Cardiovascular Magnetic Resonance; Imaging for the Echocardiographer

Cardiovascular Magnetic Resonance; Imaging for the Echocardiographer Robert W W Biederman MD, FACC, FAHA, FSGC, FASA Director of Cardiovascular MRI Department of Medicine Associate Professor of Medicine February 26, 2009 Drexel University College of Medicine Allegheny General Hospital, Pittsburgh, PA Supported in part via an American Heart Association- National Scientist Development Grant

Cardiovascular Magnetic Resonance; Not Your Grandpa’s MRI! (Basic MRI) Robert W W Biederman MD, FACC, FAHA, FSGC, FASA Director of Cardiovascular MRI Department of Medicine Associate Professor of Medicine July 11, 2009 Drexel University College of Medicine Allegheny General Hospital, Pittsburgh, PA Supported in part via an American Heart Association- National Scientist Development Grant

Disclosures  NHLBI, AHA, GE  Research funding and honoraria from Merck-Schering-Plough I will discuss off label indications for Gadolinium

December 1, 2003 Front Cover of This Week’s US New’s and World Report

Is This Just Sensationalism?  In 2003, over a million people will die of an MI pre-hospital  250,000 will survive the trip only to be dead in 30 days  Another 250,000 will be dead in 335 more  If you have the misfortune to be a woman your odds are 50% worse  Over 1 million stents will be placed (How many Sirolimus stents at 2-3K?)  How many patients are at Goal per the NCEP guidelines?  CHF admissions are not decreasing  Rise of the Metabolic Syndrome

Are we getting closer?  Stem cells research in the last 2 years  Recent identification of MEF2A gene  Sirolimus stent*  Biventricular pacing  Alternative non-HMG Co A-reductase methods  Angiogenesis  Percutaneous implantation of prosthetic valves  Artificial cardiac support devices  Use of CVMRI for detection (and manipulation) of CV disease

Cardiac Structure and Function Artifact Artifact RV RV RA QuickTime™ and a RA LV GIF decompressor LV are needed to see this picture. LA LA Ao PE PE

Cardiovascular MRI Time Line 1946 MR phenomenon - Bloch & Purcell 1952 Nobel Prize - Bloch & Purcell 1950 NMR developed as analytical tool 1960 “ 1970 “ 1972 Computerized Tomography 1973 Backprojection MRI - Lauterbur 1975 Fourier Imaging - Ernst 1977 Firstbody images 1980 MRI demonstrated – Edelstein 1982 First cardiac images-Goldman and Pohost 1986 Gradient Echo Imaging NMR Microscope 1988 Angiography - Dumoulin 1989 Echo-Planar Imaging –Sir Peter Mansfield and Doyle 1991 Nobel Prize - Ernst 1993 Functional MRI (fMRI) 1994 Hyperpolarized 129Xe Imaging 1999 Practical real-time imaging 2003 Sir Peter Mansfield and Paul Lauterbaur

T1 relaxation T1 Relaxation The return of excited nuclei from the high energy state to the low energy or ground state is associated with loss of energy to the surrounding nuclei. Nuclear magnetic resonance was originally use to examine solids in the form of lattices, hence the name "spin-lattice" relaxation. Macroscopically, T1 relaxation is characterized by the longitudinal return of the net magnetization to its ground state of maximum length in the direction of the main magnetic field. The rate of return is an exponential process as is shown in the following figure.

T2 relaxation Microscopically, T2 relaxation or spin-spin relaxation occurs when spins in the high and low energy state exchange energy but do not loose energy to the surrounding lattice. This results macroscopically in loss of the transverse magnetization. In pure water, The T2 and T1 times are approximately the same, 2-3 seconds. In biological materials, the T2 time is considerably shorter than the T1 time. For CSF, T1=1.9 seconds and T2=0.25 seconds. For brain white matter, T1=0.5 seconds and T2=0.07 seconds (70 msec). T2 relaxation occurs exponentially like T1 relaxation with 63% of the transverse magnetization gone after one T2 period as shown in the graph

T2* relaxation T2* relaxation is the loss of signal seen with dephasing of individual magnetizations. It is characterized macroscopically by loss of transverse magnetization at a rate greater than T2. It is caused by magnetic field inhomogeneity an occurs in all magnets. The relationship between T2 and T2* can be illustrated by the multiecho spin echo sequence shown in the diagram below. The 180 degree RF pulses used to generate the echo are rephasing the spins that have undergone T2* decay. The gradual decline in signal from subsequent echos reflects T2 decay (See Figure). Unlike spin echo sequences, gradient echo sequences do not refocus T2* decay. Therefore, gradient echo sequences are more susceptible to ferromagnetic foreign bodies that distort the main magnetic field homogeneity.

What is the big deal about Cardiovascular MRI imaging? …said the spider to the fly

What is the big deal about Cardiovascular MRI imaging?  The Achilles' heal for CV imaging is that, unlike the brain and the knee cap, the heart is in constant motion (unless you have an HMO).  Synchronization of complex cardiac and respiratory motion (3D) is critical requiring integrated gating algorithms which have evolved over the last 15 years, are still in evolution, and limit to an extent our ability to acquire and register data.  Thus, images are typically gated to the R wave and a breathhold sequence is utilized (in 2008).

What is New in CV MRI ?  Valvular heart disease  Viability  MR angiography  Are there any contraindications remaining?  Use in guiding surgery  Is there a role for dyssynchrony?  Discrimination of CHF  Can myocardium ‘rise from the dead’?  The Holy Grail; have we finally found it?

