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Teaching Cases Jan Bogaert Cases 81-100 ClinicalCardiac MRI SecondEdition
Cases 81-100 • Bicuspid aortic valve • RCM with secondary valve regurgitation • MV prolapse • Severe aortic valve stenosis • Parachute mitral valve • Tricuspid mitral valve • Carcinoid heart disease • Ischemic cmp secondary to aortic dissection • Stress perfusion defect in LAD Territory • Recurrent ischemia post-revascularization • ‘Fixed’ perfusion defect • Comprehensive MRI in IHD • Inducible myocardial ischemia • Post MI aneurysm • False aneurysm post MI • Aneurysm post surgery for Aortic Coarctation • Giant aortic aneurysm • Aortic dissection (Stanford B) • Cardiac paraganglioma • Congenitally corrected TGA
Abbreviations Ao, aorta / AR, aorticregurgitation / AS, aortic stenosis / ARVC-D, arrhythmogenic RV cardiomyopathy-dysplasia / ASD, atrial septal defect / AV, aorticvalve / CAD, coronaryarterydisease / CMP, cardiomyopathy / CT, computedtomography / DCM, dilated cardiomyopathy / DILV, double inlet LV / EDV, end-diastolic volume / EF, ejectionfraction / ESV, end-systolic volume / FFR, fractionalflow reserve / HCM, hypertrophic cardiomyopathy / ICD, intracardiacdevice / IVC, inferiorvenacava / LA, left atrium / LV, leftventricle / LVM, leftventricularmass / LVNC, leftventricularnon-compaction / LVOT, LV outflowtract / MAPCA, major aorticpulmonarycollateralartery / MI, myocardialinfarction / MPI, myocardialperfusionimaging / MR, mitral regurgitation / MV, mitral valve / MVL, mitral valveleaflet / PAHT, pulmonaryarterialhypertension / PAPVR – partialanomalouspulmonaryvenous return / PC-MRI, phase-contrast MRI / PCI, percutaneous coronaryintervention / PR, pulmonaryregurgitation / PS, pulmonary stenosis / PV, pulmonaryvalve / RA, right atrium / RFA, radiofrequencyablation / RV, right ventricle / RVOT, RV outflowtract / STEMI, ST-elevation MI / SVC, superior venacava / TGA, transposition of the great arteries / TOF, tetralogy of Fallot / TR, tricuspidregurgitation / US, ultrasound / UVH, univentricularheart / VSD, ventricular septal defect / WT, wallthickness.
BicuspidAorticValve 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%. Functionallybicuspidaorticvalvewithpeakvelocity of 5.5 m/s (121 mm Hg) – regurgitation of 75 ml/hb. Mildlydilatedascending aorta: 41 mm. Cardiac CT: thickened, focally calcified leaflets. Findings of pressure/volume overloaded LV due to calcified bicuspid aortic valve.
Restrictive CMP withSecondaryValveRegurgitation 72-year-old womanknownwithrestrictivecmp of unknownoriginwithsecondary mitral and tricuspidvalveregurgitation. LV EDV 287 ml – SV 171 ml - EF 60% / RV EDV 230 ml – SV 140 ml – EF 60%. SevereMR (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 ValveProlapse 37-year-old womanwith MV prolapse and severe MR. LV EDV 270 ml – SV 143 ml – EF 53% / RV EDV 147 ml – SV 74 ml – EF 51%. Severeprolapse of both MV leafletswithsevere MR and LA dilatation. Thickened, hypo-intense appearance of MV leaflets and chordae/papillarymusclesenhancingon late Gd imaging: suggestive of fibrotic changes. See Fig. 22 Valvular Heart Disease
SevereAorticValve Stenosis 56-year-old man withlong-standingcalcifiedaortic stenosis and severecompensatoryconcentric LV hypertophy. LV EDV 157 ml – EF 69% - LVM 275 gram. Maximalend-diastolic septal wallthickness 25 mm. Late Gd imaging shows multiple areas of focalmyocardialenhancement. Functionallybicuspidaorticvalvewiththickenedleaflets and restricted AV opening. PC-MRI shows peakvelocity 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 withexerciserelated pain in lefthemithorax. Cardiacauscultation: regularheartrythmwithprotosystolic click. Systolicmurmur 2/6 in L4 and R2. LV EDV 93 ml – EF 57% - LVM 129g – septal WT 11 mm. Funnel-shapedappearance 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 withknown MR, referred for MRI to rule out structural heartdiseases. • Presenceof 3-leaflet mitral valve (anterior/lateral/inferiorleaflet) withaccessorypapillarymuscle (arrow) in between anterolateral and posteriomedialmuscle. Mild MV prolapse and MR of 11 ml/hb. • Cardiac CT confirms MRI findings.
