CD springer 21-40.pptx

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Teaching Cases
JAN BOGAERT
Cases 21-40
CLINICAL CARDIAC MRI
SECOND EDITION
Cases 21-40
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Apical MI with mural thrombus

Cardiac rhabdomyoma

Iatrogenic aortic valve rupture

Bronchogenic cyst

Acute anteroapical MI

Cardiac hemangioma (2 patients)

Cor pulmonale

Coarctation + AI

ALCAPA + MI

Idiopathic DCM

Cor triatriatum

Tachycardia-induced CMP

Adverse post-infarction LV remodeling

Double-chambered RV

Idiopathic DCM with secondary VHD

ASD (type II)

Cardiac sarcoidosis (2 patients)

Lateral MI (acute phase - follow up)

Cardiac transplantation with humoral
rejection

Athlete’s heart
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 / 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 / PCMRI, 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.
Apical MI with Mural Thrombus
 55-year-old woman presenting with cardiac decompensation secondary to
recent anterior MI. Cardiac catheterization shows occlusion of mid LAD /
positive cardiac enzymes / Q-waves in II, III and aVF.
 Cardiac MRI shows dysfunctional, moderately dilated LV (EDV 203 ml - EF
16%) with dyskinetic, aneurysmally thinned LV apex. Late Gd imaging shows
transmural enhancement in LV apex with mural thrombus.
 Presence of breast implant.
See Fig. 38 Ischemic Heart Disease
Iatrogenic Aortic Valve Rupture (1)
 38-year-old woman presenting with increasing dyspnea post-partum. History
of minimal invasive surgery for MV prolapse with 4/4. Referred to MRI to
exclude post-partum CMP.
 Cardiac MRI shows severely dilated LV (EDV 392 ml – EF 31% - SV 123 ml)
with diffuse severe hypokinesia. Normovolemic and normocontractile RV. The
repaired MV seems to function with small MR (1/4).
 Diastolic regurgitant jet is visible in LVOT.
Iatrogenic Aortic Valve Rupture (2)
 Specific views along the LVOT and flow measurements at the level of the AV show
an important regurgitant jet caused by a rupture of the non-coronary cusp, causing
a severe LV volume overload.
 PC-MRI shows a regurgitant flow of 42 ml/heart beat.
 At surgery a perforation of 8 mm in the non-coronary cusp is found, treated with a
Carpentier Edwards bioprothesis.
 Though new-onset AR (2-3/4) was reported early post MV surgery on cardiac US, it
took about two years to become symptomatic. Symptoms were probably boosted by
pregnancy.
Acute Anteroapical MI
 42-year-old man admitted with ST-elevation MI treated with PCI in mid LAD.
 Cardiac MRI: LV EDV 235 ml - EF 46% / akinesia of anteroseptal anterior wall
and LV apex. Diffuse edema in LV anteroseptal wall – apex with transmural
enhancement on late Gd imaging. Presence of small apical thrombus.
 The extent of dysfunction correlates well with the extent of enhanced
myocardium of short-axis cine images (obtained post-contrast administration).
Note the small non-enhancing thrombus in the most apical short-axis slices.
See Figs. 7 and 8 Ischemic Heart Disease
Cor Triatriatum (1)
 75-year-old man presenting with decreased exercise tolerance, dyspnea grade
III. On invasive coronary angiography no significant CAD.
 Cardiac MRI shows normovolemic (EDV 161 ml) and normocontractile (EF
70%) LV / no abnormal findings on late Gd imaging.
 Incidental finding of membrane in LA separating this chamber in a dorsal and a
ventral one: cor triatriatum.
Cor Triatriatum (2)
 The thin membrane in the left atrium (arrowhead) can be well appreaciated on
cardiac MRI and CT.
 A narrow communication (*, right panel) between the dorsal and ventral
chamber can lead to increased pulmonary venous pressures.
Tachycardia-induced CMP (1)
 25-year-old man with continuous runs of atrial tachycardia (160/min) and