SSFP-2 chamber SSFP-4 chamber SSFP-3 chamber Various 2D formulae: All dependent on assumption of near perfect prolate ellipse geometry: Biplane LA: LVEDV = 8 x Av x Ah/3π x L min Biplane Ellipsoid: LVEDV = HLA π/6 x L x (4/ π x Ad/d x 4 π x A1/L)

Two-Chamber View The two-chamber view is acquired from the axial plane and provides the most comprehensive information of left ventricle (LV) structure and function because it specifically delineates the territory subtended by the left anterior descending (LAD); the anterior and apical wall. The inferior wall territory is also demonstrated. Mitral valve anatomy and pathology is delineated in this plane as well. Note the subtle descending aortic dissection also seen in the “normal” patient.

Four-Chamber View Acquired from a two-chamber view, this acquisition provides dedicated information about the inferior septum, lateral wall, and is the most definitive (2D) view for the assessment of right ventricle, including tricuspid annular excursion (TAPSE). Additional information regarding the mitral and tricuspid valves, including morphology and pathology (regurgitation and stenosis) can also be obtained).

Three-Chamber View Acquired from a coronal or a short-axis slice, this view details the anterior septum, apex, and infralateral walls, and is the key view for certain 1D LV measurements. Mitral and aortic valve pathology can be evaluated, as can the right ventricle (RV) outflow tract.

Coronal Imaging Additional evaluation of both the LV and RV can be obtained in non-conventional views afforded by the unique ability of CMR to image in any plane. This plane provides additional information about segmental wall motion, the mitral, aortic, and tricuspid valves. *This plane often yields substantial anatomic detail about extracardiac anatomy.

Normal 60 or 17 YO WF?; No history of CV disease

17 YO or 60 WM w Pulmonary Arterial Hypertension referred for CVMRI to exclude secondary causes

Why is Left Ventricle/Right Ventricle Functional Assessment by Cardiovascular Magnetic Resonance the “Gold Standard” ?  Resolution (matrix >128 x 256)  High endocardial and epicardial intrinsic contrast  Absence of foreshortening due to exact placement  Near absence of user dependence  Reproducibility and accuracy to within 5 mL  Not dependent on geometric assumptions  Ability to perform 3D imaging for exact measurements quickly (no need for 2D anymore)  Volume–time measurements  Regional LV quantification; visually mathematically  Temporal resolution

How are Left Ventricle Magnetic Resonance Images Acquired? RA, right atrium; LA, left atrium; LAA, left atrial appendage; MV, mitral valve.

Acquisition of Standard Three-Dimensional Short- Axis Images Nontriggered axial (transverse) scout Four chamber Short axis Triggered axial (transverse) scout Two chamber

Three-Dimensional Short-Axis Scans are Integrated Two-Dimensional Multiple Slices

Evaluation of Left Ventricle and Right Ventricle Morphology and Function; Semiautomated Endocardial and Epicardial Contours

Three-Dimensional Reconstruction of the Left Ventricle

Three-Dimensional Representation of Left Ventricle/Right Ventricle Mechanics

Three-Dimensional Representation of Left Ventricle/Right Ventricle Interaction; Assessment of Right Ventricle/Left Ventricle Function

LVH Geometry by CMR Diastole Normal Concentric (AS) Eccentric (AR) Mixed (CRF) Systole McGill R, Biederman RWW. J of Nephrology (In press

What about Valves? “MRI can’t image valves”…M.E. Sarono Somewhere in Rochester MN May 2008

What is the Predominant Lesion? Left ventricular outflow tract (LVOT) murmur and a 95 mmHg gradient; note the dynamic mitral valve with evidence for SAM (systolic mitral anterior motion) creating a Venturi effect with resultant suction of leaflet and mitral regurgitation (middle panel). There are multiple level of cardiac systolic murmur etiologies: 2. Anterior mitral valve leaflet 3. LVOT obstruction 4. Mild turbulence off the aortic valve (right panel)

Valvular Dysfunction and its Manifestations 37 y/o female with mildly reduced exercise tolerance and a loud decrescendo diastolic murmur. A stress echocardiogram did not demonstrate ischemia. • MRI: Cine MRI (4-chamber and oblique QuickTime™ and a QuickTime™ and a view) demonstrates significant aortic GIF decompressor GIF decompressor are needed to see this picture. are needed to see this picture. regurgitation. The left ventricle diastolic dimension is 6.4 cm and the end systolic dimension is 5.5cm and the calculated EF is 48%. This meets AHA/ACC criteria for Valve replacement

Aortic Valvar structure

CMR vs. TEE  An example of the excellent capabilities of cardiac magnetic resonance (CMR) imaging to evaluate aortic valves. (Right) The valve in this example could not be assessed by transoesophageal echocardiography (TOE) since it was not possible to define all commissural areas due to calcification. (Left) Applying the continuity equation based on transthoracic echocardiographic (TTE) assessments was also limited in this case due to a poor acoustic window and calcified deposits in the outflow tract annulus. Heart. 2004 August; 90(8): 893–901.

