Page 27 Flashcards
MC affected leaflet in Congenital cleft mitral valve
Anterior leaflet
Type of mitral valve where All chordae tendineae are attached to a single papillary muscle
Parachute mitral valve
Anomaly demonstrating apical displacement of septal tricupid valve leaflet in relation to tricuspid annulus plane w/ resultant dilation of RA and RV and tricuspid regurgitation
Ebstein anomaly
Globular or box shape heart (frontal cxr)
Ebstein anomaly
MCC of congenital tricuspid regurgitation
Ebstein anomaly
Associated conditions of tricuspid atresia
Right-sided aortic arch and TGA
What is the cutoff measurement of apical displacement of septal leaflet for Ebstein anomaly?
> 8 mm/m2 (normal heart = septal and posterior leaflets are slightly apically displace relative to anterior MV leaflet of <8 mm/m2)
Dynamic or fixed anatomic obstruction to blood flow from RV to pulm varterial vasculatures
Congenital Pulmonary stenosis - valvular, subvalvular, supravalvular
Cardiac CT or MR depict fatty or muscular separation of RA from RV
Tricuspid atresia
Cyanotic type of CHD with small and hypoplastic RV, while RA is dilated and hypertrophied
Tricuspid atresia
Type of PS in double-chambered RV
Subvalvular PS
Refers to infection of valve leaflets as wel las prosthetic valves
Valve infective endocarditis
In the setting of RIGHT heart dse, break off of fragments of vegetation will result to?
Pulmonary septic emboli
Nonbacterial heart manifestation in px with SLE
Libman-Sacks nonbacterial endocarditis (rarely embolize unlike IE)
In the setting of LEFT heart dse, break off of fragments of vegetation will result to?
TIA or stroke
Plaque-like fibrous endocardial thickening involving heart valves (tricuspid and pulmonary)
Carcinoid heart disease
Chronic exposure to excessive circulating serotonin is an imoortant contributing factor
Carcinoid heart disease
Heart disaese associated withmetastatic neuroendocrine tumors
Carcinoid heart disease
Refers to valve fibrosis and scarring caused by autoimmune rxn to infection (group A strep) resulting to stemosis/regurgitation
RHD (majority with hx of rheumatic fever)
Postoperative complications ff valve surgery
Infection, dehiscence, and perivalvular leak
Late complications ff valve surgery
Valve regurgitation, IE, anastomotic dehiscence, pseudoaneurysm, and thromboembolic events
This imaging technique is now the reference standard for assessing chamber size, LV fxn, and ventricular mass in cardiomyopathies
Cardiac MRI
Leading case of sudden cardiac death in young adults and athletes
Hypertrophic cardiomyopathy (HCM) -AD genetic cardiomyopathy
Imaging hallmark of HCM
focal, regional, or diffuse LVH measuring >20mm at end-diastole (w/ classic hazy midmyocardial enhancement)
HCM variant with characteristic “spade-like” configuration of LV on vertical long axis
Apical HCM variant
MC location of asymmetric septal HCM
Anteroseptal segments (base of LV)
Ejection fraction in cardiac amyloidosis
Mildly reduced (cardiac amyloidosis is a restrictive cardiomyopathy)
MC form of HCM
Asymmetric septal involvement (other variants =apical, symmetric, midventricular, mass-like and noncontiguous)
Ejection fraction in HCM
Normal or increased
Ejection fraction in dilated cardiomyopathy
Decreased
Fabry disease vs HCM
In Fabry disease, hazy midmyocardial delayed enhancement is siolated to inferolateral segments of LV despite relative diffuse hypertrophy
Mimicker of HCM, an x-linked disorder with accumulation of glycosphingolipid in diff tissues including the heart
Fabry disease
Imaging hallmark of cardiac amyloidosis
Diffuse concentric LVH (also, diffuse subendocardial hypoperfusion and delayed enhancement), biatrial enlargement
Restrictive CM involvingg 1 or both ventricles with classic circumferentialRestrictive CM involvingg 1 or both ventricles with classic circumferential subendocardial patternl of delayed enhancement (same with cardiac amyloidosis)
Loeffler endocarditis
Classic Cardiac manifestation of hypereosinophilic syndrome (HES)
Loeffler endocarditis
MCC of cardiac amyloidosis