Carcinoid Heart Disease 75-year-old man, presenting wiht right heartfailure (dyspnea, fatigue, swollenlegs, vagueabdominal pain), liver US and CT (left panel) show diffuse livermetastasis. Liverbiopsy: metastases of neuro-endocrinecarcinoma. Cardiac MRI: LV EDV 100 ml – SV 70 ml – EF 70% / RV EDV 197 ml – SV 147 ml – EF 74%. Thickened, nearlyimmobile, TV withnon-closure of TV duringsystole and severe TR (PC–MRI: regurgitant volume of 92 ml/hb). Severe RA dilatation. Thickenedappearance of RV chordaebut overall preserved RV contractility. See Fig. 34 Valvular Heart Disease
Ischemic CMP secondary to AorticDissection 54-year-old man with recent history of type B aorticdissectioncomplicatedwith acute ischemia of lowerlimbs, necessitating urgent axillofemoralgraft. 10 days later suddenantegradeextension of dissection (conversioninto type A dissection) with acute cardiovascularcollapse, urgent aorticsurgerybutprolangedmyocardialischemia and post-surgerycardiacfailure. LV EDV 358 ml – EF 22% - diffuse severehypokinesia. Late Gd imaging shows diffuse 25% to 75% transmural enhancement, representing diffuse subendocardial myocardialfibrosissecondary to cessation of coronaryperfusion. Bilateralpleuralfluid. Residualdissection in descending aorta.
Stress Perfusion Defect in LAD Territory STRESS MPI • REST MPI See Fig. 8 MyocardialPerfusion
RecurrentIschemiaPost-Revascularization (1) • 43-year-old womanwithrecenthistory of CAD,with LAD stent for ACS complicatedwith LM dissection, urgent CABG (GSV end-to-side LAD, GSV side-to-sideramusangularis, GSD end-to-sideLCx). Recurrentexercise-relatedinterscapularchest pain. • Cardiac MRI shows normal LV volumes (EDV 166 ml) and function (EF 56%) at rest (left panel) butextensive and long-lastingperfusion defect duringpersantine stress (segments 1,2,6,7,8,11,12,13,14). Real-timecine MRI (right panel) immediatelyafterperfusion MRI shows severedysfunction in non-enhancedmycardialregions. 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.
RecurrentIschemiaPost-Revascularization (2) Stress perfusionimaging at 2 short-axislevels (a,b) shows extensiveanterior (includinganteroseptum and lateralwall, arrows, a,b). Cineimagingperformedimmediatelyfollowing stress perfusionimaging shows severelyimpairedmyocardialcontractility (due to myocardialischemia) in the hypo-perfusedmyocardium (arrows, c,d).
‘Fixed’ Perfusion Defect 45-year-old man withhistory of PCI for LAD stenosis (2006), MRI performed to ruleinducibleischemia. 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 perfusionabnormalities are causedbylowercapillarydensity in the scarredmyocardium and notby a trueperfusion defect.
Comprehensive MRI in IHD (1) 46-year-old patientwithmulti-vessel CAD and recent history of NSTEMI. Cardiaccatherization shows occlusion of mid RCA and 2nd lateralbranchLCx. Non-stenotic CAD in LAD. RCA fillingby LAD collaterals. PCI 2nd lateralbranchLCx. LV EDV 215 ml – SV 111 ml – EF 52%. Mild thinning of the LV mid anterolateral wallshowing mild to moderate hypokinesia.