8 Pre–Aortic Valve Replacement Post–Aortic Valve Replacement Biederman RWW et al., Circulation 2005

Aortic, Mitral, Tricuspid and Pulmonic valves

Aortic, Mitral, Tricuspid and Pulmonic valves AGH

Mechanism of Mitral Regurgitant Pathology Pt. A AGH AGH Mechanism: Pt. A Pt. B MR trace 3-4+ Age 65 66 Sex M M EF: 21% 22% LVEDVI 102ml/m 105ml/m 2 2 Pt. B AGH AGH LVEsVI 21ml/m 2 23ml/m 2 r/h 0.81 0.82 Mass/vol 1.21 1.19 Annulus 33x32mm 40x38mm Tenting 105° 125° Coapt 9mm 15mm Tenting 1.6mm 2 2.6cm 2 Biederman et al, Circ 2005

Aortic Regurgitation by MRI Phase Velocity Mapping FGRE FIESTA AGH AGH AGH AGH By Phase Velocity Mapping: Forward stroke volume: 86ml Regurgitant volume: 21ml Regurgitant fraction: 24% Correlation to pulsatile phantom r=0.989

Hyperenhancement Phenomenon AGH AGH 6 weeks following MI Hypertensive patient Biederman, RWW. J Cardiovasc Mag Res. 2006;8:4;123

Evaluation of an Uncommon Acute Coronary Syndrome Please see next slide

Corrected Cardiomyopathy: without Surgery Day 1 Tako-Tsabo cardiomyopathy Day 25

Post–Dor Procedure for Ischemic Cardiomyopathy Pre-Dor Post-Dor (A) A large myocardial infarction (MI) several years previously had resulted in marked global dilation and a large apical-anterior scar after which the 68-year-old patient underwent after an LV apical patch placement (B) to restore ventricular size and correct apical geometry (the Dor procedure). Radio-frequency tissue tags A B placed in the four-chamber view are seen at end-diastole (C) and Post-Dor Post-Dor Post-Dor in the short-axis at end-systole (D) show a weak contractile pattern in the mid-inferior wall (red arrow) while the remainder of the LV shows a prominent contractile pattern. Preliminary CMR data supports the heart transplant saving benefits of this novel and evolving surgical technique. C D Radiofrequency tissue tagging

Status Post Myocardial Infarction: Now Status Post Dor Procedure A B C (A) A large MI several years previously had resulted in marked global dilation and a large apical-anterior scar after which the patient underwent after an LV apical patch placement (arrow) to restore ventricular size and correct apical geometry (Dor procedure). RF tags placed in the short axis view are seen at end-distole (B) and at end-systole (C) show a weak contractile pattern in the midinferior wall (arrow) while the remainder of the LV (chevrons) shows a prominent contractile pattern.

Pre–Aorta Valve Replacement Post–Aorta Valve Replacement Strain deformation depicted as a color schema whereby blue is highest and red is lowest %Strain. Note, the subtle inferior wall RF tissue tagging contractile patterns present in the right column: A very quick observation leads one to believe it is contracting. Either by observing the lack of the tile deformation (top) or observing the lack of color change (bottom), the effect of wall tethering is nicely demonstrated. Thereby, ‘apparent’ endocardial excursion is present but due to tethering effects of the adjacent LV myocardium, the perceived motion is erroneous. This phenomenon is quite evident in Strain the post-myocardial infarction patient yet invisible by our current color modalities via echo, nuclear, CT or schema our cardiac catheterization techniques yet are critically important to be identified when revascularization strategies are being contemplated. (Presented at the AHA-2004 Biederman et al.)

MRI Principles  Atomic nuclei with odd numbers (1H, 31P, 23Na and 13C) have a magnetic moment allowing nuclei to precess when tipped from alignment from the main magnetic field.  The MRI signal originates primarily form the the hydrogen of water and less so from the H of lipids (ie; carboxyl group). Yet the actual appearance of the image is related more to the variety of physical properties-tissue characteristics and image parameters (sequences).  An essential difference between MRI and other imaging modalities is the control users have in how data is acquired and manipulated. The agent of this control is k-space (Fourier space). K-space is the platform onto which data are acquired, positioned, and then transformed into images.

MRI Principles (Excitation)  MRI uses high-power static magnetic fields interleaved with low-power changing magnetic fields along with radio-frequency(RF) pulses to generate tomographic images.  Application of weak RF-modulated pulses of a specific frequency will partially align the magnetic moments of protons within the tissue sample against the magnetic field and will induce their resonance; the effect of this RF field is maximal when the nuclei have been deflected by 90o  The energy for image generation and the key to the physical process is: when the RF pulse ceases the protons return to general equilibrium and release energy which can be measured by induction coils (antenna).

Applications of CVMRI  Evaluations of:  “Gold standard” for LV structure (mass)(Cranney et al, Circulation, 1990:154-63)  “Gold standard” LV function (EF) (Cranney et al, Circulation, 1990:154-63)  “Gold standard” for evaluation of anomalous coronary arteries  “Gold standard” for ‘hard to find lesions’ (Biederman et al , Current Problems in Cardiology, 2001, 1-64)  Congenital heart disease  Aortic pathology-Dissections, Aneurysms and interrupted aortas  LV masses  Arythmogenic Right Ventricular Dysplasia/RVOT  Cardiomyopathy

Emerging uses  Dobutamine Stress Test (Hundley et al, Circulation, October 1999 and accompanying Editorial: Pohost and Biederman)  Real time cardiac imaging currently up to 66 phases per cardiac cycle (13ms)  Valvular evaluation ( Hundley et al, Circulation 1996-Regurgitant volume calculation and AGH-gradient quantification by Phase Velocity Mapping)  Ischemia-Delayed enhancement-probably a time related exponential estimation of region at risk within the LV (Rogers et al, Circulation, 2000, and Kim et al, Circulation 2000  Catheter coil interrogation ( Rogers et al)  Intraluminal and aortic wall pathos ( Fayad and Fuster et al Circulation 2000 and Rogers et al ATVB, 2000