AL (Amyloid light chain) or primary amyloidosis -deposition of amyloid fibrils within heart
Loeffler endocarditis vs cardiac amyloidosis
Both have same circumferential subendocardial delayed enhancement. Loeffler -presence of adherent ventricular thrombi (low signal on LGE). Overtime, subendocardial fibrosis leads to obliteration of LV cavity and result in restrictive CM)
Cardiac chamber dilation with impaired contractility of LV
Dilated CM
AD, RV predominant disease including RV dilatation, reduced RV ejection fraction, and focal areas of RV dyskinesia leading to small aneurysms
Arrhythmogenic RV cardiomyopathy (ARCV) or arrhythmogenic RV dysplasia (ARVD)
Imaging findings of dilated CM
Normal to mildly thinned LV myocardium with absent delayed dnhancement. (If present - linear midmyocardial distribution)
Imaging findings of Acute myocarditis
Global or regional areas of T2 hyperintensities (myocardial edema) with relative diffuse linear midmyocardial and subelicardial delayed enhancement
Myocardial fibrosis vs repaired myocardium in myocarditis
Ff up imaging - Delayed enhancement that persists (fibrosis), delayed enhancement that resolves (repaired injured myocardium)
Systemic inflammatory disorder characterized by deposition of noncaseating nonnecrotic granulomas including the heart
Cardiac sarcoidosis
MC involvement of LVNC
Anterolateral and inferolateral segments at the base and mid-cavity levels and much of cardiac apex (sparing the septum)
Imaging findings of cardiac sarcoidosis
Nonspecific mild LV dilatation w/ corresponding nodular midmyocardial LGE (involving inferolateral segment at midcavity level). FDG-PET =Patchy/focal areas of myocardial uptake along anterior and inferior LV wall. (In the background of bilateral mediastinal and hilar lymphadenopathies)
Hypertrabeculation of LV myocardium with relative thinning of adjacent compacted myocardium
Left ventricular noncompaction (LVNC)
Takatsubo vs STEMI and myocarditis
Signal abnormality/edema on T2 in regions of wall motion extending across vascular teritories w/o corresponding delayed enhancement. However edema resolves w/n 2 weeks in contrast to STEMI/myocarditis where it persists 2-3months after
Hallmark of Takatsubo CM
Transient hypokinesis or akinesis of mid and apical segments of LV w/ hypercontractility of basilar segments (leading to hallmark configuration of LV -resembling Takatsubo = japanese octopus pot)
Stress-induced CM frequently seen in postmenopausal women after severe emotional/physical event
Takotsubo CM/Apical ballooning syndrome/Broken heart syndrome
Findings of cardiac MR T2* shortening
Iron overload cardiomyopathy
Potential space where visceral and parietal serous layers are not attached
Pericardial cavity
2 layers of pericardium
1) visceral pericardium - innermost layer that lines the epicardial surface of heart separated from the outermost myocardium by epicardial fat, 2) parietal pericardium -has 2 layers (inner and outer=fibrous)
Staging of Iron overload CM (thru MR T2* mapping)
Normal >20ms (mean 40ms); MILD-MODERATE =10-20ms; SEVERE <10ms (stratify px at risk for heart failire and arrhythmia)
What forms the serous pericardium?
Visceral pericardium and inner layer parietal pericardium =adherent
Normal pericardial thickness on CT
Thin 1-2mm. >4mm is abnormal
Blood supply to pericardium
Branches from thoracic aorta and pericardiophrenic arteries
Cardiac recess: superior to LA, posterior to aorta and MPA, but anterior to oblique sinus
Transverse sinus
Cardiac recess: posterior and superior to the LA
Oblique sinus
MRI Appearance of pericardium
Hypointense to adjacent myocardium on all sequences
Normal volume of pericardial fluid
15-35 ml
T or F. Fibrous (outer) parietal layer is continues over aortic arch and blends w/ deep cervical fascia.
TRUE
Divisions of visceral pericardium
Arterial mesocardium = Portion of visceral pericardium covering the AA and pulmonary trunk; Venous mesocardium = covering the SVC, IVC, and 4 PV
Venous drainage
Thru venae pericardiales draining to azygos v, SVC, or brachiocephalic v.