tachycardia-induced cardiomyopathy.
 Pre-ablation cardiac MRI shows severely dilated and dysfunctional LV (EDV
504 ml – EF 9%). Image quality deteriorated by fast, irregular heart rithm.
See Fig. 49 Heart Muscle Diseases
Tachycardia-induced CMP (2)
 Follow-up cardiac MRI (9 months post-ablation) shows significant decrease in
LV EDV 236 ml (vs 504 ml) and improvement in EF 49% (vs 9%).
 Residual region of lower contractility in LV mid inferolateral wall,
corresponding to focal subendocardial enhancement. Though invasive coronary
angiography revealed no abnormalities, the nature of enhancement is most
suggestive of ischemic, possibly emboligenic.
See Fig 19 Ischemic Heart Disease and Fig. 49 Heart Muscle Diseases
Adverse Post-Infarction LV Remodeling
 46-year-old man with large transmural anteroseptoapical MI (infarct size by late Gd
imaging: 49 g).
 Cardiac MRI performed at 1week (left), 4 months (middle left), 1 year (middle right)
and 5 years (right). Concomitant severe concentric LV hypertrophy (LVM 270g –
WT 21 mm) at baseline. FU shows thinning of the infarct area (see LV apex), with
progressive increase in LV EDV, i.e., 167 ml, 180 ml, 230 ml, 257 ml, respectively.
 Thinning of the non-infarcted myocardial walls at FU.
 Findings of adverse LV remodeling that may ultimately progess towards ischemic
heart failure.
See Fig. 3 Ischemic Heart Disease
Double-Chambered RV
 11-year-old asymptomatic boy presenting with a loud systolic precordial
murmur, having a history of a spontaneously regressed RV rhabdomyoma.
 Presence of fibro-muscular web dividing the RV in a high-pressure inlet.
chamber and a low-pressure outlet. Orifice 1.5cm2 with pressure gradient of 77
mm Hg (see right panels)
 Surgical resection of the web and enucleation of small residual rhabdomyoma
in ventricular septum.
ASD (type II)
 42-year-old man presenting with severe PAHT (55 mm Hg), MRI performed to
exclude CHD.
 Severely dilated RV (EDV 477 ml – EF 45%) with inversion and paradoxical
motion of ventricular septum. Dilated RA. Presence of a large ASD. Normal
entrance of pulmonary veins in LA. Severely dilated pulmonary arteries. PCMRI shows aortic flow (63 ml/hb) and pulmonary trunk (231 ml/hb), yielding
Qp/Qs of 3.6.
See similar case Fig. 14 Congenital Heart Disease
Lateral MI (Acute Phase)
 49-year-old man admitted with ST-elevation MI, occlusion of 1st lateral branch
LCx.
 Cardiac MRI performed at day 3 post-PCI shows dysfunctional LV (EDV 167 ml
- EF 22%) with akinesia of the LV lateral wall. Images post contrast
administration shows transmural enhancement in LV lateral wall with presence
of large no-reflow zone.
See similar case Fig. 34 Ischemic Heart Disease
Lateral MI (Healed Phase)
 Follow up study one year post-infarction.
 LV EDV 255 ml – EF 36%.
 Infarct healing with fibrotic repair and thinning of the lateral wall (strongly
enhancing on late Gd imaging). Negative LV remodeling with significant
increase in LV volumes and loss in EF.
See similar case Fig. 34 Ischemic Heart Disease
Athlete’s Heart
 26-year-old man – semi-professional soccer player.
 LV EDV 243 ml – SV 176 ml – EF 72% / RV EDV 230 ml - SV 170 ml - EF 73 %.
 Septal WT 12.4 mm – lateral WT 12 mm, normal regional contractility.
 PC-MRI shows normal inflow physiology.
 Findings compatible with exercise-related (physiological) biventricular
remodeling.
Cardiac Rhabdomyoma
 One-month-old girl presenting with a large paracardiac mass on cardiac
ultrasound.
 Cardiac mass shows a large well-defined mass along the left ventricle, clearly
distinguishable from the adjacent myocardium. dynamic (cine) imaging shows
that the myocardial contractility is not affected.
See Fig. 13 Cardiac Masses
Bronchogenic Cyst
 48-year-old man presenting with repeated





