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40 Cards in this Set

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Pericardial effusion
HICCUP
-Heart attack (post MI, AKA Dressler's syndrome)
-Infection (TB/viral pericarditis)
-Cancer (look for nodularity/pericardial mass)
-Collagen Vascular Disease
-Uremia
-Post-op
Others: Radiation therapy, Trauma (hemopericardium)
1. What are the causes of PRECAPILLARY pulmonary HTN?
2. What are the causes of CAPILLARY pulmonary HTN?
3. What are the causes of POSTCAPILLARY pulmonary HTN?
4. How do you recognize main pulmonary arterial enlargement on frontal radiograph?
5. What pressure defines pulmonary HTN?
1. Precapillary pulm HTN is due to increased blood flow in the pulmonary arteries. Therefore, it is seen in L to R shunt (ASD, PAPVR, VSD, PDA).

2. Capillary causes of pulm HTN include:
- Idiopathic (primary Pulmonary HTN)
- Chronic PE
- Chronic Lung disease: fibrosis, COPD, emphysema

3. Postcapillary causes of pulm HTN include:
- L sided valvular lesion
- Left heart failure

4. Look for focal convexity between the aortic arch and the left main bronchus (2nd mogul).
5. mean pulmonary artery pressure greater than 25 mm Hg. On chest radiographs, PAH is diagnosed when the transverse diameter of the right interlobar pulmonary artery >15-16mm. Calcifications of the pulmonary artery indicate chronic severe PAH.
MASSIVE cardiac enlargement
- Dilated cardiomyopathy
- Multivalvular disease
- Pericardial effusion (mimic)
- Ebstein's anomaly (kids)
1. What is the etiology of rheumatic heart disease?
2. Which valves are affected?
1.
- Autoimmune response to an initial infection with Group A Beta-hemolytic Streptococcus.
- Antibodies cross react with various tissues in the body including the heart.
2.
- LEFT SIDED VALVULAR INVOLVEMENT
- Fibrosis and fusion of mitral leaflets leading to mitral stenosis and insufficiency => left atrial enlargement.
- Aortic valve can also be affected.
1. What signs on the PA radiograph suggest left atrial enlargment?
2. What signs on the lateral radiograph suggest left atrial enlargement?
1. FINDINGS OF LEFT ATRIAL ENLARGEMENT ON FRONTAL CXR:
- Prominent left atrial appendage
- Double density adjacent to the right heart border
- Splaying of the bronchi with elevation of the left mainstem bronchus
2. FINDINGS OF LEFT ATRIAL ENLARGEMENT ON LATERAL CXR:
- LA extends posterior to the back wall of the trachea.
- Posterior displacement of the esophagus (better seen on esophagram)
Black blood vs white blood technique
Vascular imaging with MR usually employs both black blood and white blood imaging techniques.

Black blood imaging:
- refers to spin-echo sequences.
- result in signal void (black blood) from flowing blood within vascular structures.
- excellent for demonstrating the anatomy of vascular structures, including vascular walls and luminal diameter
- not good for assessing luminal flow.

White blood techniques:
- preferable for assessing luminal flow.
- variety of white blood techniques, including cine gradient-echo (GRE), two-dimensional (2D) segmented time-of-flight, 2D gadolinium-enhanced rapid GRE imaging, and gadolinium-enhanced 3D angiography.
- These white blood techniques can readily differentiate slow flow from thrombus.
How do you interpret gated wall motion studies?
- Hypokinesis can be graded into mild, moderate, or severe.
- if there is no wall motion, it is called akinesis.
- if there is paradoxical motion of the wall, it is called dyskinesis.
Absence of the pericardium
Can be partial or complete:

PARTIAL:
- can be symptomatic due to herniation and strangulation of the atria or appendages.
CXR
- deviation of the heart to the left side.
- left atrial appendage is prominent at it herniates through the pericardial defect.
CT
- clockwise rotation of the heart
- horizontal positioning of the interventricular septum
- **herniation of lung b/w main pulmonary artery and aorta

