ECOCARDIORESONANCIA MEGNETICA Y SU FUNCION pptx

La resonancia magnética cardiaca (RMC) es un estudio no invasivo que permite obtener imágenes detalladas del corazón y los grandes vasos que lo rodean. Se realiza con imanes y ondas de radio potentes, sin utilizar radiación

1. Routine Cardiac MRI: Systematic Approach to Interpretation Aeman Muneeb, MD • Sonia Betancourt-Cuellar, MD • Diana M. Palacio, MD

2. Author affiliations.— From the Department of Radiology, Division of Cardiothoracic Imaging, University of Texas Medical Branch at Galveston, 301 University Blvd, Galveston, TX 77550 (A.M., D.M.P.); and Department of Radiology, Division of Cardiothoracic Imaging, University of Texas MD Anderson Cancer Center, Houston, Tex (S.B.C.). Address correspondence to: Aeman Muneeb, MD ( [email protected] ) Presented as an education exhibit at the RSNA 2022 Annual Meeting. Acknowledgments.— The authors would like to thank Richard Pena, Sarah Curtis, and Ryan Foster, MR technologists at UTMB Galveston. Without their dedication and help, this presentation would not be possible. Disclosures of conflicts of interest.— A . M. Support for attending the 2022 RSNA Annual Meeting from the University of Texas Medical Branch radiology residency program. All other authors have disclosed no relevant relationships.

3. Objectives Road Map

4. Road Map Road Map Top right corner of the slide indicates the current section of the presentation. *Familiarity with the basics of MRI physics is recommended for an optimal learning experience * There are multiple cine clips throughout this presentation. Please click to play Preliminary axial chest image assessment

5. 2Ch = Two chamber 3Ch = Three chamber 4Ch = Four chamber Afib = Atrial fibrillation AO = Aorta ARVC = Arrhythmogenic right ventricular cardiomyopathy AV = Aortic valve BMI = Body mass index BSA = Body surface area CAD = Coronary artery disease EF = Ejection fraction FF = Forward flow FSE = Fast spin echo Gad = Gadolinium GRE = Gradient echo HASTE = Half-Fourier acquisition single-shot turbo spin-echo HCM = Hypertrophic cardiomyopathy HOCM = Hypertrophic obstructive cardiomyopathy IAS = Interatrial septum IR = Inversion recovery IVS = Interventricular septum LA = Left atrium LGE = Late gadolinium enhancement LV = Left ventricle LVOT = Left ventricular outflow tract MS = Mitral stenosis MV = Mitral valve Myo = Myocardial muscle PA = Pulmonary artery PV = Pulmonic valve RA = Right atrium RV = Right ventricle SA = Short axis SGRE = Spoiled GRE Skel = Skeletal muscle SNR = Signal-to-noise ratio STIR = Short inversion time inversion-recovery SSFP = Steady-state free precession TD = Transverse diameter TOF = Tetralogy of Fallot TSE = Turbo spin echo TV = Tricuspid valve VENC = Velocity encoding Road Map Abbreviations

6. Anatomy C A C ( A–C) Commonly used dark-blood imaging sequences: T1- and T2-weighting refers to nonsuppressed solid tissues (myocardium, chest wall,  cerebrospinal fluid , etc ). As these sequences are mostly performed to assess anatomy, weighting is not as relevant. The double inversion pulse refers to suppression of the blood pool and recovery of the myocardial signal. Triple IR refers to additional nulling of the fat in addition to the blood pool, which can also be performed with T1 (not shown here). ( A ) Double IR T1-weighted TSE image. ( B ) T2-weighted HASTE image. ( C) T2-weighted fat-saturated (SPAIR) image. ( D) Bright-blood SSFP (single-shot) image. B D Recognizing Sequences

7. 1.1 Preliminary Axial Chest MR Images C A B VENTRICLES and SEPTUM ( A ) Normal ventricular size. Normal septum position (arrow). ( B) Dilated right chambers, RV/LV ratio less than 1; s eptal bowing (arrow). ( C ) Dilated LV. F E D G ATRIA ( D ) Normal RA size. ( E ) Normal LA size. ( F ) RA enlargement. ( G ) LA enlargement. Anatomy Overall assessment: Axial SSFP single-shot images are usually available. Normal Appearance VENTRICLES: RV/LV ratio ( < 1) The normal chamber size parameters in conventional chest MR sequences have not been validated. The values extrapolated from published data in chest noncardiac-gated CT images are suggested but require confirmation on dedicated CMR images. LV and RV : S eptum to free wall distance less than 5.5 cm ( female patients) <6 cm (male patients) (A–C). SEPTUM : S lightly bowed to the right LA : AP diameter less than 4.5 cm ( female patients), less than 5 cm ( male patients) (E–G) RA TRANSVERSE DIAMETER : less than 6.5 cm (female patients), less than 7 cm (male patients). SYSTEMIC AND PULMONARY VEINS: Patency, confirm normal drainage GREAT VESSELS: PA and AO—Caliber, filling defects, wall abnormalities. AO/PA ratio less than 1. OTHER: Filling defects

8. Anatomy Normal pericardium (arrows). ( A ) SSFP. ( B ) T1-weighted contrast-enhanced dark-blood image. (C) Precontrast MR image . ( D ) T1-weighted contrast-enhanced GRE image. G E Thin smooth curvilinear structure surrounded by epicardial and mediastinal fat of high signal intensity. The signal intensity characteristics closely follow the skeletal muscle, with intermediate-to-low signal intensity on T1- and T2-weighted black-blood and SSFP sequences. THICKNESS: Less than 3–4 mm ENHANCEMENT: The pericardium should not enhance with early or late gadolinium interrogation. INFILTRATION: Benign and malignant processes may affect the pericardium. * Mild pericardial enhancement may be seen in patients with prior sternotomy. 1.2 Preliminary Chest MR Sequences: Normal Pericardium B D A C

9. Anatomy A B C D E G F H ( A, B ) 4Ch view . ( A ) SSFP. ( B ) SGRE. ( C, D ) 3Ch view. ( A ) SSFP. ( B ) SGRE. (E, F) 2Ch (long axis) view. ( E ) SSFP. ( F ) SGRE. ( G, H) SA view. ( A ) SSFP. ( B ) SGRE. 2.0 Dedicated CMR Sequences and Planes *SPGR = spoiled gradient-recalled echo † AICD = automated implantable cardioverted defibrillator

10. Anatomy ( A ) Obtaining a 2Ch view. Left panel: Axial c hest image shows a prescribed plane through the center of the mitral valve intersecting the apex. Right panel: resulting 2Ch view image. ( B ) Obtaining a 4Ch view . Left panel: from the 2Ch view, a plane is prescribed intersecting the center of the MV and LV apex . Right panel: resulting 4Ch view image. ( C ) Obtaining an SA cine stack. Left panel: 4Ch and 2Ch view images from which the SA plane is prescribed orthogonal to the myocardial walls. Right panel: Representative SA images shown here from base (close to the mitral valve) to the apex. Approximately 10–18 sections are obtained depending on the heart size. ( D ) Obtaining a 3Ch view. Left panel: Basal SA image. A plane intersecting the mitral (white arrows) and aortic (red arrow) valves is prescribed. Right panel: Resulting 3Ch view image containing the LA, LV, and AO. LV LA AO RA RV LA LV B LA LV A D C 2.1 CMR Planes