symptoms of malaise, retrosternal chest and
fever.
Incidental finding of infracarinal mass.
Cardiac MRI performed for further
investigation.
Presence of a well-defined structure between
ascending aorta and thoracic spine,
compressing the SVC and LA.
An intra-lesional fluid-fluid level is clearly
visible.
At surgery, a chocolate-colored fluid,
proteinaceous fluid was found. Histology
showed presence of respiratory epithelium,
cartilage islands, and hair cells: findings
compatible with a bronchogenic cyst.
See Fig. 31 Cardiac Masses
Cardiac Hemangioma (patient 2)
 One-day-old girl with prenatal diagnosis of pericardial effusion and RA mass.
MRI performed after urgent pericardiocentesis because of cardiac tamponade.
Large mass attached to RA wall extending to RA appendage.
 First-pass perfusion MRI shows strong enhancement similar to the
enhancement of the surrounding blood, suggestive of benign highly vascular
tumor (type hemangioma).
 Surgery shows capillary hemangioma (2g).
See Fig. 17 Cardiac Masses
Cardiac Hemangioma (patient 2)
 50-year-old man presenting with a thickened appearance of the LV basal
anteroseptal wall, maximal wall thickness of 29 mm.
 Though findings are compatible with asymmetric septal form of HCM, first pass
perfusion MRI (panel, middle right) shows very strong, well-defined
enhancement of the thickened myocardium.
 Invasive coronary angiography shows a network of small arterial branches
supplied by the LAD coronary artery.
 Findings primarily suspected of cardiac hemangioma.
See Fig. 18 Cardiac Masses
Cor Pulmonale
 29-year-old man presenting with dyspnea (NYHA grade III-IV). Severe
pulmonary arterial hypertension (mPAP 59 mm Hg, PCWP 19 mm Hg, no
nitric-oxide response). Obesitas (BMI: 40) and obstructive sleep apnea
syndrome.
 Cardiac MRI: LV EDV 153 ml – EF 49% / RV EDV 216 ml – EF 35% hypertrophic and hypokinetic RV wall. Early diastolic inversion of ventricular
septum. Dilated pulmonary trunk (42 mm) and arteries: findings compatible
with severe cor pulmonale with RV pressure overload, diastolic and systolic
dysfunction.
See similar case Fig. 1 Pulmonary Hypertension
Endocarditis + Aortic Coarctation (1)
 19-year-old man presenting palpitations and decreased exercise tolerance
since 1.5 years, admitted with fever, weight loss (-10 kg), hemorrhagic sputa.
 Cardiac US (TEE) shows bicuspid aortic valve with prolapse and a 1cm
floating structure attached: findings compatible with endocarditis.
 Cardiac MRI shows dilated LV (EDV 377 ml / EF 42%), a functionally bicuspid
aortic valve with an important AI (54% regurgitant fraction), a moderate
pericardial effusion.
 The valvular vegetation can be suspected on dynamic cine images.
Cardiac US: courtesy of Prof. Dr. JU Voigt
Endocarditis + Aortic Coarctation (2)
 As an incidental finding, the patient had an aortic coarctation (suggested by
cardiac US). The minimal diameter is 8 mm, presence of important collateral
vessels.
 Patient underwent aortic valve replacement (homograft), at surgery 2 valvular
vegetations were found with presence of abscesses in the subaortic curtain. The
aortic coarctation was treated with a balloon dilatation and stenting.
 Follow up cardiac MRI 3 years later (right panel) shows normalization of LV
EDV (161 ml) but persistence of LV dysfunction (EF 39%).
ALCAPA with secondary MI (1)
 68-year-old woman presenting with atypical angina and dyspnea (NYHA II).
 Invasive coronary angiography shows tortuous heavily dilated coronary arteries
with a suspicion of LAD originating from pulmonary trunk.
 Cardiac MRI: both the RCA and LCx have a normal origin but show heavily tortous
and dilated (max. diameter 10 mm). The LAD, however, arises from the pulmonary