COMPLETE:
- usually an incidental finding and not symptomatic
- complete absence of pericardium may refer to absence of pericardium overlying the LV, RV, or LV+RV.
- can be associated with cardiac abnormalities = ASD, bicuspid aortic valve, PDA, TOF, etc.
What is the DDX of cardiac mass?
- Cardiac metastases
- Lipomatous hypertrophy of the interatrial septum/Lipoma
- Cardiac myxoma
- Angiosarcoma: most commonly involve the right atrium and presents as an irregular infiltrative mass.
- Lymphoma: usually seen in immunocompromised pts. Presents as multiple masses invading multiple chambers and involving the pericardium.
Patterns of delayed contrast enhancement:
1. What is the pattern of contrast enhancement in MI?
2. What is the pattern of enhancement in sarcoidosis and myocarditis?
3. What is the pattern of enhancement in amyloidosis, endomyocardial fibrosis, and hypereosinophilic cardiomyopathies?
1. Delayed enhancement in myocardial infarction starts in the subendocardial regions and extends to involve the mid-myocardial and then subepicardial regions.
2. Delayed enhancement in sarcoidosis or myocarditis can be diffuse, patchy, or linear and can involve any region of the heart including the subendocardium, subpericardium, or mid myocardium and is in a noncoronary distribution. Myocarditis progresses from a focal myocardial disease to generalized disease over several days. Thus repeat imaging may be helpful if findings are equivocal.
Myocardial edema is typical on T2WI.
Clinical sequelae of sarcoid granulomas within the myocardium range from asymptomatic conduction abnormalities to fatal ventricular arrhythmias. There may also be contraction abnormalities.
Sarcoidosis most commonly involves the septum and spares the right ventricle.
3.
- Circumferential subendocardial enhancement. However, in many cases, there is widespread enhancement involving all layers due to the diffuse infiltrative nature of this disease.
- Absence of edema.
- Thickening of the myocardium due to extracellular deposition of amyloid.
- Can involve the right ventricle.
- Amyloid cardiomyopathy is the most common cause of a restrictive cardiomyopathy in the United States. It is often seen in pts with multiple myeloma.
- **Difficult to suppress the signal of normal myocardium on delayed gadolinium images.
- NOTE: circumferential subendocardial enhancement is seen in a few infiltrative processes, such as endomyocardial fibrosis and hypereosinophilic (Loeffler) cardiomyopathies. These entities also have associated intraventricular thrombus.
Endomyocardial fibrosis can present with linear calcifications of the endocardium.
Coronary arterial anomalies:
1. What is a malignant course of a coronary artery?
2. What is a benign course of the LCA?
3. What is Bland-White-Garland syndrome?
4. What is a coronary fistula?
5. What is the septal/subpulmonic course of left coronary artery?
1. Malignant course refers to artery located between the pulmonary artery anteriorly and the aorta posteriorly.
2. Origin of the LCA from the right coronary sinus coursing either anterior to the pulmonary artery or posterior to the aorta.
3. Anomalous origin of the left coronary artery directly from the pulmonary artery. The flow in the affected coronary artery is reversed and is toward the pulmonary artery. This leads to ischemia with infarction children. Extensive collateral formation between the left and right coronary arteries is suggested by right coronary artery dilation.
4. In a coronary fistula, there will be an aberrant connection between a coronary artery and another vascular structure or cardiac chamber. The vessel will be enlarged and collaterals are often present.
5. LCA arises from the right cusp and traverses the basilar aspect of the muscular interventricular septum. So, it goes through a muscle to get to the epicardial space.
1. What is left ventricular non-compaction syndrome?
2. What are the imaging findings?
1.
- rare congenital cardiomyopathy
- 2/2 failure of normal myocardial development during embryogenesis.
- can involve both ventricles.