Emerging uses (Build a better mouse trap…Ralph Waldo Emerson)  CABG grafts patency (Aurigemma et al,Circulation, 1989:80;1595-1605)  Coronary imaging (Galjee et al, Circulation1996:93;660-668)  Quantification of coronary stenosis (Rogers et al, Proc Soc Mag Res 1994;1;370-377)  Myocardial perfusion (WISE) (Doyle, submitted to JACC)  Post Infarct LV Remodeling (Foster, et al Am Heart J, 1998;136:269-275, Mankad et al Circulation, 2001)  Post surgical assessment of LV reconstruction of (Batista and Dor procedures), White and Biederman  Constrictive pericarditis with application of RF tags (Sechtem et al, AJR 1986 and Hasada et al Cardiol 1999;92(3);214-6)

Efficiency Entwined with Precision  Bottini et al, Am J Hyperten. 1995; 8(3); 221-228. (MRI vs Echo)  Bellinger et al. European Heart J, 2001 (MUGA vs Echo vs MRI  Swan J et al AJR Aortic imaging by CVMRI vs X-ray angiography “Emerging concepts of precision, efficiency, cost containment and front loaded patient care”… Biederman, 2001

Integrated “One Stop Shop”  Cardiovascular anatomic morphology (LV mass and function), thickness of LV walls, post MI remodeling, thrombus  Global and regional contractile function  Myocardial perfusion studies with paramagnetic contrast (at rest and stress)  Morphologic assessment of coronary tree and assessment of CABG bypass graphs  Myocardial metabolism by NMR spectroscopy  (Adapted from Pohost and Biederman, Circulation Editorial, 1999)

Left Ventricular Hypertrophy Regression and Left Ventricular Strain Pre–Aortic Valve Replacement Late (13 months) following AVR End-diastole End-systole End-diastole End-systole (Biederman, RWW et al., Circulation 2005)

Left Ventricular Reconstruction (Dor Procedure) Pre Post (1month) Late (1year) LVEDV: 300 mL, LVEDV: 158 mL, LVEDV: 194 mL, LVEDV 223 mL, LVEDV 118 mL, LVEDV 137 mL, LVSV 77 mL, LVSV 40 mL, LVSV 57 mL, LVEF 25%, and LVEF 30%, and LVEF 24%, and MR 1–2+ MR 2+ MR 2–3+

Aortic Valve Replacement-SSFP Imaging Pre–AVR Post–AVR

Rotational Patterns in the Heart- HARmonic Phase (Biederman, RWW et al., Circulation 2005)

Systolic Torsion and Diastolic Untwisting in Aortic Stenosis; Pathologic or Expected Reduction Following Aortic Valve Replacement? 30 30 25 25 20 30 20 15 15 20 10 10 5 5 10 0 0 1 2 3 4 5 6 7 8 9 10 11 12 13 1415 1617 18 19 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 0 -5 -5 10 13 16 19 1 4 7 -10 -10 -10 Systolic torsion Systolic torsion and diastolic Systolic torsion and and diastolic untwisting untwisting—(6 months diastolic untwisting— —(pre— AVR) following AVR) (14 months following AVR) (Biederman, RWW et al., Circulation 2005)

HARmonic Phase Analysis for Rapid Radio frequency— A B Tag Analysis HARP LV end-diastolic (A) and end-systolic (B) images demonstrating tags (Rathi V et al., submitted to JACC overlaid by epi, endo and mid-wall contours (semiautomatic). A strain map Biederman et al., Circulation 2005) is then generated demonstrating intramyocardial deformation. 30 30 30 25 25 25 20 20 20 15 15 15 Torsion (°) 10 10 10 5 5 5 0 0 0 1 2 3 4 5 6 7 8 9 10 11 12 1314 15 16 1718 1920 1 2 3 4 5 6 7 8 9 10 11 1213 1415 16 17 1819 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 -5 -5 -5 -10 -10 -10 A B C HARP offline analysis of base to apex torsion in a patient with aortic stenosis. (A) is pre–aortic valve replacement (AVR), (B) is 6 month post AVR and (C) is 14 months post–AVR. Y axis = Torsion (°), X axis = time (ms)

Is “Exuberant Hypertrophy” Hype, Hyperbole or History? Male Aortic Stenosis —pre–Aorta Valve Diastole Systole Replacement Female Diastole Systole 2D cardiovascular magnetic resonance imaging (CVMRI) images of geometry in (A) 65 YO WM with a small thick LV and (B) 68 YO MN with a larger, thinner LV, both with similar mean gradient (52±4 mm Hg), BSA (2.1±1), and LVMI corrected for end diastolic volume (EDV) (1.33±0.10) but with dissimilar LVMI. BSA = body surface area, LVMI = LV mass index

Circumferential Strain—Normal (Courtesy of Elliot McVeigh, PhD, NIH)

Dilated Cardiomyopathy— Resynchronization with Pacing (Courtesy of Elliot McVeigh, PhD, NIH)

What about MRI for Myocardial Necrosis?  Ubiquitous process but difficult to quantitate  Techniques have relied on invasive or inexact techniques:  Microsperes with gamma/beta counters  X-ray angiography (subtended vessels)  Radionuclide techniques  Electrocardiography  Contrast Echocardiography

How about for the Myocardium?… Delayed Hyperenhancement (DHE) AGH AGH AGH Pt 1 Pt 2 Pt 3

MRI Delayed Hyperenhancement  Gadolinium DPTA is a chelate that decreases T1 of blood approximately 15 fold when administered IV  Gadolinium has the following ideal characteristics:  Inert  Safe  Non-radionuclide imaging  Is imaged without x-ray  Remains interstitial  High degree of discrimination between normal and infarct  High degree of sensitivity and specificity (>95%) in MI  Can image in under 30 minutes  Can combined with LV function analysis, “Gold Standard”  Acute or chronic imaging  High reproducibility  The 2003 reference standard,“Gold Standard” for viability

Comparison of SPECT, contrast-enhanced CMR, and histology in a dog with a nearly transmural infarct  Short axis views from three dogs with subendocardial infarcts Wagner et al, Lancet 2003;361:234-246

Why is CV MRI like Shania Twain?  They both are both sensational (to look at too)  They both keep you up at night  They both have a lot of heart  When they are good, they are very, very good  But they are only good to a select few  Only one looks good in a pair of jeans  But only one can be my mistress!

