Teaching Cases
JAN BOGAERT
Cases 81-100
CLINICAL CARDIAC MRI
SECOND EDITION
Cases 81-100


‘Fixed’ perfusion defect

Comprehensive MRI in IHD

Inducible myocardial ischemia

Post MI aneurysm
Bicuspid aortic valve

RCM with secondary valve regurgitation

MV prolapse

Severe aortic valve stenosis

Parachute mitral valve

False aneurysm post MI

Tricuspid mitral valve


Carcinoid heart disease
Aneurysm post surgery for Aortic
Coarctation

Ischemic cmp secondary to aortic
dissection

Giant aortic aneurysm

Aortic dissection (Stanford B)

Cardiac paraganglioma

Congenitally corrected TGA

Stress perfusion defect in LAD Territory

Recurrent ischemia post-revascularization
Abbreviations
 Ao, aorta / AR, aortic regurgitation / AS, aortic stenosis / ARVC-D,
arrhythmogenic RV cardiomyopathy-dysplasia / ASD, atrial septal defect / AV,
aortic valve / CAD, coronary artery disease / CMP, cardiomyopathy / CT,
computed tomography / DCM, dilated cardiomyopathy / DILV, double inlet LV /
EDV, end-diastolic volume / EF, ejection fraction / ESV, end-systolic volume /
FFR, fractional flow reserve / HCM, hypertrophic cardiomyopathy / ICD,
intracardiac device / IVC, inferior vena cava / LA, left atrium / LV, left ventricle /
LVM, left ventricular mass / LVNC, left ventricular non-compaction / LVOT, LV
outflow tract / MAPCA, major aortic pulmonary collateral artery / MI, myocardial
infarction / MPI, myocardial perfusion imaging / MR, mitral regurgitation / MV,
mitral valve / MVL, mitral valve leaflet / PAHT, pulmonary arterial hypertension /
PAPVR – partial anomalous pulmonary venous return / PC-MRI, phase-contrast
MRI / PCI, percutaneous coronary intervention / PR, pulmonary regurgitation /
PS, pulmonary stenosis / PV, pulmonary valve / RA, right atrium / RFA,
radiofrequency ablation / RV, right ventricle / RVOT, RV outflow tract / STEMI,
ST-elevation MI / SVC, superior vena cava / TGA, transposition of the great
arteries / TOF, tetralogy of Fallot / TR, tricuspid regurgitation / US, ultrasound /
UVH, univentricular heart / VSD, ventricular septal defect / WT, wall thickness.
Bicuspid Aortic Valve
 48-year-old man with bicuspid aortic valve, mixed aortic stenosis and
regurgitation.
 Cardiac MRI: LV EDV 263 ml – SV 164 ml – EF 53% - LVM 235 g / RV EDV 174
ml – SV 92 ml – EF 53%. Functionally bicuspid aortic valve with peak velocity
of 5.5 m/s (121 mm Hg) – regurgitation of 75 ml/hb. Mildly dilated ascending
aorta: 41 mm. Cardiac CT: thickened, focally calcified leaflets.
 Findings of pressure/volume overloaded LV due to calcified bicuspid aortic
valve.
Restrictive CMP with Secondary Valve Regurgitation
 72-year-old woman known with restrictive cmp of unknown origin with
secondary mitral and tricuspid valve regurgitation.
 LV EDV 287 ml – SV 171 ml - EF 60% / RV EDV 230 ml – SV 140 ml – EF 60%.
 Severe MR (80 ml regurgitant volume) and TR (47 ml regurgitant volume).
 Giant atria: LA 13,5 x 12,9 cm – 1700 ml / RA 17,3 x 9,2 cm – 1300 ml.
Mitral Valve Prolapse
 37-year-old woman with MV prolapse and severe MR.
 LV EDV 270 ml – SV 143 ml – EF 53% / RV EDV 147 ml – SV 74 ml – EF 51%.
Severe prolapse of both MV leaflets with severe MR and LA dilatation.
Thickened, hypo-intense appearance of MV leaflets and chordae/papillary
muscles enhancing on late Gd imaging: suggestive of fibrotic changes.
See Fig. 22 Valvular Heart Disease
Severe Aortic Valve Stenosis
 56-year-old man with long-standing calcified aortic stenosis and severe