2.
- ratio of non-compacted to compacted myocardium of greater than 2.3:1 in diastole and hypokinesis of the affected segments. LV myocardium is thinner than normal but the trabeculation is markedly prominent. In systole, the myocardium may appear to be thickened.
NOTE: Occasionally, the myocardium of the left ventricle can be heavily trabeculated. However, hypokinesis of the heavily trabeculated segments should be present to suggest the diagnosis of left ventricular (LV) non-compaction.
1. What is the etiology of death in hypertrophic cardiomyopathy?
2. Describe the imaging findings in hypertrophic cardiomyopathy?
3. Describe the imaging findings in the septal variant of HCM?
4. Which other processes lead to concentric wall thickening?
1. Areas of myocardial scarring, as manifest by delayed enhancement, lead to conduction abnormalities and ventricular arrhythmias.
2.
- diffuse, ill-defined mid-myocardial enhancement
- concentric hypertrophy of the myocardium, most prominent in the septum which may lead to aortic outflow obstruction.
- Delayed patchy mid myocardial enhancement of the hypertrophied walls.
3.
- Asymmetric hypertrophy of the septal portion of the left ventricular wall at the base resulting in narrowing of the aortic outflow tract.
- Systolic anterior motion of the anterior leaflet of the mitral valve (SAM) further contributes to the narrowing of the aortic outflow tract. Look for turbulent flow jet across the aortic valve.
- SAM also leads to eccentric mitral regurgitation as the mitral valve is pulled open during systole.
- Delayed enhancement at the junction of the right ventricle wall and septum is common in the septal variant of HCM. NOTE: mild enhancement at the right ventricular insertion points can be seen in patients with pulmonary hypertension, so its presence alone should not make a diagnosis of HCM.
4.
- Systolic HTN and aortic stenosis can lead to concentric wall thickening; however, there is no delayed enhancement in these.
- Restrictive cardiomyopathy can also lead to diffuse myocardial thickening. However, this thickening is often diffuse and is not associated with outflow tract obstruction. In restrictive cardiomyopathy, the atria are usually dilated. Mid-myocardial enhancement can be present.
1. What are the imaging findings of true cardiac aneurysms?
2. What are the imaging findings of false cardiac aneurysms?
3. What entity can be confused for aneurysm?
1. True aneurysms:
- More common than false aneurysms
- Wide-necked (neck is as wide as the widest portion of the aneurysm)
- Occur at the left ventricular apex
- Involve all layers of the myocardium.
- Slow flow and akinesis of the aneurysmal segments can lead to thrombus formation
- Little risk of myocardial rupture.
2. False aneurysms:
- Represent contained myocardial rupture by pericardium or scar tissue
- Patients are often sent for emergent surgery.
- Narrow necked (neck is narrower than the widest portion of the aneurysm)
- Occur at the base along the left circumflex artery territory.
- MCC = MI; followed by surgery for mitral valve repair, trauma, infection.
3. Ventricular diverticulum: pouchlike or sac like projection from the cardiac lumen that is connected by a wide or narrow neck. Wall of diverticulum contains all layers of normal ventricular myocardium. However, unlike aneurysms that have dyskinetic motion, diverticula have normal wall motion.
What are the features of a papillary fibroelastoma?
1. Papillary fibroelastoma is the most common valvular neoplasm.
2. Most common location is in the aortic valve (~50%) followed by the mitral valve.
3. Usually small, lobulated mass < 2 cm in size.
4. Usually asymptomatic, however, may lead to distal arterial embolization.
5. Distinguished from valvular endocarditis vegetation by symptoms. Also, infected vegetations lead to rapid destruction of the valve.
What are the radiographic findings of Erdheim Chester disease
CHEST: large heart, septal thickening, GGO, pleural effusion, pleural thickening.
Other: periarticular soft tissue, perirenal soft tissue.
1. What are the imaging findings of arrhythmogenic right ventricular dysplasia?
2. What entities mimic ARVD?
1.
- Right ventricular dilation
- Right ventricular free wall microaneurysms (crenulated appearance of anterior wall of the RV).
- Wall motion abnormalities (dyskinesis)
- Right ventricular fibrofatty infiltration which may have delayed enhancement.
- + Family history
2.
Epicardial fat pad:
- difficult to separate normal epicardial fat from intramyocardial fat.
- NOTE: intramyocardial fat does not have to be present on imaging to make the diagnosis. However, the wall motion abnormality and right ventricular dilation suggests ARVD.