Explanation:Delayed Hyperenhancement Hypothetical representation of contrast distribution in blood (left) and myocardial tissue (right) under equilibrium conditions. The extracellular space in this text refers to the sum of the interstitial plus the intravascular volumes minus the volume occupied by red blood cells within the myocardial intravascular space. Lima J et al Circulation. 1995;92:1117-1125

Spatial Resolution Changes all the Rules Wagner.Lancet .Feb 2003;361:374379

Three short-axis views (apical, equatorial, and basal) of a PET viability study with assessment of rest perfusion (NH3) and glucose metabolism (FDG). Below, MRI images in corresponding slices showing hyperenhancement. Note that in segments with reduced perfusion and metabolism, there is an increased signal in MRI. Because of better spatial resolution in MRI, distinction between transmural, subendocardial, and papillary defects can be made. The border between enhanced and normal areas is distinct. Klein C et alCirculation. 2002;105:162

Myocardial Viability Typical Contrast-Enhanced Images Obtained by MRI in a Short-Axis View (Upper Panels) and a Long-Axis View (Lower Panels) in Three Patients. Hyperenhancement is present (arrows) in various coronary-perfusion territories — the left anterior descending coronary artery, the left circumflex artery, and the right coronary artery — with a range of transmural involvement. Kim et al. NEJM 2000;343 (20): 1445

Relation between the Transmural Extent of Hyperenhancement before Revascularization and the Likelihood of Increased Contractility after Revascularization. Data are shown for all 804 dysfunctional segments and separately for the 462 segments with at least severe hypokinesia and the 160 segments with akinesia or dyskinesia before revascularization. For all three analyses, there was an inverse relation between the transmural extent of hyperenhancement and the likelihood of improvement in contractility. Kim et al. NEJM 2000;343 (20): 1445

RF Tissue Tagging Demonstrates Return of Function week 1 week 6

67 YO F Status Post Myocardial Infarction 1 Year Ago Wanted: Alive or dead?

67 YO F s/p “MI” Wanted: Alive or dead? AGH Brown

Viability: Is there more that meets the eye? 59 YO WF, school teacher,with NYHA IV symptoms Told,” all dead nothing we can do; go home” AGH AGH AGH AGH LVEF 18% LVEDV 255ml Geometry: 1.2

Why is This? Nuclear(incl PET) MRI Spatial 1.0-1.3cm 1.0-1.5mm Resolution Voxel 3-5cm 8-10mm resolution SNR 6 20 CNR 8 >100 Difference in 1 60-80 resolution

Why is CV MRI like Shania Twain?  They both are both sensational (to look at too)  They both keep you up at night  They both have a lot of heart  When they are good, they are very, very good  But they are only good to a select few  Only one looks good in a pair of jeans

Can viability return in wall thickness <5mm? AGH AGH

Can Kloner and Braunwald be wrong and CMR be right? Is thinned myocardium obligatorily beyond salvage? DHE (Viability) SSFP (Systolic imaging) Pre CABG Post CABG Pre (top row) and post (bottom row) demonstrating remarkable improvement in wall thickness following intervention despite substantial DHE but a viable rim of 5mm. Courtesy of Ron Mikolich, MD.

Evaluation of cardiomyopathy: part of an integrated approach First pass perfusion Delayed hyperenhancement

55 YOM Presents with similar story but for >1 year AGH lendyak

Does DHE Predict Transplantation need? Role of MultiHance in predicting Cardiac transplantation Heart MACE Unchanged/ Worsening Transplant Worsening EF NYHA 5 7 8 8 +DHE/ +Stripe (9) 0 1 1 1 +DHE/ _ Stripe(2) 0 0 0 0 _ DHE/ _ Stripe (2) Biederman, RWW et al. JCMR 2009 (abst) and ISHLT Paris April 2009

Oh Please Dr. Biederman, don’t stop now! Hint!

Cardiovascular Magnetic Resonance; Not Your Grandpa’s MRI! (Advanced MRI) Robert W W Biederman MD, FACC, FAHA, FSGC, FASA Director of Cardiovascular MRI Department of Medicine Associate Professor of Medicine July 11, 2009 Drexel University College of Medicine Allegheny General Hospital, Pittsburgh, PA Supported in part via an American Heart Association- National Scientist Development Grant

How About for Congenital Heart Disease?

Aortic Dissection LSA RSA C C A A LR M RR A MA A A  Rotating MRA of entire thoracic/abdominal aorta with a spiral Type III dissection. Image acquisition was performed in 22 seconds. Note the spiral nature that is characteristic of a Type III dissection as the aorta is rotated (large arrow). Other arteries are seen including the mesenteric artery (MA), celiac artery (CA), left and right and renal arteries (LRA and RRA) in the proximal and mid sections, as well as, large sections of the left and right subclavian arteries (LSA and RSA) arising from the true lumen.

Sinus Venosum  A persistent left superior vena cavae (VC) is visualized suggesting the possibility of a previously unrecognized unroofed coronary sinus ASD. V However, a confluence of C right upper pulmonary veins entering the high right atrium/right superior vena cavae is seen, consistent with a sinus venosum defect.  The sinus venosum defect is seen in a coronal image depicting the entry site into the RA (arrow) and right SVC (chevron).

