JAN BOGAERT

Teaching Cases

CLINICAL CARDIAC MRISECOND EDITION

Cases 81-100

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, 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 end-to-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

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.

Comprehensive MRI in IHD (3)

Inducible Myocardial Ischemia

60-year-old man with history of 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.

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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