Right ventricular infarct:
- Chronic infarcts may be fatty replacement and there may be dilation of the ventricle.
Myocardial viability
Delayed enhancement that involves less than 50% of the myocardium are considered viable and should be sent for revascularization.
Takotsubo cardiomyopathy
- Sudden onset of transient akinesia or dyskinesia of the left ventricular (LV) apex in absence of coronary artery stenosis.
- Brought on by severe emotional distress.
- 6 times more common in women than men.
-Occurs from myocardial stunning, likely from excess catecholamine release.
- Delayed enhancement is absent.
- Normal contraction of the left ventricular base and proximal mid-cavity but dyskinesis and ballooning of the distal mid-cavity and apical segments.
Coronary artery stenosis
Hemodynamically significant stenosis is considered greater than 70% narrowing of the vessel lumen except for the left main coronary artery where 50% narrowing is considered significant
Coronary artery fistula (CAF)
- Shunt vascularity in which blood flows from the high pressure aorta via the coronary artery to the low pressure cardiac chamber or coronary vein.
- Results in a steal phenomenon and may cause myocardial ischemia.
- The affected coronary artery is diffusely dilated.
- Look for normal origin from the aorta to rule out Bland White Garland syndrome
Atrial fibrillation
The left atrial appendage closure device (watchman closure device - looks like an IVC filter) is used in patients with atrial fibrillation that cannot be anticoagulated to prevent risk from thrombus formation in the native appendage and subsequent embolization.

Pulmonary vein stenosis and/or pulmonary vein thrombosis are uncommon but serious complications after pulmonary vein radiofrequency ablation procedures performed for atrial arrhythmias. Severe stenosis is described as greater than 70% narrowing of the luminal diameter. Treatment includes stent balloon angioplasty or stent placement if the patient is symptomatic.
Mixing of contrast
On CT, the mixing of cotnrast with non-contrast enhanced blood is an unusual finding in the left ventricle, but it may be seen in the right side of the heart.
DDX of dilated coronary arteries
1. Kawasaki disease
2. Polyarteritis nodosa
3. Scleroderma
4. Ehlers-Danlos
5. Coronary fistula
6. Bland-White-Garland syndrome
What are the imaging features of infarcted myocardium on CT
- thinning of the myocardium
- decreased attenuation of the muscle due to fatty or fibrous degeneration.
- look for associated thrombus
and aneurysm formation
Myocardial bridge
Intramyocardial segment of an epicardial artery in which the vessel is embedded within the myocardium.
- results in systolick compression of tunnelled segment by teh overlying myocardium.
- tunneled segment of the coronary artery is rarely affected by atherosclerosis, but the segment proximal to the myocardial bridge is at increased risk of plaque development.
Calcium socring
Most widely used system for calcium scoring is the Agatston score in which the calcium area is multiplied by the CT density number.
- Coronary artery calcification is predictive of coronary artery disease. However, even pts with a CAC score of 0, may have significant non-calcified plaque.
- CAC increases with aging, so an elevated calcium score has less clinical significacnce and a lower positive predictive value for coronary artery disease in the elderly.
Acute vs. chronic infarct
- acute and chronic infarcts demonstrate endocardial enhancement on delayed images.
- myocardial wall is often normal in thickness or mildly thickened in acute MI due to edema
- myocardial wall is thinned in chronic infarcts.
- On perfusion images, look for decreased enhancement in ischemic or infarcted regions. If there is thinning of the myocardium, it is likely old. There may be fat infiltration of the myocardial wall.
cystic lesions around the heart
- pericardial cyst: mc location is in teh cardiophrenic angle, right > left.
- duplication cyst
- bronchogenic cyst
- thymic cyst
Cardiomyopathies
- Can be divided into dilated, hypertrophic, and restrictive.