Coarctation  A markedly narrowed coarctation is seen in (a) with a high velocity jet (braces) extending 80mm into the descending aorta.  (b) The dilated internal mammary artery (arrow) carrying blood to the intercostal arteries and eventually to collateralize the lower extremity is seen.  The degree of narrowing of the coarctation is appreciated in cross-section in (c) (arrow) as are a the enlarged internal mammary arteries (chevrons).Since there is a high risk of intercerebral aneurysm and polycystic kidney disease.  (d) and (e) provided additive information c b compared to traditional angiography. Note, in (d) that possible indications are present of early renal cystic changes. d e

Patent Ductus Arteriosum  Gradient echo image showing high velocity jet (arrow) in late systole from the aortic arch entering into the pulmonary artery via a15mm communication (PDA).  HR axial image showing anterior lumen off the descending aorta (arrow) at the site of the PDA entrance.  Contrast enhanced MRA images of a cranial view of the aortic arch revealing the PDA (arrow) and a pre ductal coarctation (chevron).

Anomalous Pulmonary Great Vein- at Transplanatation Vessels  During orthotopic cardiac PV transplantation an anomolous Aorta C pulmonary vein entering the brachiocephalic vein was seen in the P recipient requiring the creation of a A LUPV pulmonary venous conduit (from donor vein) to the superior left LA atrium (LA). Follow up using 3D MRI six months later revealed a patent conduit to the left upper pulmonary Descending vein (LUPV). Aorta

27 YO BF s/p Jatene

Tetralogy of Fallot with Aortic Aneurysm and Dissection

Ostium Secundum Defect (ASD) SSFP 4-ch GRE-4-ch SSFP-axial PVM 4-ch

WHO 2 (Mitral Regurgitation) RVOT view TV annular ring

“Positive” Bubble Study

MIPP Source MIPP Anomalous Left Upper Pulmonary Vein Draining Into the Vertical Vein (“Partially Partial Anomalous”)

Interrupted IVC Is this Nl or pathologic?

41 YO WM with diagnosis of l- transposition since a child. Cong corr

Pulmonary veins by CMR

RV Function: ARVD 45 YO WM with Sudden Death T2 (TIR) T2 (TIR) T2 (TIR) McKenna et al Working Group Classification 1994: 1) Thinning/Fat deposits in anterior wall RV (Apoptosis, Fat Transformation or Dysontogenetic theory) 2) Enlarged RV 3) Focal RV free wall motion abnormalities (aneurysms, crenulations) *4) Contrast enhancement

Abnormal Septal Motion: Etiology?

Thickened Pericardium; Constrictive Pericarditis?

Constrictive Pericarditis: Adherence Pattern between Visceral and Parietal Pericardium by MRI

Large Lipoma; Extreme Lipomatous Inner Atrial Hypertrophy

What about MRI for Myocardial Necrosis?  Ubiquitous process but difficult to quantitate  Techniques have relied on invasive or inexact techniques:  Microsperes with gamma/beta counters  X-ray angiography (subtended vessels)  Radionuclide techniques  Electrocardiography  Contrast Echocardiography

MRI Delayed Hyperenhancement  Gadolinium DPTA is a chelate that decreases T1 of blood approximately 15 fold when administered IV  Gadolinium has the following ideal characteristics:  Inert  Safe  Non-radionuclide imaging  Is imaged without x-ray  Remains interstitial  High degree of discrimination between normal and infarct  High degree of sensitivity and specificity (>95%) in MI  Can image in under 30 minutes  Can combined with LV function analysis, “Gold Standard”  Acute or chronic imaging  High reproducibility  The 2003 reference standard,“Gold Standard” for viability

Mechanism of Delayed Hyperenhancement  A probe for cellular membrane integrity  Molecular size large enough to to freely exist in the vascular space and rapidly distribute  Gadolinium increases the T1 signal in myocardium  Gadolinium is excluded from myocardial cells with intact membranes  Signal attenuation depends on microheterogeneity of distribution in tissue because the media resides in extracellular not the intracellular space

Mechanism, cont.  Using IR prep EPI, the volume of distribution (Vold) provides an index of the percentage of necrotic myocardial cells within a zone of ischemic injury  Indicator achieves a near equilibrium state due to the observed proportionality constant between ∆T1 relaxation rate of myocardium and blood pool  Vold is slightly increased by H20 but substantially increased by loss of myocyte cellular integrity  Extent of enhancement represents the percentage of non-viable cells  Not accurate if the ROI is subtended by a no- reflow zone (central core of necrotic cells), but after 20 minutes this region is in equilibrium

Attributes Cross-platform for MI Imaging Characteristic SPECT ECHO MRI Spatial resolution ↑ ↑↑ ↑↑↑ Sensitivity ↑↑ ↑ ↑↑↑ Specificity ↑ ↑ ↑↑↑ Quantitation ↑ ↑ ↑↑↑ Speed ↑ ↑↑ ↑↑↑ Cost ↑↑↑ ↑ ↑↑ Cost-effectiveness ↑↑ ↑ ↑↑↑ Platform availability ↑↑↑ ↑↑ ↑ Claustrophobia ↑ ↑ ↑↑ Proven in MI ↑↑↑ ↑ ↑↑ User-independent ↑ ↑ ↑↑↑ Reproducibility ↑↑ ↑ ↑↑↑ Subendocardial imaging -- -- ↑↑↑ Variability ↑ ↑ ↑↑↑ Viability ↑↑ ↑ ↑↑↑