trunk and has dilated and tortuous appearance.
 Findings of (partial) anomalous left coronary artery arising from pulmonary artery
(ALCAPA syndrome).
See Fig. 16 Coronary Artery Disease – See similar case Fig. 45 Congenital Heart Disease
ALCAPA with secondary MI (2)
 LV EDV 379 ml, EF 25% / thinning and a-to dyskinesia of the LV apical
anteroseptal wall showing >50% transmural enhancement on late Gd imaging.
 The extensive infarcisation in the LAD perfusion territory is most likely
secondary to chronic hypo-oxygenation.
 Conservative treatment for heart failure symptoms.
See Fig. 16 Coronary Artery Disease – See similar case Fig. 45 Congenital Heart Disease
Idiopathic DCM
 11-year-old girl presenting with DCM.
 Cardiac MRI shows severely dilated and dysfunctional ventricles (LV EDV 324
ml - EF 9% / RV EDV 520 ml – EF 7%) with left-sided cardiac rotation / dilated
atria and dilated IVC / mild pericardial effusion.
 Late Gd imaging shows diffuse strong enhancement of epicardial LV borders
and diffuse RV enhancement. Myocardial biopsy shows myocardial
replacement fibrosis.
See Fig. 27 Heart Muscle Diseases
Idiopathic DCM with secondary VHD
 58-year-old man presenting with cardiac decompensation, history of idiopathic
DCM with secondary MR and AR, treated with AV replacement and MV plasty.
Aneurysmal dilation of ascending aorta (53 mm).
 Cardiac MRI shows severe dilated LV (EDV 470 ml – EF 19%), regional
moderate to severe hypokinesia, moderately severe MR with LA enlargement,
and right-sided pleural effusion. Late Gd imaging shows midwall septal
enhancement, suggesting replacement fibrosis as seen in DCM.
Cardiac Sarcoidosis (patient 1)
 47-year-old man presenting with cardiomyopathy of unknown origin, cardiac
US shows low EF (40%), mediastinal and hilar lymph nodes on chest CT.
 Cardiac MR image quality limited by arrhythmias. Real-time cine MRI shows
dilated dysfunctional ventricles (LV EDV 193 ml – EF 35% / RV EDV 270 ml EF 25%), with flattening of ventricular septum. Dilated RA. Late Gd imaging
shows diffuse patchy subepicardial enhancement in LV, and diffuse RV
enhancement.
 Cardiac and skin biopsy show granulomatous inflammation (sarcoidosis).
See Fig. 60 Heart Muscle Diseases
Cardiac Sarcoidosis (patient 2)
 42-year-old man with sarcoidosis (positive
lymph node biopsy) referred for cardiac MRI
because cardiac US shows borderline to mild
LV hypertrophy, diastolic dysfunction with
moderately dilated LA and 1st degree AV
block (PR 248 ms).
 Cardiac MRI: EDV 184 ml – EF 58%.
Thnning of mid anteroseptal wall, apical
inferior wall (segments 7,8,11,15), while
segment 14 is mildy thickened. Hypokinesia
apicoinferior (segments 14,16).
 Late Gd imaging shows patchy enhancement
in segments 2,3,8,9,14,15,16,17 – focal
enhancement of RV anterior/inferior wall.
 Findings of biventricular involvement of
sarcoidosis.
Cardiac Transplantation with Humoral Rejection
 26-year-old man with cardiac transplant (2005) for familial cmp, admitted with
progressive graft deterioration and dysfunction.
 Cardiac MRI shows biventricular systolic dysfunction (LV EDV 216 ml – EF 37% /
RV EDV 171 ml – EF 42%) with thickened walls (LVM 252 g – septum 19 mm).
Moderate pericardial effusion. Strong, diffuse enhancement in LV and RV wall.
 Although cardiac MRI findings are compatible with cardiac amyloidosis, in the
clinical context findings are suspected of diffuse fibrose/inflammation.
 Myocardial biopsy is negative for cellular rejection, but CD4 staining and HLA-AS
are positive suggesting humoral rejection.
See Fig 9 Heart Failure and Heart Transplantation
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