Comprehensive MRI in IHD (2) • STRESS MPI • REST MPI
Comprehensive MRI in IHD (3) Rest MPI(previousslide) shows a perfusion ‘defect’ in the LV anterolateral wall, corresponding to the area of enhancementon late Gd imaging. Stress MPI shows extensive and long-lastingperfusion defect in LV inferiorwall (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 extensivestress-inducedperfusion defect in RCA territory. Rest cardiac volumes/functionwithinnormallimits.
InducibleMyocardialIschemia 60-year-old man withhistory of PCI (stent) in proximal LAD and re-stenosis. Coronaryangiography shows 60% stenosis in proximal LAD withcollateralsfromLCx to LAD. FFR > 0.75. Cardiac MRI shows normal LV volumes (EDV 198 ml) and function (EF 73%). Severelydecreasedwall motion and wallthickened in LV midanteriorwallduring 40 gamma dobutamine. Though FFR values are withinnormallimits, stress dobutamine MRI clearly shows inducibleischemia in midanteriorwall. rest 20 gamma dobutamine 40 gamma dobutamine
Post-MIAneurysm 63-year-old patientwithpreviousinferiorwallinfarction. Cineimaging shows relativelybroad-basedaneurysmwithextensivewallthinning and dyskineticwall motion. Strong enhancement of the aneurysmalwallon late Gd imaging. Aneurysmal volume 235 ml. Aneurysmalneck: 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
FalseAneurysm Post MI 85-year-old man withhistory of lateral MI. LV EDV 211 ml – SV 58 ml – EF 27%. Presence of largeaneurysm (24x43x43mm) arisingfrom LV laterobasalwall (arrows), withpresence of a muralthrombus (arrowhead). The aneurysm is pulsatile, and enhanceson late Gd imaging. Because of the patient’sageconservativetreatment. The findings favor the presence of a false and not a trueaneurysmwith complete rupture of the myocardialwall, containedbypericardialadhesions.
Aneurysm Post Surgery for Aortic Coarctation 33-year-old womanwithDacronpatchangioplasty for aortic coarctation (1981, age 5 years). Progressiveincrease over time of the diameter of the repair site from 30 mm (2002)(upper row) to 48 mm (2008)(middlerow). Redosurgerywithtubulargraft (22 mm), follow up MRI (2009)(lowerrow) shows mild dilatation of graft (25 mm).
GiantAorticAneurysm 42-year-old man withhistory of surgery for aortic coarctation and bicuspid AV. Follow up cardiac US shows dilatedascending aorta. Cardiac MRI shows extensivedilatation of the ascending aorta (85 mm) withnormalization of the diameter distally. No evidence of aneurysmformationor stenosis at the coarctation site. Functionallybicuspid AV withsevere AR (regurgitant fraction 41%) and secondary LV volume overload. Bentallsurgery
AorticDissection (Stanford B) 36-year-old womanwithhistory of aorticdissection (Stanford B) for 10 years, conservativetreatment. Important dilatation of the entiredescending aorta (proximal 52 mm, distal 34 mm), withpresence of anintimal flap originatingjustbelow the level of the leftsubclavianartery and descendingdistally (rentry at the level of the renal arteries). The truelumen is the smalllumenlocatedanteromedially. Both lumen are patent. The size of the aneurysm is relativelystable over time (increase of 5 mm over a period of 10 years).
CardiacParaganglioma 68-year-old man withlargeparacardiacmass, compressing the LA. Though the mass has a relativelyhomogeneousappearanceon T1w-imaging (left panel), cineimaging (left, middle panel), perfusionimaging (right, middle panel) and late Gd imaging (right panel) show inhomogeneousappearancewithstrongperipheralenhancement and central non enhancementrepresentingliquefactionnecrosis. See Fig. 16 CardiacMasses
CongenitallyCorrected TGA 58-year-old woman presenting withcongenitalcardiopathy, referred to MRI for morphological and functionalevaluation. Situssolitus, meso-todextrocardia, congenitallycorrected TGA with atrioventricular and ventriculardiscordance, right-sidedlocatedmorphologic LV, left-sidedlocatedmorphologic RV, largeoutlet VSD, (supra)valvular PS withgradient > 40 mm Hg, leftsidedaorticarch, RV wallhypertrophy. Seesimilar case Fig. 12 and Fig. 30 Congenital Heart Disease