Technique  1.5 General Electric clinical CV MRI scanner  Routine standard imaging-(non-research mode):  Cardiac phased array coil, non-invasive monitor  Respiratory and cardiac gating  First pass and delayed hyperenhancement imaging  Selective saturation pulse to null myocardium and blood pool  Segmented EPI gradient (FSPGRE)  Imaged every other heart beat  Inversion recovery sequence  Spatial resolution: 1.3-1.7mm in-plane  0.1mMol/kg gadolinium dimeglumine  Infarct definition: myocardium with higher signal intensity than NL  Quantitative analysis using ROI’s at baseline and 30 days

Regression of MDE-with matched Improvement in Function Week Week Ti=200ms week 6 Ti=200ms 1 6 week 1 EDV(ml) 71 83 SV(ml) 38 50 EF(%) 53 60 LVM(g) 99 116 week 1 Ti=200ms week 6 Ti=200ms

RF Tissue Tagging Demonstrates Return of Function week 1 week 6

Comparison of SPECT, contrast-enhanced CMR, and histology in a dog with a nearly transmural infarct  Short axis views from three dogs with subendocardial infarcts Wagner et al, Lancet 2003;361:234-246

Spatial Resolution Changes all the Rules Wagner.Lancet .Feb 2003;361:374379

First Pass Perfusion-Syndrome X Images of Myocardium at Peak Myocardial Enhancement during the First Pass of Gadolinium in a Patient with Syndrome X at Rest (Panel A) and during Stress (Panel B), Showing a Ring of Delayed Subendocardial Enhancement (Arrows in Panel B). Panting et al. Abnormal Subendocardial Perfusion in Cardiac Syndrome X Detected by Cardiovascular Magnetic Resonance Imaging NEJM 2002 ;346 (25): 1948.

Myocardial Perfusion  Perfusion study obtained after dipyridamole infusion from a patient with single vessel coronary artery disease (80% RCA stenosis). (a) Prior to contrast agent arrival, myocardium appears to have uniformly low intensity; (b) a a b b contrast arrival in the RV; (c) contrast in the LV and the myocardium, where a contrast deficit in the inferior wall is apparent (arrow); (d) the deficit improves in a later frame. Frames (c) and (d) resemble the thallium redistribution phenomenon. c d c d

Myocardial Viability Typical Contrast-Enhanced Images Obtained by MRI in a Short-Axis View (Upper Panels) and a Long-Axis View (Lower Panels) in Three Patients. Hyperenhancement is present (arrows) in various coronary-perfusion territories — the left anterior descending coronary artery, the left circumflex artery, and the right coronary artery — with a range of transmural involvement. Kim et al. NEJM 2000;343 (20): 1445

Myocardial Viability Typical Cine Image and Contrast-Enhanced Image Obtained by MRI before Revascularization. Registration of the images was not required, because both types were acquired during the same MRI session. Twelve equal circumferential segments were analyzed in each short-axis view. For contrast-enhanced images, the transmural extent of hyperenhancement was determined for each segment with use of the following equation: percentage of area that was hyperenhanced = 100 x area A ÷ (area A + area B). Kim et al. NEJM 2000;343 (20): 1445

Relation between the Transmural Extent of Hyperenhancement before Revascularization and the Likelihood of Increased Contractility after Revascularization. Data are shown for all 804 dysfunctional segments and separately for the 462 segments with at least severe hypokinesia and the 160 segments with akinesia or dyskinesia before revascularization. For all three analyses, there was an inverse relation between the transmural extent of hyperenhancement and the likelihood of improvement in contractility. Kim et al. NEJM 2000;343 (20): 1445

Representative Cine Images and Contrast-Enhanced Images Obtained by MRI in One Patient with Reversible Ventricular Dysfunction (Panels A and B) and One with Irreversible Ventricular Dysfunction (Panels C and D). The patient with reversible dysfunction had severe hypokinesia of the anteroseptal wall (arrows), and this area was not hyperenhanced before revascularization. The contractility of the wall improved after revascularization. The patient with irreversible dysfunction had akinesia of the anterolateral wall (arrows), and this area was hyperenhanced before revascularization. The contractility of the wall did not improve after revascularization. Kim et al. NEJM 2000;343 (20): 1445

Explanation:Delayed Hyperenhancement Hypothetical representation of contrast distribution in blood (left) and myocardial tissue (right) under equilibrium conditions. The extracellular space in this text refers to the sum of the interstitial plus the intravascular volumes minus the volume occupied by red blood cells within the myocardial intravascular space. Lima J et al Circulation. 1995;92:1117-1125

Three short-axis views (apical, equatorial, and basal) of a PET viability study with assessment of rest perfusion (NH3) and glucose metabolism (FDG). Below, MRI images in corresponding slices showing hyperenhancement. Note that in segments with reduced perfusion and metabolism, there is an increased signal in MRI. Because of better spatial resolution in MRI, distinction between transmural, subendocardial, and papillary defects can be made. The border between enhanced and normal areas is distinct. Klein C et alCirculation. 2002;105:162