11. Figure. Polar map reflects the SA distribution: Base: Segments 1–6. Midcavity : Segments 7–12. Apical cavity: Segments 13–16. Apex: Segment 17 SEGMENTATION CMR mirrors the established echocardiogram myocardial nomenclature, which contains 17 segments (Figure). A A Anatomy 2.2 CMR LV Segments and Nomenclature

12. For clinical CMR interpretation, it is common to refer to regions of the heart affected by disease rather than specific LV segment numbers. Their denominations and boundaries are as follows: Base (segments1–6): From the mitral annulus to the tip of papillary muscles. Midcavity (segments 7–12): From the base to tip of papillary muscles. Apical cavity (segments 13–16): From the base of the papillary muscles to just before the cavity ends. Apex (segment 17): Area of the myocardium beyond the end of the LV cavity. (A-C) SSFP image and corresponding sketch of the regions of the heart according to plane obtained. Regional abnormalities should be evaluated in the cardiac planes where the specific region or regions are displayed. (A) 2Ch view AW = a nterior wall IW = i nferior wall (B) 4Ch view S = s eptum LW = l ateral wall (C) 3Ch view: ISW = i nferoseptal wall ALW = a nterolateral wall Anatomy 2.2 CMR Regions and LV Nomenclature A

13. Causes of RA enlargement include pulmonary hypertension, TV regurgitation, and atrial fibrillation. The RA is measured in the 4Ch view at the end of systole. The top normal area accepted is 30 cm 2 (15 cm 2 /m 2 ) (A, B). The anterior-posterior diameter is drawn from the posterior wall to the center of the closed TV plane. The diameter is normal up to 6.6 cm. The normal TD from lateral wall to interatrial septum should be not more than 5.8 cm. Dimensions may also be obtained in a right 2Ch view. However, images obtained in a right 2Ch view are not routinely obtained. LANDMARK The crista terminalis is a muscular ridge that separates the smooth and muscular portions of the RA and is seen at the edges between the superior vena cava and inferior vena cava laterally . This is a pitfall for an RA mass (C). ( A, B) 4Ch view showing dimensions of the RA. Area (red contouring), AP diameter ( blue line ), TD (white line). (A) Normal size. ( B) RA enlargement. D imensions listed: a rea, 35 cm 2 , TD, 6.8 cm, AP, 6.5 cm. The LA was also enlarged. ( C ) Left and right p anels : 4Ch contiguous views near the inferior vena cava shows p seudo - filling defect corresponding to the RA crista terminalis (arrows). ( D) Left panel: 4Ch image . Right panel: Delayed enhancement 4Ch view image shows a real filling defect, representing a thrombus (arrows). A B D Anatomy 3.1 RA Assessment C

14. The RV has an inlet portion immediately distal to the TV, an outlet or infundibular portion continuous to the pulmonic valve, and a trabecular apex. The RV equals the LV in volume. The RV surface of the septum has several muscular attachments that differentiate it from the LV. Moderator band ( septomarginal trabecula): M uscular structure connecting from apical septum to apical free wall that is involved in the cardiac electrical conduction system ( A). Chordae of the TV septal leaflet (B) Crista supraventricularis : A ridge separating the infundibulum and the inlet part (C). The crista supraventricularis may be a cause of septum thickness overestimation as it inserts adjacent to the septum. Caution should be taken by measuring the septum as it departs from this band (D). (A) Moderator band of the RV (arrow). Abnormal RV/LV ratio greater than 1 in this case. ( B ) Chordal attachment of the TV septal leaflet. ( C ) Crista supraventricularis . ( D ) Overestimation of septal thickness (incorrect) versus correct measurement of the septum in a patient with a prominent crista supraventricularis (arrow). A B C Anatomy D 3.2 RV Assessment

15. The LA may dilate due to pressure overload (mitral stenosis), volume overload (mitral regurgitation), high cardiac output , or atrial fibrillation. As with the RA, manual tracing of the LA can be performed using 4Ch views but, unlike the RA, can also be performed with 2Ch views, ensuring exclusion of the pulmonary veins. The LA volume can also be obtained with the biplane area-length method in the horizontal and vertical long axes as with echocardiography, where the LA v olume i ndex (LAVI) can be estimated according to BSA. This is considered normal up to 28 mL/m 2 (A). A normal LA volume varies by patient sex. The normal range is approximately 100 ± 30 mL. STRUCTURE: Cardiac CT is the reference standard for thorough LA anatomy evaluation. However, assessment of potential endoluminal lesions and p ulmonary v ein connections should be performed in all CMR studies. LANDMARK: The wall separating the LA from the inferior pulmonary vein may appear as a filling defect or masslike lesion in some patients. This is referred to as the coumadin ridge, a pitfall for thrombus. B A ( A ) Left panel: 4Ch view. Right panel : 2Ch view image shows the LA contouring. The LAVI can be obtained using online calculators or a CMR aquisition (s ee text). ( B ) Axial SSFP image shows the coumadin ridge separating the LA appendage from the left inferior pulmonary vein. Anatomy 3.3 LA Assessment

16. The visual impression of size is correlated with the semiautomated quantified end- d iastolic v olume (EDV) and EDV i ndex (EDVI) adjusted to the patient's BMI and sex (usually available in any CMR postprocessing software) (A). These volumes are usually written as mL/m 2 : volume in milliliters divided by th e BSA (m 2 ). Grossly, with an LVEDVI value of greater than 100 mL/m 2 and an RVEDVI value greater than 111 mL/m 2 , dilatation may be considered (B, C). Alternative LV dimension assessment (less often used) : In the SA view, at the level of the papillary muscle base, the LV end-diastolic dimension (EDd) distance is measured between the septum and lateral walls. N ormal range values are between 41 and 63 mm (D). On the 4Ch view images, two distances are obtained (D ). Between the MV plane and the LV apex, n ormal values range between 67 and 116 mm. Between the septum and the lateral wall at the basal level, normal values are approximately 39–64 mm. (A) Typical postprocessing of SA cine stack images for function calculation and size. ( B ) Severe LV dilatation , d iastolic volumes (red contouring). The LVEDVI was 158 mL/m 2 . ( C ) Severe RV dilatation (y ellow contouring). The estimated RVEDVI was 215 mL/m 2 . ( D ) Normal LVEDd in the SA (left) and 4Ch plane (right). See the text for description. A B C D 3.4 Biventricular Assessment: Size Anatomy