Innervation
Predom thru branches of phrenic n (sime of posterior pericardium -vagal innervation from esophageal plexus)
Lymphatic drainage
Toward tracheobronchial nodes (and less frequently prepericardial LV and nodes)
Congenital lesion appearing as Smooth, ovoid mass along the hemidiaphragm, (x section) homogeneous thinned-wall without septations and no internal enhancement
Pericardial cyst
Pericardial cyst vs pericardial diverticulum
Diverticula often cannot be distinguished from cyst. Though diverticulum can change can change over time (may disappear)
Pericardial cyst vs cystic tumor
Internal enhancement, heterogeneous signal, thick wall, numerous septations, or invasion into surrounding structures raise rhe possibility of cystic tumors
MC location of congenital pericardial defect
Left side
MCC of pericardial defect or absence of pericardium
Postsurgical
Types of pericardial effusion
Transudative, exudative, hemorrhagic, or pyogenic
Causes of transudative pericardial effusion
CHF, pulm HPN
Associated congenital anomalies of congenital pericardial defect
ASD, PDA, bicuspid aortic valve, or pulmonary abnormalities
Causes of exudative pericardial effusion
Infection (pericarditis), inflammation, malignancy, autoimmune, and trauma
Best radiographic clue of pericardial defect
Interposition of lung b/w MPA and transverse aorta (complete or large defects), bulging of left upper heart border (small defect consistent with LA herniation)
MRI appearance of complete left-sided pericardial defect
Entire heart is typically displaced to the left and cardiac apex is positioned posteriorly
This condition occurs when the pressure in the pericardial space exceeds that of the RV
Pericardial tamponade
MC cause of cardiac tamponade
Pericardial effusion (as little as 100-200 ml especially for noncompliant pericardium dt inflammation or scarring)
Causes of hemorrhagic pericardial effusion
Trauma or aortic dissection
Causes of pyopericardium
MRSA infection
T or F. Most pf idiopathic or viral pericarditis undergo complete resolution
TRUE
Conditions leading to chronic pericardial fibrosis and adhesions
Pericarditis dt TB, radiation, chronic renal failure, or collagen vascular dse (RA, SLE, scleroderma), trauma
Typical CT findings of cardiac tamponade
Moderate/large pericardial collection with compression/flattening of RA and/or RV, flattening or bowing of interventricular septum towards the LV
T or F. Pneumopericardium can cause cardiac tamponade.
True -esp large volume of intrapericardial air
MCC of pericarditis
Viral infection
T or F. Causes of calcific pericarditis are the same as those that lead to fibrous pericarditis.
TRUE
T or F. Patients with fibrous/calcific pericarditis are at increased risk of developing constrictive pericarditis,
TRUE
Condition in which reduced compliance of pericardium leads to elavated ventricular diastolic pressure
Constrictive pericarditis (CP)
T or F. Absence of pericardial thickening exclude the diagnosis of constrictive pericarditis.
FALSE
Imaging findings of diffuse pericardial thickening (bestsee anteriorly) w/ calci, without pericardial effusion and conical shale heart
Constrictive pericarditis
Rare entity presenting both latge pericardial effusion and stiff noncompliant pericardium
Effusive CP
Constrictive pericarditis vs restrictive cardiomyopathy (via MRI)
(Interventricular interdependence). In CP, inspiration leads to flattening of interventricular septum and expiration leads tonormal configuration of septal bowing to the right. This fing is absent in restrictive CM
Pericardial neoplasm associated with HIV infection
Primary effusion lymphoma (appearing as large pericardial effusion)
Similar appearance with epiploic appendagitis centered in juxtapericardial fat assoc. w/pericardial thickening and effusion
Epicardial fat pad necrosis / pericardial fat necrosis (self-limited)
MC primary pericardial neoplasm
Primary pericardial mesothelioma -although rare
CT/MRI demonstrate heterogeneous pericardial effusion and thickening with FDG uptake of the thickening
Primary pericardial mesothelioma
Ddx for fat-containing intrapericardial tumor
Teratomas or lipoblastoma (children); lipoma (adult)
Pericardial lymphangioma vs pericardial cyst
Both show fluid attenuation. Enhancing septations are seen in lymphangioma, absent in pericardial cysts
This malignancy should be considered in any pediatric px w/ heterogeneous
intrapericardial mass located b/w the aortic root and LA
Malignant germ cell tumors
MC pericardial malignancy
Mets
Pericardial lymphangioma vs pericardial hemangioma
Both are T2 hyperintense and have septations. Lymphangiomas show no internal enhancement. Hemangiomas show nodular enhancement w/nprogressive filling
MC malignancies to involve the pericardium thru direct invasion or metastatic spread
Breast ca and lymphoma (others, melanoma and renal cell ca)
Defining feature of LV
aortomitral fibrous tissue (aortic annulus and mitral annulus are coupled together)
Aortic root diameter on CT
Male = 3.63-3.91 cm; female =3.5-3.72cm
MC congenital cardiovascular anomaly
Bicuspid aortic valve (fish mouth appearance
MC type of bicuspid aortic valve
Bicuspid valve w/ raphe (fusion of 2 cusps) = MC fused are (left and right cusps)
Complications of bicuspid aortic valve
Aortic stenosis, COA, aneurysm (repair is recommended b/w 4.5-5cm diameter compared to general population at 5.5cm diameter)
MC position of unicuspid aortic valve
Left posterior position
Clover-leaf morphology of the aortic valve
Quadricuspid aortic valve - very rare
Condition presenting with diminished upper limb pulses or ischemia secondary to narrowing of ipsilateral proximal subclavian artery
Subclavian steal syndrome
Physiologic narrowing of ipsilateral proximal subclavian artery Subclavian steal syndrome Physiologic narrowing of aortic arch b/w L subclavian a. And ligamentum arteriosum
Aortic isthmus
Focal prominence of aorta at ligamentum arteriosum, a normal variant
Ductus diverticulum / ductus bump
T or F. Aortic arch is right-sided.