compensatory concentric LV hypertophy.
 LV EDV 157 ml – EF 69% - LVM 275 gram. Maximal end-diastolic septal wall
thickness 25 mm. Late Gd imaging shows multiple areas of focal myocardial
enhancement. Functionally bicuspid aortic valve with thickened leaflets and
restricted AV opening. PC-MRI shows peak velocity over AV of 5.6 m/s
(gradient of 125 mm Hg).
See Fig. 15 Valvular Heart Disease
Parachute Mitral Valve
 15-year-old man presenting with exercise related pain in left hemithorax.
Cardiac auscultation: regular heart rythm with protosystolic click. Systolic
murmur 2/6 in L4 and R2.
 LV EDV 93 ml – EF 57% - LVM 129g – septal WT 11 mm. Funnel-shaped
appearance of mitral valve without evidence of MS (orifice of 2.9cm2 –
gradient 3 mm Hg). Common origin of papillary muscle along the LV lateral
wall: findings of parachute mitral valve.
Tricuspid Mitral Valve
 42-year-old man with known MR,
referred for MRI to rule out structural
heart diseases.
 Presence of 3-leaflet mitral valve
(anterior/lateral/inferior leaflet) with
accessory papillary muscle (arrow) in
between anterolateral and
posteriomedial muscle. Mild MV
prolapse and MR of 11 ml/hb.
 Cardiac CT confirms MRI findings.
Carcinoid Heart Disease
 75-year-old man, presenting wiht right heart failure (dyspnea, fatigue, swollen
legs, vague abdominal pain), liver US and CT (left panel) show diffuse liver
metastasis. Liver biopsy: metastases of neuro-endocrine carcinoma.
 Cardiac MRI: LV EDV 100 ml – SV 70 ml – EF 70% / RV EDV 197 ml – SV 147
ml – EF 74%. Thickened, nearly immobile, TV with non-closure of TV during
systole and severe TR (PC–MRI: regurgitant volume of 92 ml/hb). Severe RA
dilatation. Thickened appearance of RV chordae but overall preserved RV
contractility.
See Fig. 34 Valvular Heart Disease
Ischemic CMP secondary to Aortic Dissection
 54-year-old man with recent history of type B aortic dissection complicated
with acute ischemia of lower limbs, necessitating urgent axillofemoral graft.
 10 days later sudden antegrade extension of dissection (conversion into type A
dissection) with acute cardiovascular collapse, urgent aortic surgery but
prolanged myocardial ischemia and post-surgery cardiac failure.
 LV EDV 358 ml – EF 22% - diffuse severe hypokinesia. Late Gd imaging
shows diffuse 25% to 75% transmural enhancement, representing diffuse
subendocardial myocardial fibrosis secondary to cessation of coronary
perfusion. Bilateral pleural fluid. Residual dissection in descending aorta.
Stress Perfusion Defect in LAD Territory
 STRESS MPI
 REST MPI
See Fig. 8 Myocardial Perfusion
Recurrent Ischemia Post-Revascularization (1)
43-year-old woman with recent history of CAD, with LAD stent for ACS complicated with LM
dissection, urgent CABG (GSV end-to-side LAD, GSV side-to-side ramus angularis, GSD endto-side LCx). Recurrent exercise-related interscapular chest pain.
 Cardiac MRI shows normal LV volumes (EDV 166 ml) and function (EF 56%) at rest (left
panel) but extensive and long-lasting perfusion defect during persantine stress (segments
1,2,6,7,8,11,12,13,14). Real-time cine MRI (right panel) immediately after perfusion MRI
shows severe dysfunction in non-enhanced mycardial regions. Late Gd imaging shows
smal(ler) transmural enhancement in anterolateral wall (segments 1,7,12).
 Cardiac catheterization shows occlusion of LAD and venous graft to LAD with filling of distal
LAD by RCA collaterals, slow flow in venous graft to LCx.