17. The LV is conical in shape with an antero-inferiorly projecting apex that is longer with thicker walls than the RV (A; left). See the middle and right panels for comparison displaying LV pathologic shapes. The RV has a semilunar shape in the SA view, a pyramidal shape in the 4Ch view, and a smooth contour in normal conditions. The RV equals the LV in volume. The ventricular wall and trabeculations are substantially thinner. (A) Left: Normal LV shape in the 2Ch view. Middle: Ballooning of the midanterior cavity due to Takotsubo cardiomyopathy (arrow). Right: Apical aneurysm ( * ) in a patient with midcavity (arrows) HCM. (B) Left: Normal appearance of the RV in the 4Ch plane. Right: Unusual contour of the RV, overpassing the LV apex. This is an anatomic variant called “butterfly” RV (arrows). B RV C A LV * (C) Two 4Ch images through the cardiac cycle in a patient with subtle outpouchings or microaneurysms during systole due to ARVC. Anatomy 3.5 Biventricular Assessment: Shape

18. THICKNESS: Assessed on the cine images, ensuring the dimensions are obtained at end diastole. Although the measurements can be obtained in any plane, the SA stack is preferred. Measurements should be radial, perpendicular to the measured wall. Hence, for the apex, either a 2Ch or 4Ch view should be used. Normal ranges from about 5 to 6 mm to 12 to 13 mm ( A, C). Compare these to Figures B and D, which are abnormal. The ventricular wall is thickest at the base and thins to only 1–2 mm at the tip of the apex. Polar maps of the LV thickness in systole and diastole are generated by the postprocessing software (from the SA image contouring) and presented as polar maps of the 16 cardiac segments, except for the apex (E). C D E (C) Midcavity SA image in diastole with normal LV thickness. (D) Same plane and phase in a patient with severe midcavitary HCM and near occlusion of the LV cavity. A B (A) 4Ch view in diastole. Note the normal LV thickness and orientation of measurements. (B) Asymmetric septal thickening with HCM (arrow). (E) Polar maps with measurements of myocardial thickness in systole and diastole. Anatomy D 3.6 Biventricular Assessment: Thickness

19. There are two LV muscles, anterolateral (AL) and posteromedial (PM). Thickness should not exceed the thickness of the adjacent myocardial wall or septum in normal patients (A). On CMR images, papillary muscle thickness greater than 1.1 cm or greater than the LV free wall thickness is abnormal (B–C). Each muscle can have one or several muscle heads with a single or separate basal segments. On occasion, papillary muscle configurations may contribute to LVOT obstruction. The papillary muscles may also suffer from ischemia, undergo necrosis, and become atrophic. (B, C) Two different patients with HCM. (B) Note a thickened AL muscle (arrow). (C) Thickened PM muscle (arrow). A C PM AL A B C (A) SA view. Normal AL and PM papillary muscles measuring less than 1.1 cm in thickness. Anatomy 3.7 Biventricular Assessment: Papillary Muscles

20. A The myocardial wall components include a compact layer and a trabecular layer, where trabeculae and intertrabecular recesses alternate. During embryogenesis, the trabeculated myocardium is favored and contributes to cardiac output and nutrition of trabecular myocytes prior to coronary vascularization. With maturation, the compact myocardium and the coronary artery system develop simultaneously, while trabeculae remodel. In a normal heart, the trabeculae are mechanically active during early systole and expand the contact surface of the endocardium and nearby blood, improving perfusion. Noncompacted myocardium refers to absence or reduction of the compact layer of the LV. On CMR images, the compacted to noncompacted myocardium is measured orthogonal to the LV wall. The noncompacted (NC) to compacted (C) ratio is considered abnormal if greater than or equal to 2.3 (B). However, without mention of LV dysfunction, the findings may also be seen in normal individuals. Hypertrabeculation may also affect the RV (B). (A) Left panel: 4Ch view. Right panel: SA view at the midcavity shows normal trabeculation (arrows). (B) Left panel: SSFP 4Ch view. Middle and right panels: SSFP SA views without and with measurements, respectively, show hypertrabeculation of the mid to distal LV wall (arrows). The RV is also affected. The C/NC ratio met criteria for noncompaction cardiomyopathy. Anatomy 3.8 Biventricular Assessment: Trabeculation B

21. E C D When obstructed, the LVOT may show acceleration (dephasing jet) flow, best seen in the 3Ch cine views. See Figure D under section 4.8. The LVOT/AO ratio may help in determining whether LVOT obstruction is present (B). An LVOT/AO ratio less than 0.45 appears to predict LVOT obstruction. The IVS is smooth on the LV side from which no structures should attach (E). On occasion, fibrotendinous bands may be seen, in some cases associated with arrhythmia (F). (A, C) 3Ch view images in diastole (left panels). (B, D) 3Ch view images in systole (right panels). LVOT/AO ratio: The AO diameter is a line that is drawn at annulus in diastole (yellow lines) (A, C). The LVOT diameter is a line that is drawn from the septum to the mitral valve at narrowest portion in systole (white lines) (B, D). (A-B) These images show a patient with concentric hypertrophy due to systemic hypertension without obstruction with an LVOT/AO ratio of 0.54. (C-D) These images show a patient with an LVOT/AO ratio of 0.27 and asymmetric septal hypertrophy due to HCOM. E A B C D (E) 4Ch view. Normal IVS. No structures attached to the LV surface (arrow). (F) Reformatted axial oblique image shows the course of an anomalous musculotendinous band from the anterior wall to the septal LV wall (arrow). F Anatomy 3.9 LVOT and Septum E

22. Although detailed valvular assessment requires dedicated sequences, gross assessment of the anatomy and hemodynamic consequences of valvular disease are possible on standard CMR images when flows are obtained ( see Section 6). STRUCTURE: All valves should appear as paper-thin structures. Normal TV implantation is slightly apical than the MV (A). The distance between the valve annuli in reference to the BSA can be indexed. Length/BSA ratio greater than 8 mm/m 2 is abnormal and may raise the possibility of Ebstein anomaly. MOTION ABNORMALITIES: Re striction to motion of the TV and MV is common in rheumatic or infiltrative diseases. Insufficient coaptation may be associated with ventricular dilatation. T ethering and excessive motion and floppy prolapsed valves may be seen, especially for the AO valve and MV ( C). On HCM images, displacement of the anterior mitral leaflet towards the septum may be seen, suggesting obstruction (systolic anterior motion; S AM) (D). FOCAL LESIONS: This should be assessed for each valve in the conventional views (including tumors, thrombi, etc ; E). ( A ) Normal MV and TV. Note the TV is more apical than the MV. ( B) Implantation index measurement shown in the yellow line (see text). (C) MV prolapse: There is displacement (typically >2 mm ) into the LA, beyond the annulus axis ( blue line ). ( D) 3Ch SSFP cine clip (hover over to p lay). The anterior mitral leaflet moves towards the septum in early systole (SAM) in a patient with asymmetric HOCM. A subtle dephasing jet near the basal septum ( arrow) is also noted. E ( E) Contiguous T1-weighted double IR image in the true axial plane of the PV. Top: T he valve is seen. Bottom: Attached to the valve is a mass (arrow). Anatomy 4.0 Valvular Structure MV TV A B C D