FALSE
Left AA variant: R inominate and L com carotid have common origin
Two-vessel aortic arch
Left AA variant: L vertebral a has an independent origin from AA (b/w L com carotid and subclavian a)
Four-vessel aortic arch
L AA variant: R subclavian a arises from L subclavian gravelling behind the esophagus to supply the R UE
L aortic arch w/ aberrant R subclav a
L AA bariant: absent diverticulum of Kommerell
Aberrant R subclav a
What is diverticulum of Kommerell?
Aneurysmal dilatation at the origin of the aberrant R subclav a., an embryologic remnant of dorsal aortic arch
R arch variant: 1st branch is L brachiocephalic (divides into L comm carotid and L subclavian a) ff R comm carotid and R subclavian a
R arch with mirror-image
Symmetric four-vessel branching at the thoracic inlet w/ bilateral indentations at
lower trachea and compression of posterior esophagus
Double aortic arch
R arch variant: 1st branch is L comm carotid, ff R carotid, R subclav, and aberrant L subclav arteries
R AA w/ aberrant L subclavian artery
High location of aortic arch above the level of clavicle extremely rare)
Cervical aortic arch
Discontinuity of aa in which there is complete absence or fibrous remnant of
interrupted segment
Interrupted AA
In double aortic arch, which arch is larger?
RIGHT arch is larger
All types of interrupted aa require a PDA for survival
TRUE
Most common type of interrupted aa
Type B -interruption b/w L comm carotid and L subclavian (A- distal to L subclav; C -b/w R brachio and L comm carotid
Focal narrowing of aorta adj to ductus arteriosus
Juxtaductal COA
Anomaly associated with bicuspid aortic valve and Turner syndrome
COA
Type of COA: severe, longer segment involvement, present in infancy w/ systemic hypoperfusion
Preductal COA
Type of COA: present in adulthood w/ HPN and signs of L heart failure
Postductal COA
T or F. Extensive collateral formation in COA may equalize UE and LE blood pressure.
TRUE
Frontal xray finding of “figure of 3” sign
COA
Rib notching in COA involves what ribs?
Bilateral central rib notching (posterior 4th to 8th ribs)
COA vs pseudocoarctation
Both = assoc w/ bicuspid aortic valve. Pseudocoarctation lacks pressure gradient and arterial collateral formation, though may be assoc w/ HPN nad aneurysm
Congenital elongation w/ prominent kinking of aorta at the aortic isthmus
Pseudocoarctation
This is an indirect sign of previous atherosclerotic plaque rupture and can lead to thrombiembolic events
Plaque ulceration
MCC of acquired sinus Valsalva aneurysm
Pseudoaneurysms (resulting from bacterial aortic valve endocarditis or aortic surgery)
This is a sign of intimal disruption
Penetrating atherosclerotic ulcer
Connective tissue disordrss associated with Congenital sinus Valsalva aneurysms
Marfan, Ehlers-Danlos, Loey-Dietz syndromes
MC involved sinus in aneurysm
RIGHT sinus of Valsalva
Congenital heart disease associated with congenital sinus Valsalva aneurysms
Bicuspid aortic valve, VSD
MC involved structure to rupture as a complication of aneurysm
RV and RA
Term used when aortic annulus and prox ascending aorta are dilated
Annuloaortic ectasia (characteristic “tulip” appearance of aortic root)
Definition of thoracic aortic aneurysm (TAA)
> 4cm diameter (intact vessel wall)
MC location of TAA
50% ascending (prox to R brachiocephalic a); 40% descemding aorta (distal to L subclavian); 10% aortic arch
MCC of TAA
atherosclerosis (MC descending aorta)
Conditions associated with ascending aortic aneurysm
Giant cell arteritis, rheumatic fever, relapsing polychondritis
Independent risk factor for ascending TAA, unrelated to presence of associated aortic stenosis
Bicuspid valve
Complications of ascending aortic aneurysms
Dissection or rupture (rupture is the leading cause of death)
Condition associated with aneurysm of the ascending aorta, aortic arch, arch vessels, abdominal aorta and pulmonary arteries
Takayasu arteritis
Sign of impending rupture of aneurysm
Focal cresentic hyperateenuation in mural thrombus