Recurrent Ischemia Post-Revascularization (2)
Stress perfusion imaging at 2 short-axis
levels (a,b) shows extensive anterior
(including anteroseptum and lateral
wall, arrows, a,b).
 Cine imaging performed immediately
following stress perfusion imaging
shows severely impaired myocardial
contractility (due to myocardial
ischemia) in the hypo-perfused
myocardium (arrows, c,d).

‘Fixed’ Perfusion Defect
 45-year-old man with history of PCI for LAD stenosis (2006), MRI performed to
rule inducible ischemia.
 Though LV volumes and function at rest are normal (EDV 115 ml – EF 60%),
the basal and mid LV inferolateral wall show mild hypokinesia. During both rest
perfusion (left middle panel) and persantine stress perfusion (right middle
panel) presence of subendocardial perfusion defect in the inferolateral wall, and
corresponds nicely with the zone of subendocardial enhancement on late Gd
imaging (arrow, right panel). The perfusion abnormalities are caused by lower
capillary density in the scarred myocardium and not by a true perfusion defect.
Comprehensive MRI in IHD (1)
 46-year-old patient with multi-vessel CAD and recent history of NSTEMI.
Cardiac catherization shows occlusion of mid RCA and 2nd lateral branch LCx.
Non-stenotic CAD in LAD. RCA filling by LAD collaterals. PCI 2nd lateral
branch LCx.
 LV EDV 215 ml – SV 111 ml – EF 52%. Mild thinning of the LV mid
anterolateral wall showing mild to moderate hypokinesia.
Comprehensive MRI in IHD (2)
 STRESS MPI
 REST MPI
Comprehensive MRI in IHD (3)
 Rest MPI(previous slide) shows a perfusion
‘defect’ in the LV anterolateral wall,
corresponding to the area of enhancement on
late Gd imaging.
 Stress MPI shows extensive and long-lasting
perfusion defect in LV inferior wall (segments
3,4,9,10,15).
 Late Gd imaging (suboptimal image quality)
shows almost complete transmural enhancement
of the LV anterolateral wall (segments 6,12,16).
 Findings of anterolateral transmural MI, and
extensive stress-induced perfusion defect in RCA
territory. Rest cardiac volumes/function within
normal limits.
Inducible Myocardial Ischemia
20 gamma
dobutamine
40 gamma
dobutamine
PCI (stent) in proximal LAD and
re-stenosis. Coronary angiography
shows 60% stenosis in proximal
LAD with collaterals from LCx to
LAD. FFR > 0.75.
 Cardiac MRI shows normal LV
volumes (EDV 198 ml) and
function (EF 73%).
 Severely decreased wall motion
and wall thickened in LV mid
anterior wall during 40 gamma
dobutamine. Though FFR values
are within normal limits, stress
dobutamine MRI clearly shows
inducible ischemia in mid anterior
wall.
rest
 60-year-old man with history of
Post-MI Aneurysm
 63-year-old patient with previous inferior wall infarction.
 Cine imaging shows relatively broad-based aneurysm with extensive wall
thinning and dyskinetic wall motion. Strong enhancement of the aneurysmal
wall on late Gd imaging. Aneurysmal volume 235 ml. Aneurysmal neck: 68x70
mm.
 LV EDV 448 ml – EF 18%.
 Surgical aneurysmectomy, histology shows completely fibrosed myocardial wall
without residual myocardial tissue: ‘true’ aneurysm.
See Fig. 36 Ischemic Heart Disease
False Aneurysm Post MI
 85-year-old man with history of lateral MI.
 LV EDV 211 ml – SV 58 ml – EF 27%.
 Presence of large aneurysm (24x43x43mm) arising from LV laterobasal wall
(arrows), with presence of a mural thrombus (arrowhead). The aneurysm is
pulsatile, and enhances on late Gd imaging.
 Because of the patient’s age conservative treatment.
 The findings favor the presence of a false and not a true aneurysm with
complete rupture of the myocardial wall, contained by pericardial adhesions.
Aneurysm Post Surgery for Aortic Coarctation
 33-year-old woman with Dacron
patch angioplasty for aortic
coarctation (1981, age 5 years).
 Progressive increase over time of
the diameter of the repair site
from 30 mm (2002)(upper row) to
48 mm (2008)(middle row).
 Redo surgery with tubular graft
(22 mm), follow up MRI
(2009)(lower row) shows mild
dilatation of graft (25 mm).
Giant Aortic Aneurysm
 42-year-old man with history of surgery for aortic coarctation and bicuspid
AV. Follow up cardiac US shows dilated ascending aorta.
 Cardiac MRI shows extensive dilatation of the ascending aorta (85 mm) with
normalization of the diameter distally. No evidence of aneurysm formation or
stenosis at the coarctation site. Functionally bicuspid AV with severe AR
(regurgitant fraction 41%) and secondary LV volume overload.
 Bentall surgery
Aortic Dissection (Stanford B)
 36-year-old woman with history of aortic dissection (Stanford B) for 10 years,
conservative treatment.
 Important dilatation of the entire descending aorta (proximal 52 mm, distal 34
mm), with presence of an intimal flap originating just below the level of the left
subclavian artery and descending distally (rentry at the level of the renal
arteries). The true lumen is the small lumen located anteromedially. Both
lumen are patent. The size of the aneurysm is relatively stable over time
(increase of 5 mm over a period of 10 years).
Cardiac Paraganglioma
 68-year-old man with large paracardiac mass, compressing the LA. Though the
mass has a relatively homogeneous appearance on T1w-imaging (left panel),
cine imaging (left, middle panel), perfusion imaging (right, middle panel) and
late Gd imaging (right panel) show inhomogeneous appearance with strong
peripheral enhancement and central non enhancement representing
liquefaction necrosis.
See Fig. 16 Cardiac Masses
Congenitally Corrected TGA
 58-year-old woman presenting with congenital cardiopathy, referred to MRI
for morphological and functional evaluation.
 Situs solitus, meso-to dextrocardia, congenitally corrected TGA with
atrioventricular and ventricular discordance, right-sided located morphologic
LV, left-sided located morphologic RV, large outlet VSD, (supra)valvular PS
with gradient > 40 mm Hg, left sided aortic arch, RV wall hypertrophy.
See similar case Fig. 12 and Fig. 30 Congenital Heart Disease