DILATED CARDIOMYOPATHY: Dilated LV + normal-decreased myocardial thickness.
- further divided into primary and secondary
- Causes of secondary dilated CM include:
*infection (coxackie, HIV)
*ischemic heart diseae
*substance abuse (alcohol)
*peripartum cardiomyopathy

HYPERTROPHIC CM: Small LV chamber + thickened myocardium

RESTRICTIVE CM: Normal sized LV chamber + normal wall thickness
- least common type.
- reduced diastolic volume of ventricles.
- **pericardium is normal (important to differentiate from constrictive pericarditis)
- can be idiopathic or secondary to infiltrative diseases
- causes of infiltrative diseases leading to restrictive CM:
*amyloidosis: MCC
*Loeffler endocarditis
*endomyocardial fibrosis
*hemochromatosis
*sarcoidosis
*scleroderma
1. What conditions result in poor contractility and thinning of the myocardium?
2. How can you differentiate between the two?
1. Ischemic and dilated cardiomyopathies.
2. With ischemic cardiomyopathy, subendocardial delayed enhancement would be present. Delayed mid-myocardial enhancement is seen in about 50% of dilated cardiomyopathies. The enhancement in dilated CM is diffuse, whereas with ischemic cardiomyopathy, it tends to be localized to a vascular territory.
caseous calcification of the mitral annulus
- large, round, tumorlike, broad-based calcification closely associated with posterior mitral annulus.
- Calcifications may be denser in the periphery.
- MRI shows a low SI mass...CT confirms dense calcifications. No enhancement.
- Usually asympotmatic but can be associaed with mitral valve stenosis/regurgitation.
Avulsion of a cusp of the aortic valve
- Occurs in the setting of dissection that involves the aortic valve separating the cusp from the annular ring.
- Look for a linear filling defect in the LVOT.
- Associated with acute onset of valvular insufficiency that leads to CHF or death.
-
Mitral stenosis
- Look for thickening of the mitral valves with limited opening during ventricular diastole.
- Associated left atrial enlargement.
- MCC = rheumatic heart disease; other causes = atrial myxoma, thrombus, severe degenerative annular calcifications.
- Results in pulmonary venous HTN --> pulmonary arterial HTN
- Can be complicated by atrial fibrillation --> emboli.
- The severity of mitral valve calcifications correlates with degree of mitral stenosis. NOTE: mitral annular calcifications is a degenerative process that usually is not assoicated with mitral valvular stenosis.
what are false tendons (cords) of the myocardium?
- linear cords of muscle with broad based attachment to the myocardium that project into the lumen of the LV and may extend through the cavity of the LV to other walls.
- May displace papillary muscles and lead to chordae or valve dysfxn.
myocardial calcification
old infarct
inflammatory disease
metabolic abnormality
endomyocardial fibrosis.
Interatrial septal aneurysm
- Abnormal protrusion of the interatrial septum toward either the right or left atrium.
- associated with interatrial shunting (PFO, ASD)
Aortic assist device vs. Intra-aortic balloon pump
AORTIC ASSIST DEVICE:
- sewn into the thoracic aorta and functions to augment the systolic effect of the LV
- inflates during systole which forces blood through the coronary arteries and great vessels
- deflates during diastole which creates a negative pressure in the thoracic aorta and drives blood into the abdomen.
- initally filled with saline; upon discharge from the hospital, the balloon eventually fills with air.
INTRA-AORTIC BALLOON PUMP:
- temporary device placed in teh lumen of the descending thoracic aorta.
Pulmonary artery stenosis
- Can be supravalvular (most common), valvular, and subvalvular
- Supravalvular obstruction = may affect the main trunk of the pulmonary artery, central arteries, or more pheripheral branches (may mimic PE on V/Q scan).
CAUSES:
- CHD: TOF, Williams syndrome, Noonan syndrome
- Congenital rubella
- Carcinoid syndrome
- Post surgical (lung transplant).
- Vasculitis (Takayasu and Behcet).
- Fibrosing mediastinitis
Constrictive pericarditis
Most commonly a sequeale of prior radiation, surgery, and TB
- **THICKENING and CALCIFICATION of the pericardium. Occasionally, seen with a large pericardial effusion.
- **Irregular calcifications may occur anywhere over the surface of the heart but the largest accumulations are usually present at the ATRIOVENTRICULAR GROOVE.
- TUBULAR configuration of ventricles
- Atrial enlargement
- SEPTAL BOUNCE can be seen on cine images.
- Associated with secondary MYOCARDIAL ATROPHY (thinning of the interventricular septum and left ventricular wall).
- Signs of impaired diastolic filling -- dilatation of the IVC and hepatic veins, hepatosplenomegaly, and ascites.