23. ( A–D) Normal anatomy and signal intensity of the pericardium in different sequences. ( A ) SA T1-weighted d ouble IR. B: 4Ch SSFP. C: SA T2-weighted STIR D : 4Ch LGE (normal pericardial nulling: no enhancement; discussed further in section 6.2). (E–H) Same order of sequences compared to A–D in a patient with exudative pericarditis. ( E) T1-weighted d ouble IR SA image. Note severe pericardial thickening (arrows). ( F) 4Ch SSFP image. Thick pericardium (arrows) surrounded by heterogeneous bright signal intensity due to complex fluid. Susceptibility artifact from right coronary artery stent noted (*). (G ) SA T2-weighted STIR image. The thickened pericardium is surrounded by high signal intensity arising from fluid and pericardial edema (arrows). ( H) 4Ch LGE image: Note avid pericardial enhancement (arrows), surrounding by lack of signal intensity due to pericardial fluid ( * ). C B B D A The pericardium is better visualized adjacent to the right heart due to a larger amount of epicardial fat. Two layers of the pericardium slide onto each other, separated by up to 50 cm 3 of physiologic fluid ( often not visualized). The normal pericardium should follow the skeletal muscle signal intensity and should not enhance (A–D). Inflammatory conditions of the pericardium are displayed as high signal intensity on T2-weighted images and usually associate with delayed enhancement (C–D). MOTION: Requires dynamic images for assessment. Please refer to function section. Anatomy 4.1 Pericardium E H * F * G

24. VISUAL ASSESSMENT: Estimation of the LV and RV systolic function by subjectively identifying the size differences between the diastolic and systolic ventricular size is a first step. This helps put in context the quantitative or semiquantitative values obtained with the dedicated software. AUTOMATED OR SEMIAUTOMATED ASSESMENT: Typically performed in the SA cine stack following the Simpson rule technique. Each section volume is calculated as the area delineated along the endocardium. All section areas are multiplied by the section thickness and the predetermined section gap. Absolute values and values normalized to BSA are obtained. CO = HR x SV SV = EDV - ESV EF = EDV - ESV EDV In the absence of intra- or extracardiac shunts, the LV and RV SV should be nearly equal. ( A ) Representative images of an SA stack in diastole. ( B) Representative images of an SA stack in systole. The red line indicates the endocardial LV contour from which the volumes will be quantified. The yellow line delineates the RV endocardium. The assessment can be performed (as in this case) including the papillary muscles in the blood pool. Alternatively, it can be performed so that the papillary muscles are excluded from the analysis. In either case, there are established parameters of normalcy for reference. Typical parameters obtained: CO = c ardiac output SV = s troke volume HR = h eart r ate EF = e jection f raction EDV = e nd -d iastolic v olume ESV = e nd - systolic volume B A REAL-TIME FREE-BREATHING CINE IMAGING: Alternative technique in the case of arrhythmia or patient motion for function calculation. H owever , the results should be considered estimates . Function 5.0 Function: Quantification

25. A B C ( A–C ) Real-time free-breathing cine clips in a patient with nonischemic c ardiomyopathy and severely depressed biventricular systolic function. In this case, the patient had an arrhythmia. The visual estimate of LVEF and RVEF was between 20 and 30%. REAL-TIME FREE-BREATHING CINE IMAGING: Alternate technique in the case of arrhythmia or patient motion that may be used for function estimation. H owever , the results should be considered estimates . Function 5.1 Function: Real-Time Cine Imaging

26. Wall motion abnormalities may be global or regional and often affect cardiac function. HYPERKINESIS: H ypercontractility usually with associated wall thickening (A). HYPOKINESIS: Hypocontractility that w hen diffuse, nonischemic cardiomyopathy or valvular diseases may be suspected other than severe three vessel coronary disease. If regional, ischemic or inflammatory causes are more likely (A). AKINESIS: Lack of contractility which is commonly seen with scarred myocardium ( typically caused by old infarcts) (B, C). Dyskinesis: Outward movement of the RV or LV myocardial wall in systole. It translates into outpouchings in systole (D). C D ( B ) Left panel: T2-weighted 2Ch STIR image shows an area of high signal intensity due to edema (arrow). Right panel: The 2Ch SSFP cine clip shows corresponding focal akinesis in the region due to focal myocarditis. B ( D ) 2Ch SSFP cine clip in a patient with Takotsubo cardiomyopathy and regional midanterior wall dyskinesis (arrow). (A) SA SSFP cine clip shows hyperkinesis of the LV in a patient with HOCM. Note near collapse of the LV cavity in systole. LVEF was calculated at 77% (hypercontractility). (C) 4Ch SSFP cine clip in a patient with LAD myocardial infarction shows akinesis of the apical inferoseptal wall. Note the associated wall thinning. C E Function 5.2 Motion Abnormalities A C

27. A D ( D ) SA SSFP image shows massive epicardial fat infiltration (*) and fatty infiltration of interatrial septum (arrow). (E) 4Ch cine clip shows hypermobile septum with suspected small PFO. cardiogram ( A ) 4Ch view with normal IAS. note thinning in the region of fossa ovalis. (B) Subtle dephasing jet due to a small PFO (arrow). (C ) Secundum type of ASD with a dephasing jet (arrow). INTEGRITY On the 4Ch views, the normal IAS may show focal thinning at the fo ssa ovalis (A). Atrial septal defects (ASD) are defined more reliably by the septal discontinuity ( C). Patent foramen o vale (PFO) diagnosis with C MR is often inadequate for defining shunts due to the common lack of dephasing jet visualization. MOBILITY: IAS motion is influenced by the pressure gradient between the atria. Hypermobility in any direction is abnormal and if the excursion is greater than 1 cm, it is referred to as IAS aneurysm (sometimes associated with PFO or mitral prolapse) (E). The IAS bowing to the left with each beat may be indicative of high right-sided pressures but has also been noted in healthy hearts. LESIONS ALONG THE SEPTUM: Look for intrinsic septal lesions or lesions attached to the IAS (D). Function 5.3 IAS B E C * D