Indication for TAA repair in the setting of connective tissue disease (Marfan)
> 5 cm
Indication for repair of acsending thoracic aneurysm
> 5.5 cm and/or interval growth of >0.5 cm (in 6 months) or 1 cm (in 1 yr)
MCC of descending thoracic aortic aneurysm
Atherosclerotic disease
Complications of descending TAA
Dissection, rupture, fistula formation to esophagus/airways
Risk factors for rupture of descending TAA
Age, size >5cm, HPN, smoking, and COPD
Conditions included in Acute Aortic Syndrome (AAS)
Aortic dissection, acute intramural hematoma (IMH), and Penetrating aortic ulcer (PAU)
Indication for descending TAa repair
Size >6.5 cm and/or interval growth of >0.5 cm in 6months or 1cm in 1 yr
T or F. AAS share common clinical presentation but can be distinguished thru imaging
TRUE
stanford system: type of dissection involving ascending aorta (proximal to
innominate a)
Type A - require immediate surgical management w/ stent-graft placement
Stanford system: type of dissection involving only the descending aorta (distal to L subclavian artery)
Type B - managed medically unless w/ evidence of end-organ ischemina or impending rupture
MCC of aortic dissection
Marfan and Ehler-Danlos syndromes (congenital); chronic hypertension (acquired)
Stanford system: dissection involving the aortic arch but do not extend proximal to
innominate
Type B with aortic arch involvement
MCC location of intimomedial tear
Along R lateral wall of ascending aorta, 1-2cm from sinotubular jxn, or in prox descending aorta nezr insertion of of ligamentum arteriosum
CXR findings of aortic dissections
Tracheal deviation, mediastinal widening, loss of aortic knob contour, enlargement of ascending/descending aorta, pericardial effusion, inward displacement of intimal calcifications
True vs false lumen in aortic dissection
True lumen has smaller lumen with increase contrast opacification and acute angle of dissection flap in relation to false lumen, (dt increased pressure)
Described as acute hemorrhage within the aortic wall without communication w/ aortic lumen (dt rupture of vasa vasorum w/n media)
Intramural hematoma (IMH)
NECT findings of continuous, cresentic, hyperdense thickening of aortic wall w/
inward displacement of atherosclerotic calcifications
IMH
T or F. IMH os also classified by Stanford system (similar w/ Aortic dissections).
TRUE
Internal erosion into aortic media on the background of severe atherosclerosis
PAU
PAU vs Ulcerated plaques
PAU =crater-like shape extending beyond the calcified intima; Complex ulcerated plaques = more jagged appearing and do not extend beyond intima
CECT findings of focal contrast outpouching in the aorta w/c extends beyond calcified
intima
PAU
MC location of PAU
Descending aorta (worse prognosis at aortic root or prox ascending aorta)
T or F. Rupture appears to more common than dissection in the setting of PAU
TRUE
MCC of aortic psuedoaneurysm
Traumatic aortic injury or in postoperative setting
MC site of traumatic thoracic pseudoaneurysms
Aortic isthmusb(narrowing b/w distal arch and ligamentum arteriosum)
Focal irregular outpouching of aorta sec to intimomedial disruption w/ extravasation contained by adventitia and surrounding mediastinal tissues
Aortic pseudoaneurysm
MC site of postoperative pseudoaneurysms
Ascending aorta at sites of aortic puncture, cannulatoon, and/or cross-clamping
Primary imaging modality for detecting pseudoaneurysms
Thoracic CTA -focal irregular outpouching of contrast beyond aortic lumen w/ narrow neck (true aneurysm has large neck neck)
What are the different forms of aortic fistulas?
Aortoesophageal, aortopleural, aortobronchial, etc
Causes of aortic fistulas
Anerysm rupture, PAU, foreign body ingestion w/ esophageal perforation, intrathoracic malignancies, and postaortic endovascular stenting
MC site in Acute traumatic aortic injury (ATAI)
Aortic root, aortic isthmus (maximum traction); diaphragmatic aortic hiatus -less common
T or F. Native aorta is resistant to infection.
TRUE
What is luetic aortitis?
Infectious aortitis caused by tertially syphilis
