy
• enlarged right atrium
• prominent pulmonary outflow tract
• enlarged pulmonary arteries
• pruning of peripheral pulmonary vessels

67. CT
• HRCT: assessing the lung parenchyma and to identify possible causative processes
• Extracardiac vascular signs
• enlarged pulmonary trunk (measured at pulmonary artery bifurcation on an axial slice vertical to
its long axis)>29 mm diameter is often used as a general predictive cut-off
• main pulmonary artery (pulmonary trunk) to ascending aorta ratio
• higher ratio correlates with higher PA pressure
• the ratio obtained on the axial image at the bifurcation of the right pulmonary artery
• adult: normal ratio is less than 1.0
• enlarged pulmonary arteries
• mural calcification in central pulmonary arteries
• evidence of previous pulmonary emboli
• a segmental artery-to-bronchial diameter ratio of 1:1-1.25 or more in three or four lobes in the
presence of a dilated (≥29 mm) main pulmonary artery and absence of significant structural lung
disease has a specificity of 100% for the presence of pulmonary hypertension

69. Vascular signs of pulmonary hypertension. Axial
multidetector CT angiogram shows dilatation (29
mm or more) of the main pulmonary artery.
The ratio of main pulmonary arterial diameter to
that of the ascending aorta is also greater than or
equal to 1, another useful sign of pulmonary
hypertension.

70. • Cardiac signs
• right ventricular hypertrophy: defined as the wall thickness of >4 mm
• straightening or bowing (towards the left ventricle) of the interventricular
septum
• right ventricular dilatation (a right ventricle–to–left ventricle diameter ratio of
more than 1:1 at the midventricular level on axial images)
• decreased right ventricular ejection fraction
• ancillary features
• dilatation of the inferior vena cava and hepatic veins
• pericardial effusion

73. Ischemic heart disease

75. Coronary CT angiography: Indications
• noninvasive evaluation of coronary artery anomalies and other
thoracic vessels
• symptomatic patients with low/moderate probability of CAD
• evaluating the patency of a CABG/coronary artery stents
• preoperative assessment for transcatheter aortic valve implantation
(TAVI/TAVR)
• new onset heart failure with no prior history of CAD,
low/intermediate probability

76. Coronary CT angiography: contraindications
• Having acute MI
• screening of asymptomatic patients with low-to-intermediate risk of
CAD
• evaluation of coronary artery stents <3 mm
• evaluation of asymptomatic patients post CABG (<5 years old) and
post stent (<2 years old)

77. Calcium scoring
• Nonenhanced, low-dose technique
• detection of calcifications of the coronary arteries
• Agatston score:
• no evidence of CAD: 0 calcium score
• minimal: 1-10
• mild: 11-100
• moderate: 101-400
• severe: >400
• allows for an early risk stratification of patients with a high Agatston
score (>160) have an increased risk for a major adverse cardiac event
(MACE)

79. 4 chamber view 3 chamber view

80. 5 chamber view 2 chamber view

81. Each stenosis detected at coronary CTA was graded as mild (< 30%), moderate
(30% to 50%), or severe (≥ 70%).

82. Three-dimensional (3D) volume rendering from left anterior oblique perspective, demonstrate significant
coronary artery stenosis (arrowhead) in the proximal left anterior descending coronary artery (LAD) caused
by predominantly noncalcified plaque.

83. A hypodensity (arrow) in the lateral
wall of the left ventricle indicative of
myocardial ischemia.
B, Reduced uptake of contrast in the
left ventricular wall (arrow) suggestive
of myocardial ischemia.
C, A reformatted short-axis view of
the left ventricle from the computed
tomography scan shows
hypoperfusion (arrow) in the posterior
wall.

84. Cardiac MRI: Indications
• Coronary artery disease
• Assessment of global ventricular function and mass
• Detection of CAD
i. Regional LV function at rest and during dobutamine stress
ii. Assessment of myocardial perfusion (adenosine stress)
iii. Coronary MRA (anomalies)
• Acute and chronic myocardial infarction
I. Detection and assessment
II. Myocardial viability
• Cardiomyopathies
• Valvular heart disease: quantification of regurgitation

85. Vertical long axis view

86. Horizontal long axis view

87. Short axis view

88. Three chamber view

90. Aortic view

91. Pulse sequences in cardiac MRI
• Spin echo (SE) has high resolution images, black-blood technique and
are used to study the anatomy of the heart and mediastinium as well
as the thoracic aorta and great vessels. Each image requires a single
breath hold.
• Gradient echo (GRE), has fast imaging speed, bright-blood technique
and is the workhorse of cardiac imaging because of its speed and
versatility.
• Gradient echo imaging is employed in the assessment of ventricular function,
blood velocity and flow measurements, assessment of valvular disease,
myocardial perfusion, delayed enhanced imaging, and magnetic resonance
angiography

92. 17-Segment model
• Myocardial segments with
abnormal enhancement or wall
motion disturbances are named
and localized according to the 17
segments model of the American
Heart Association.
• Individual myocardial segments
can be assigned to the 3 major
coronary arteries with the
recognition that there is anatomic
variability.

93. • Dobutamine stress test
• Dobutamine is the agent of
choice when evaluating for
stress induced wall motion
abnormalities. Dobutamine
increases both the contractility
of the heart and heart rate.
Atropine can be added if the
target heart rate is not
obtained.
• Cardiac perfusion imaging
• Adenosine is administered to
maximally vasodilate the entire
coronary bed to uncover regional
differences in blood flow due to a
stenosis.
• Ischemic areas are identified by
decreased enhancement during
first pass imaging after intravenous
administration of gadolinium and
adenosine.
• Rest images are then acquired by
repeating the technique in the
absence of adenosine. If a
perfusion defect persists on rest
images, this may represent an
infarction which can be confirmed
with delayed enhanced image
https://www.med-ed.virginia.edu/courses/rad/cardiacmr/MP4/cadStressRest.mp4
https://www.med-ed.virginia.edu/courses/rad/cardiacmr/MP4/cadDetectionUpper.mp4
https://www.med-ed.virginia.edu/courses/rad/cardiacmr/MP4/cadDetectionLower.mp4

94. Enhancement pattern
Administration of Gadolinium results in uptake of the
contrast agent into both normal and injured
myocardium.
In normal myocardium there will be early wash
out of contrast.
In injured myocardium the wash out is very
slow resulting in delayed enhancement after 10
- 15 minutes compared to the normal
myocardium.
Delayed enhancement of myocardial tissue is
seen in many pathophysiologic scenarios:
Retention of contrast material by fibrous tissue
Increased extravascular space
Inflammation
Tumor neovasculature in primary and
secondary tumors

95. • Stunned myocardium is myocardium with normal perfusion,
abnormal function, and absence of delayed enhancement;
• it represents transient myocardial dysfunction after a bout of acute ischemia
with restoration of blood flow.
• Hibernating myocardium has poor function, low resting perfusion,
and absence of delayed enhancement;
• it represents chronic ischemia and down regulated metabolic needs of the
myocardium.

96. Thank you!