28. The IVS is shared with the RV but functionally behaves like a wall of the LV throughout the cardiac cycle, maintaining a concave contour from the LV perspective (A, B). Normal motion: The IVS moves t owards the left in systole and toward the right during diastole. The net motion determined by the biventricular pressures and the intrinsic active tension and stiffness of the IVS. As the two ventricles compete for space within the pericardium and share the IVS, filling in one ventricle affects filling in the other. This is a normal phenomenon known as ventricular interdependence. Variations of the normal septal motion are referred to as paradoxical , a broad term with many different variations.  SEPTAL BOUNCE: Abnormal deviation of the septum from right to left in early systole or early diastole as a manifestation of exaggerated ventricular interdependence (C–F). (D) SA sketch demonstrates the IVS bowing to the left in septal bounce (arrows). (E, F) Examples of early diastolic septal bounce. ( E) SA cine clip shows patient with pulmonary hypertension. (F) 4Ch cine clip shows right heart strain following correction of pulmonic stenosis from TOF . ( G) SA cine clip shows s ubtle early systole leftward deviation or “septal flash” in a patient with left bundle branch block. C D E (A) Sketch of the normal IVS position in the SA view (orange shaded) and arrow in C with concavity to the left in a normal patient. (B ) SA cine clip (arrow). (C ) 4Ch cine clip. RV LV A RV LV D E C F G B Function 5.4 IVS C

29. Function Septal bounce may occur in reference to the respiratory cycle (inspiration vs expiration or continuous). These characteristics should be described as they may present different scenarios: Early diastole: c onstrictive pericardium, mitral stenosis, pulmonary h ypertension . With inspiration: constrictive pericarditis, cardiac tamponade, and COPD ( C, D). Early systole: l eft bundle branch block, RV pacing (septal flash). Throughout systole: RV dysfunction. C * * * (A, B) Sketches of the IVS position in SA view during inspiratio n and expiration (orange shaded). The diaphragm is shown down and up (black curved band), respectively. In RV LV B RV LV A D Inspiration Expiration ( C, D) Free-breathing SA cine clips in patients with respirophasic septal bounce (arrows) , noted predominantly in inspiration. (C) C onstrictive effusive pericarditis. Note fluid surrounds the pericardium (*). ( D) S eptal b ounce in a patient with constrictive pericarditis (arrow). 5.4 IVS

30. This technique uses radiofrequency prepulses known as spatial modulation of magnetization (SPAMM), complementary SPAMM (CSPAMM), or delays alternating with nutation for transient excitation (DANTE) applied to the heart just before the start of systole. This creates tag lines that deform along with the myocardium, and measurements of the boxes can be used to quantify regional ventricular function . The complex way in which the heart contracts and deforms during the cardiac cycle is not detected by traditional CMR or other imaging. Three orthogonal components of myocardial motion (longitudinal, circumferential, and radial), rotation, and torsion are explored with this technique. Alterations of these mechanisms may be seen with cardiomyopathies, even in the setting of normal conventional CMR imaging. The implementation is less straightforward for the myocardial strain analysis as it requires specialized software not widely available. Additionally, tagging can be applied to images of pericardial disease to evaluate for areas of thickened pericardium adhered to the myocardium (A–E). ( A–D) 4Ch view images in a patient with severe exudative pericarditis. (A) SSFP image shows thickened pericardium. (B) T2-weighted STIR image shows extensive edema (high signal intensity). ( C) Postcontrast T1-weighted GRE and (D) LGE images demonstrate a combination of fluid and severe enhancement and thickening. ( E) Myocardial tagging image shows that there is no deformation of the myocardial grids near the pericardium due to tethering by adhesions from the inflammatory process. 5.5 Myocardial Tagging E A B C E D Function

31. Tissue ACUTE EDEMA INFLAMMATION T2-weighted imaging of the heart is done through m ultiecho spin-echo (SE) techniques, known as TSE or FSE. Thes e techniques produce black-blood images of the heart within a breath hold and can be performed with or without fat suppression ( A, B). Single heartbeat T2-weighted imaging performed in diastole, with fat nulling by a third inversion pulse ( STIR), highlights the signal intensity from long-T1, long-T2, such as fluid and edema (D, E). Regional edema may be readily seen. However, diffuse changes may require comparing absolute values. These are abnormal if the myocardium has more than two times the skeletal muscle signal intensity. T2 mapping evaluation is an alternative method used to assess for diffuse edema. ARTIFACTS: The b lood suppression techniques may not fully null the blood signal intensity, especially if flow is not perpendicular to the image plane. This may result in intraluminal areas (often close to the subendocardial layer) with high signal intensity (C, F). ( A ) Axial T2-weighted TSE (HASTE) image. ( B ) Axial T2-weighted TSE spectral fat-saturated (SPAIR) dark-blood image shows normal intermediate myocardial signal intensity compared to muscle (*). (C ) Artifactual high-signal intensity o n axial T2 HASTE image due to stagnate blood along the LV endocardium (arrows) is seen. B C ( D–E ) SA T2-weighted STIR images. ( A) Normal isointense signal intensity of the myocardium compared to skeletal muscle. ( B) Abnormal high signal intensity in the mid lateral wall due to acute myocardial infarction in a patient with a history of cocaine abuse (arrows). Note the signal intensity is seen within the myocardium. ( C) Artifactual high signal intensity at the interface of the blood pool in the medial aspect of the LV midcavity . D * F E * B * * A C 6.1 Tissue Characterization: T2-weighted Imaging

32. Tissue GAD contrast-enhanced images take advantage of the fact that the contrast material takes longer to wash in and out of infiltrated or infarcted tissue compared to normal cells and even longer in regions affected by microvascular obstruction. Techniques: IR or phase-sensitive IR (PSIR) using electrocardiogram- gated segmented FLASH readout, (spoiled gradient-recalled-echo SPGR). IR or PSIR with SSFP, also known as true-FISP or balanced-TFE, are preferred. IR images are typically acquired in mid to late diastole to minimize cardiac motion. The IR time attempts to null the normal myocardium for best tissue contrast between normal and ab normal myocardium. A T1-weighted scout series with progressively larger T1 values is obtained, and the image that best shows the myocardial nulling is selected (D). With PSIR , two data sets are acquired, a conventional image and a reference-phase data set, which are compared to reconstruct the final image. These data sets are acquired during two consecutive heartbeats but at the same time point in the cardiac cycle (MAG and PSIR image pair). W hen two sets of images (MAG IR and PSIR) are available, the PSIR images are more reliable as they eliminate errors associated with incorrect selection of the T1 value by the operator (E). A C B A C N ormal LGE images . ( A ) SA, ( B ) 3Ch, and ( C ) 4Ch view images. Note the entire myocardium remains dark (no late GAD enhancement). ( E ) Magnitud e (MAG) IR SA LGE image. (F) Corresponding PSIR image. Note the less optimal quality of the MAG image compared to the PSIR image. This may be due to motion correction but also due to the suboptimal selection of IR. E F 6.2 Tissue Characterization: LGE ( D ) T1-weighted scout images obtained at incremental values. The T1 value selected (image with red circle) shows the best myocardial nulling (where it appears the darkest). The value was 260 ms in this case. D

33. ISCHEMIC PATTTERN NONISCHEMIC PATTERN Suben docardial Transmural Midmyocardial Diffuse Subendocardial Epicardial Gadolinium deposition in the myocardium results in various degrees of hyperenhancement in the LGE sequences, where the myocardium has purposely been nulled using a specific inversion time. This is performed to amplify the difference between normal and abnormal myocardium. Whenever there is hyperenhancement in these sequences, it indicates injury ( fibrosis, necrosis, edema ) or infiltration by inflammatory cells or material that expands the extracellular component of the myocardial tissue. The patterns of LGE help suggest specific causes, and the extent of enhancement predicts prognosis. On the right panel, several common patterns are depicted. Tissue 6.2 Tissue Characterization: LGE

34. ( A) 4Ch view: Apical anteroseptal wall transmural LGE. Note an area of microvascular obstruction displayed as absence of signal intensity (arrow). ( B ) SA view: Basal lateral wall epicardial (arrows) and subtle anteroseptal midmyocardial (smaller arrow) LGE due to sarcoidosis. ( C ) SA view: Midcavity near transmural anteroseptal (larger arrow) and patchy midmyocardial i nferoseptal (smaller arrow) LGE in a patient with advanced asymmetric septal predominant HCM. Mild subepicardial anteroseptal enhancement was also noted (arrowheads). ( D ) 2Ch view: Zebralike pattern of LGE due to amyloidosis with predominantly concentric subendocardial but also midmyocardial (small arrow) and epicardial involvement (larger arrows) , throughout the LV. Tissue 6.2 Tissue Characterization: LGE A B C D

35. Tissue ( A ) Example of semiautomated scar quantification. A pixel value of normal myocardium is selected and any pixel over two standard deviations of normal will be considered in a cumulative value of pixels with some degree of scar per segment. This is then depicted on the polar map in the right panel. From the information of myocardial mass, a percentage of myocardial mass containing scarring is then defined. Polar maps can be created to assess for scar quantification (beyond visual analysis) and can provide the percentage of scar that is of prognostic value in these patients. A 6.3 Tissue Characterization: Scar Quantification

36. Subtle changes in the myocardial signal intensity characteristics can be difficult to visualize on conventional images. To overcome this obstacle, relatively recent advances now permit pixel by pixel quantification of T1, T2, or T2* values using short breath-hold mapping sequences. The results are displayed in color-coded pixel maps representing a time value for T1, T2, or T2* in milliseconds (A–C). Native T1 ( precontrast ) is high in diseases that increase total myocardial water, such as acute myocardial infarction (AMI), myocarditis, or stress cardiomyopathy. The myocardial extracellular volume (ECV) (B) can also be calculated from the native and postcontrast T1 values of myocardial tissue and the blood pool together with the information of the patients’ hematocrit values. Normal ECV values are in the range of 28–32%. T2 mapping depicts myocardial edema and inflammation. ( B ) Example of a report by segments of the T1 pre- and postcontrast T1 values and ECV in a patient with borderline elevated ECV values. (A–C) Myomaps in a normal patient . ( A) T1 map. ( B) T2 map. (C) Postcontrast T1 map. Note the scales run from 0 to 2000 ms for T1 pre- and postcontrast T1 values and 0-120 ms for T2 values. Accepted normal values: T2 values, around 50–60 ms ; precontrast T1 values, around 900–1100 ms ; and postcontrast T1 values, 300–400 ms. 2000 ms 0 ms 2000 ms 0 ms 120 ms 0 ms A B C Tissue 6.4 Tissue Characterization: Myo-maps

37. Patients with thalassemia and transfusion-related anemias may develop systemic iron overload resulting in end-organ damage due to formation of reactive oxygen species and lipid peroxidation. Chelation therapy may improve prognosis in these patients. A series of breath-hold GRE images at progressively increasing echo times (TE) are obtained. The signal intensity is measured over the ventricular septum (less susceptible to cardiac veins and air-containing lung artifact). The curve is fitted to a simple exponential resulting in an estimate of myocardial T2*. The liver may also be interrogated with multiecho GRE images in the same study to calculate hepatic T2* values and the degree of iron overload presented in a similar scale. Typically, T2* values less than 20 ms are associated with a higher risk of arrhythmia and systolic dysfunction, and levels less than 10 ms predict heart failure. In patients with myocardial infarction, T2*-mapping values less than 20 ms may indicate microvascular injury. (A–C) Semiautomated T2* mapping. ( A) T2* color map. ( B) Estimation of T2* value using signal intensity data at different TEs fitted to a first-order exponential model. ( C) Typical septal measurement in a patient with suspected hemochromatosis. However, this was not confirmed with CMR. The T2* value was 39 ms. Tissue A B C 6.4 Tissue Characterization: T2* Assessment

38. ASSESSMENT OF EDEMA AND INFLAMMATION Typically, T2-weighted STIR imaging is performed in cases where acute edema or cellular infiltration are suspected. Regional hyperintense foci may be easily identified. A ratio between skeletal muscle ( skel ) and myocardial muscle ( myo ) signal intensity values greater than 2 is considered compatible with edema and acute inflammation (A–B). The T2 map information is more sensitive to determine the presence of edema, especially when diffuse, as it may not be as apparent on the T2 STIR images. ( A ) Left panel : SA T2-weighted STIR image. Middle panel: s eptal and lateral wall measurements with skeletal muscle correlation. The skel / myo ratio is less than 2 , within normal limits . Right panel: c orresponding T2 map in a normal patient. T2 times were quantified between 51 and 56 ms. Tissue 6.5 Tissue Characterization: Suggested Approach ( B ) Left panel : SA apical cavity T2-weighted STIR image. Middle panel: region of interest measurements of the anteroseptal and inferoseptal wall. Right panel: corresponding T2 map. Note prolonged T2 values in the same regions in a patient with preexistent severe coronary disease and a new myocardial infarction . The quantified T2 values in these regions were up to 68 ms . A B A

39. HYPEREMIA ASSESSMENT Pre- and postcontrast T1-weighted double IR images may be available. These may provide information of hyperperfusion and can be assessed by special software and manually with the formula below. The myocardial signal intensity (SI) and the skeletal muscle ( skel ) signal intensity is assessed in both sequences and the following formula is applied: Myocardium enhancement = (post SI - pre SI) / pre SI Skel muscle enhancement = (post SI - pre SI) / pre SI Finally, the following ratio is used: Myocardium enhancement:skel muscle If this value is greater than 4 , it is considered suggestive of hyperemia. Tissue 6.5 Tissue Characterization: Suggested Approach ( D–F ) Mid cavity SA views . Same case as on slide 37 Figure B. Focal hyperemia in a patient with a chronic CAD and new acute myocardial infarction . ( D ) Left panel: p recontrast double IR T1-weighted image . Right panel: s ame image showing regio n-of-interest measurements at the anteroseptal, inferoseptal walls, and skeletal muscle. ( E) Left panel : p ost contrast image. Right p anel : s ame image with region-of-interest values as in D. ( F ) Left panel: c orresponding T1 native map image. Right panel: postcontrast T1 map image. The myocardial:skel ratio was 9 for the inferoseptal wall and 18 for the anteroseptal wall. This corresponded to elevated T1 native values of 1154 ms and 1172 ms , respectively, and visual low postcontrast T1 values (arrows in F). Postcontrast T1-weighted map quantification was not available. A A ( A–C ) Mid cavity SA views with normal T1-weighted appearance. (A) L eft panel: p recontrast double IR T1-weighted image . Right panel: s ame image showing region-of-interest measurements at the septum, lateral wall, and skeletal muscle. (B) Left panel : post contrast image. Right p anel : s ame image showing region-of-interest measurements at the septum, lateral wall, and skeletal muscle. ( C) Left panel: c orresponding T1 native map image. Right panel: postcontrast T1 map image. Applying the formula described in the text, the highest ratio wall myocardial:skel enhancement obtained out of the two measurements (septum and lateral) is 2.5 (within normal limits). C B A F E D

40. ( A–C ) Left panel: bright-blood SSFP Images. ( A) 4Ch, ( B) 3Ch, and ( C) SA views. Right panel: corresponding LGE images. ( D) Precontrast T1 map. ( E ) Postcontrast T1 map. A B C D E Tissue 6.5 Tissue Characterization: Suggested Approach INFILTRATION AND FIBROSIS SEQUENCES Next, late gadolinium interrogation images are assessed and compared to their respective plane cine images (A). The cine SSPF images provide the roadmap to the expected thickness of the myocardium and help avoid confusion with false delayed enhancement that may originate at the blood pool interface in the subendocardium or due to pericardial fat in the subepicardium . Lastly, the SA delayed enhancement images should be paired with the pre- and postcontrast T1 maps. Most infiltrative diseases that cause delayed enhancement will increase the T1 native value and decrease the postcontrast T1 value (exceptions include cases of fibrofatty infiltration and iron deposition). H

41. Tissue ( A, B ) 4Ch and SA T2-weighted STIR images show myocardial thickening and high signal intensity in the mid- to subepicardial region due to edema (arrows). ( C) LGE SA image reveals enhancement in the same area (arrow). (D ) Corresponding T2 color map shows elevated T2 values in the same region (arrow). This was above 65 ms when quantified (not shown). A B C D 6.6 Practice Examples. Case I: Myocarditis

42. ( A) 4Ch SSPF cine clip shows akinesis of the mid lateral wall. ( B ) 4Ch T2-weighted STIR image reveals high signal intensity along the lateral wall from edema (arrow). ( C ) Corresponding 4Ch view image shows transmural delayed enhancement in the same region (arrows). This is due to a large left circumflex coronary artery acute myocardial infarction . Note the fine foci of lack of enhancement along the endocardial border, secondary to microvascular obstruction (microthrombosis) in C (small arrows). B C A Tissue 6.6 Practice Examples. Case II: Ischemic Cardiomyopathy

43. Tissue ( A) SA T2W STIR image shows concentric LV thickening and diffuse , predominantly subendocardial, high signal intensity from edema and acute infiltration (arrows). SA images at the (B) midcavity and (C) apical segments show c orresponding diffuse delayed enhancement involving all layers of the myocardium (arrows). However, these images show higher subendocardial signal intensity, consistent with active amyloidosis. A B C 6.6 Practice Examples. Case III: Amyloidosis

44. ( A–C ) SA section images show transition of normal myocardial perfusion from left to right. A B C First-pass myocardial perfusion involves imaging the LV myocardium during the passage of the gadolinium contrast bolus at rest and following pharmacologic stress, like cardiac SPECT. It is of limited value in absence of stress perfusion. Typically, the electrocardiogram -gated T1-weighted GRE or SSFP images include three LV SA sections (base, mid, and apex) that are obtained. The perfusion is considered abnormal if a low signal intensity is detected in the myocardium that persists for a period of at least five heartbeats. Hemodynamics 7.1 First-Pass Myocardial Perfusion

45. (A– D) Midventricular section during rest perfusio n CMR. Dark-rim artifact (arrows). ( A) F rame 1 . ( B ) Frame 4. ( C) Frame 7. ( D ) Frame 9. Typically, the artifact disappears after 8–10 frames. A B C D Dark-rim artifact: Dark rind between the myocardium and gadolinium-enhanced blood pool, generally seen in the phase-encode direction. Factors involved include inadequate spatial frequencies sampling, susceptibility effect, motion, and intravoxel phase cancellations. A true perfusion defect during a first-pass study is seen in at least 3–4 frames during peak enhancement of the myocardium with a consistent size from frame to frame and corresponds to a known coronary artery distribution. A dark-rim artifact appears at the arrival of contrast material in the left ventricular cavity and before contrast material arrival in the myocardium (A–D). Hemodynamics 7.1 First-Pass Myocardial Perfusion

46. (A) 4Ch first-pass perfusion image shows a rim of hypointensity (arrow) and thinning of the myocardium due to chronic ischemia in a patient with LV apical aneurysm from terminal sarcoidosis. ( B ) C orresponding transmural delayed enhancement image is consistent with a chronic scar (arrow). ( C) Perfusion imaging is useful in the characterization of intracavitary lesions and helps in the process of differentiating thrombi versus masses. Here, a thrombus (lack of enhancement) is noted along the lateral wall of the right atrium. A B C Hemodynamics 7.1 First-Pass Myocardial Perfusion

47. (A–F) Phase-contrast images of the AO and PA. (A–C) Cine images of the AO flow typically include a ( A) magnitude image. The brightness in the vessel raises as blood flows into the section and decreases due to repeated excitations as it remains in the plane. ( B) Phase image shows the signal intensity proportional to the velocity of flow, in this case encoded from head to foot. White and black signal intensity denote flow into and out of the selected plane (ascending and descending aorta, respectively) (arrows). (C) An angiographic image was produced as a result of the magnitude and phase images. (D–F) Static phase-contrast images of the PA (arrows). (D) Magnitude image. ( E) Phase image. ( F) Angiographic image. Flow interrogation at CMR is possible through cardiac-gated phase-contrast imaging (A–F). This technique modifies the phase signal intensity from flowing blood by applying specially designed gradients while stationary tissue phase signal intensity remains at zero. Quantification of flow is possible through velocity encoding (VENC). The VENC values represent a range of velocities ( – VENC … + VENC) selected depending on the interrogated vascular structure or shunt. The selected VENC value will determine the maximal velocity that can be recorded. Typically, a thin ( 3-mm thick or less) cross-sectional image of the vessel of interest is obtained. In cases of a slight suboptimal selection of the true perpendicular vessel plane by the operator, the calculations obtained with this technique may not be significantly affected. A C Hemodynamics 7.2 Flow Quantification D F E B A C D

48. (A) AO representative magnitude image where the aorta region of interest is drawn across all frames on the phase-contrast images ( red circle). ( B) The flow velocity information is extracted and plotted in a graph against time. (C) Magnitude image displays the region of interest for the PA ( green circle). ( D) Corresponding plotted graph. The area under the curve above zero is the forward flow, and the retrograde flow is the area below the zero level. In absence of regurgitation, the AO and PA forward flow should be close to the LV and RV stroke volume, respectively. Semiautomated flow calculations are obtained by drawing a region of interest around the vessel for each acquired time frame over the cardiac cycle (A, C). Tracing the boundaries near the edges of the vessel should be carefully performed to eliminate contamination from other vessels or excess static tissue. Basic statistics such as average velocity and peak velocity are plotted as a function of time, and curves can be generated (B, D). In addition, pressure gradient (mm Hg) calculation is possible through the Bernoulli equation ( 4 x velocity peak 2 ). These curves are used not only to determine flows but quantification of shunts. A B C D Hemodynamics 7.2 Flow Quantification

49. (A–C) Phase-contrast images of the aorta. ( A) Magnitude, ( B) phase-contrast, and ( C) angiographic images in a patient with LVOT obstruction. The VENC is 200 cm/s. Note aliasing (arrow in B). (D–F) With the corrected VENC of 275 cm/s, the aliasing resolves (arrow in E) . (D) Magnitude image. (E) Phase-contrast image. (F) Angiographic view image. When VENC is incorrectly selected as lower than the actual vessel flow velocity, aliasing occurs. The VENC represents the maximum velocity present in the imaging volume. Therefore, any velocity greater than the preselected VENC causes aliasing. In theses cases, undersampling results in coding of the high velocity flow as flowing in the opposite direction. The visual result is a central small area of disturbance encoded, contrary to the rest of the blood flow (B). The solution to aliasing is to increase the VENC, which can be done in 50 cm/s increments (D–F). Conversely, if maximum velocities are much smaller than VENC, only small phase differences are seen, resulting in low contrast to stationary tissue and a bad SNR ratio. Typical VENC values: AORTA: The first measurement is usually set at 200 cm/s . The usual peak velocity is 100–160 cm/s. PULMONARY ARTERY: The first measurement is 180 cm/s . The usual velocity for peak velocity measurement is 60–120 cm/s. Shunts can be interrogated with flows around 50–150 cm/s. E A B D F C Hemodynamics 7.3 Flow Quantification: Aliasing

50. (A–C) Phase-contrast images through the p ulmonic valve. (A) Magnitude, ( B) phase-contrast, and ( C) angiographic phase images show stenotic orifice (arrows). The area of the orifice can be measured (planimetry) and compared to normal values. Phase-contrast imaging may be used to determine severity of valvular stenosis. Once the direction of the peak velocity is identified on cine images, a through-plane acquisition perpendicular to the jet direction will be used to obtain the peak velocity (A–C). If there are several jets, the plane of highest velocity may not be captured and the stenosis severity underestimated. Most current clinical systems use segmented techniques that yield average velocities over multiple cardiac cycles. B C A Hemodynamics 7.4 Flow Quantification: Example

51. (A, B) 3Ch and LVOT cine images through the LVOT in a patient with HOCM. (C–E) Phase-contrast magnitude, phase, and angiographic view images of the through plane LVOT flow (arrows). (F) Flow-graph and (G) magnitude image show the region of interest. The gradient obtained was 39 mm Hg (severe obstruction). Interestingly, the AO/LVOT ratio was 0.25, which is also consistent with severe obstruction. F G A B C D E Hemodynamics 7.2 Flow Quantification: Example F G

52. (A ) 4Ch cine view. Example of a tricuspid regurgitant jet (arrow) due to hypertrophic changes of the RV in a patient with prior TOF correction. Detailed valve disease requires extra specific sequences beyond the scope of this presentation. However, in a standard CMR, besides anatomic evaluation, the dynamic images may reveal regurgitant or stenotic jets (dephasing jets) which occur due to flow disturbances and loss of laminar flow. When flow quantification is performed for the PA and AO , an indirect quantification of atrioventricular valve regurgitation is possible by subtracting the net FF of either the AO or PA from the ventricular stroke volume for the respective cardiac chamber, provided there are no cardiac shunts. Mitral regurgitation = LVSV - FFAO Tricuspid regurgitation = RVSV - FFPA (B) 4Ch cine view. Note severely thickened mitral valve leaflets. A regurgitant jet is apparent (mitral regurgitation). Regurgitation by indirect calculation is estimated at 20%. There is also a double lesion of the AO valve. Note both dephasing in systole from stenosis (aortic stenosis) and a regurgitant jet (aortic regurgitation). AS = aortic stenosis, MR = mitral regurgitation. A Hemodynamics 8.0 Valves AS AS MR B

53. Suggested Readings Attili AK, Schuster A, Nagel E, Reiber JH, van der Geest RJ. Quantification in cardiac MRI: advances in image acquisition and processing. Int J Cardiovasc Imaging 2010;26(suppl 1):27–40. Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation 2002;105(4):539–542. Ferreira VM, Piechnik SK, Robson MD, Neubauer S, Karamitsos TD. Myocardial tissue characterization by magnetic resonance imaging: novel applications of T1 and T2 mapping. J Thorac Imaging 2014;29(3):147–154. Hota P, Simpson S. Going beyond Cardiomegaly: Evaluation of Cardiac Chamber Enlargement at Non-Electrocardiographically Gated Multidetector CT: Current Techniques, Limitations, and Clinical Implications. Radiol Cardiothorac Imaging 2019;1(1):e180024. Kawel -Boehm N, Hetzel SJ, Ambale -Venkatesh B, et al. Reference ranges (“normal values”) for cardiovascular magnetic resonance (CMR) in adults and children: 2020 update. J Cardiovasc Magn Reson 2020;22(1):87. Kramer CM, Barkhausen J, Bucciarelli-Ducci C, Flamm SD, Kim RJ, Nagel E. Standardized cardiovascular magnetic resonance imaging (CMR) protocols: 2020 update. J Cardiovasc Magn Reson 2020;22(1):17. Messroghli DR, Moon JC, Ferreira VM, et al. Clinical recommendations for cardiovascular magnetic resonance mapping of T1, T2, T2* and extracellular volume: A consensus statement by the Society for Cardiovascular Magnetic Resonance (SCMR) endorsed by the European Association for Cardiovascular Imaging (EACVI). J Cardiovasc Magn Reson 2017;19(1):75. Nayak KS, Nielsen JF, Bernstein MA, et al. Cardiovascular magnetic resonance phase contrast imaging. J Cardiovasc Magn Reson 2015;17(1):71. O’Brien AT, Gil KE, Varghese J, Simonetti OP, Zareba KM. T2 mapping in myocardial disease: a comprehensive review. J Cardiovasc Magn Reson 2022;24(1):33. Tseng WY, Su MY, Tseng YH. Introduction to Cardiovascular Magnetic Resonance: Technical Principles and Clinical Applications. Zhonghua Minguo Xinzangxue Hui Zazhi 2016;32(2):129–144.