Visual assessment of MRI data is more accurate, yet, overestimates scar compared with PET Why?  MRI can delineate segments more accurately, because the border between hyperenhanced and normal areas is distinct, whereas in non-gated PET images, the border between normal and defect areas is less well defined. (Fifty-five percent of segments showing a subendocardial enhancement by MRI were classified as normal by PET. Since the assessment of wall thickness is limited by the spatial resolution of non-gated PET, epicardial tracer activity may mask small subendocardial defects. Therefore, MRI might provide, with its better spatial resolution, a more subtle delineation of scar tissue than PET.  FDG is a marker for viability, whereas Gd-DTPA is considered a marker for scar tissue. Thus, a relatively small number of viable cells may show increased FDG uptake probably due to a hypermetabolic state, indicating local viability, whereas structural changes may already coexist and altering Gd-DTPA kinetics. Therefore, PET imaging may show viability in segments with hyperenhancement, but in areas that are in fibrotic scarred tissue, incapable of contracting.  An increase in regional signal intensity (Gd-DTPA) is easier to interpret by CV MRI than a regional comparison of both flow and metabolism by PET. Personal discussions with Markus Schwaiger, MD, München, Germany

Non-Ischemic Cardiomyopathy 54 y/o male with increasing dyspnea. No prior cardiac history, however has a long history of ETOH abuse. • Peak CK: ruleout; Troponin: ruleout QuickTime™ and a GIF decompressor • Cath Report: Clean coronaries are needed to see this picture. • MRI: Interventricular septum is dyskinetic with severe hypokinesis of the remainder of the LV (cine MRI). Contrast enhanced MRI showed no hyperenhancement anywhere, including the focal region of dyskinesis (arrow).

Same patient: clot or necrosis? 10 minutes 30 minutes 10 minutes 30 minutes

67 YO F s/p MI 1 year ago Wanted: Alive or dead? Brown

The Chairman of CT surgery wants to know: Alive or Dead? Phelan

Why is This? Nuclear(incl PET) MRI Spatial 1.0-1.3cm 1.0-1.5mm Resolution Voxel 3-5cm 8-10mm resolution SNR 6 20 CNR 8 >100 Difference in 1 60-80 resolution

41 YO s/p large MI 6 months ago Fluck

Viability: Is there more that meets the eye? 59 YO WF, school teacher,with NYHA IV symptoms Told,” all dead nothing we can do; go home” AGH AGH AGH AGH LVEF 18% LVEDV 255ml Geometry: 1.2

MRI Viability: How Low Can You Go? DHE All Viable Except for 0.5g of Myocardium 53 YOWM referred for Viability by Tony Farah/Rob Maholic: Answer?

38 YO WF with acute chest pain, minimally elevated troponin-i trivially elevated creatine kinase-myocardial bound (CK- mb) (7 IU) and normal coronary arteries by x-ray angiogram. CMR performed to evaluate high coronary artery disease (CAD) suspicion despite above results.

What is this? FIESTA Delayed Hyperenhancement Perfusion 1) Tumor 2) Infiltration 3) Thrombus 4) Acute MI 5) LV contusion

What does it mean to you as a Cardiologist? …as a CT surgeon? What does it mean to you as a Cardiologist? …as a Patient? Pt A Diastole Systole Viability …as a CT surgeon? …as a Patient? Post CABG Representative Cine Images and Contrast-Enhanced Images Obtained by MRI in One Patient with Reversible Ventricular Dysfunction (Panels A and B) and One with Irreversible Ventricular Dysfunction (Panels C and D). Pt B Diastole Systole Viability The patient with reversible dysfunction had severe hypokinesia of the anteroseptal wall (arrows), and this area was not hyperenhanced before revascularization. The contractility of the wall improved after revascularization. The patient with irreversible dysfunction had akinesia of the anterolateral wall (arrows), and this Post CABG area was hyperenhanced before revascularization. The contractility of the wall did not improve after revascularization. Kim et al. NEJM 2000;343 (20): 1445

55 YOM Presents with similar story but for >1 year AGH lendyak

67 YO BF presents last week with 2 yrs of fatigue, SOB and weight gain and peculiar findings on echo AGH AGH AGH tucker

Does DHE Predict Transplantation need? Role of MultiHance in predicting Cardiac transplantation Heart MACE Unchanged/ Worsening Transplant Worsening NYHA EF 5 7 8 8 +DHE/ +Stripe (9 pts) 0 1 1 1 +DHE/ _ Stripe (2 pts) 0 0 0 0 _ DHE/ _ Stripe (2 pts) Biederman, RW, submitted to AHA

AGH AGH 6/6/06 AGH 25 YO WM with FH of SCD presents for evaluation of ‘peculiar’ EKG AGH

Thrombus vs. Fat vs. Fluid vs…

Quantitative Velocity Imaging  The conventional image and the corresponding velocity encoded image  Acquired in a plane parallel to the mitral valve  A graph of the flow is shown for the region encompassing the mitral valve

Infarct, mass, or diverticulum?

35 YO M with peculiar story as a child

Why is LV/RV Functional Assessment by CMR the ‘gold standard’ ?  Resolution (matrix >128x256)  High endocardial and epicardial intrinsic contrast  Absence of foreshortening due to exact placement  Near absence of user dependence  Reproducibility and accuracy to within 5ml  Not dependent of geometric assumptions  Ability to perform 3D imaging for exact measurements quickly no need for 2D anymore  Volume-time measurements  Regional LV quantification; visually, mathematically  Temporal resolution

SSFP-2 chamber SSFP-4 chamber SSFP-5 chamber Various 2D formulae: All dependent on assumption of near perfect prolate ellipse geometry: Biplane LA: LVEDV = 8 x Av x Ah/3π x L min Biplane Ellipsoid: LVEDV = HLA π/6 x L x (4/ π x Ad/d x 4 π x A1/L)

Methodology for LV/RV function and Mass Assessment  Localizer defined LV short axis. Images acquired from low left atrium to beyond apex of the left ventricle  EKG-gated to R-wave with breath-hold segmented k space dynamic (SSFP preferred) imaging using contiguous 7mm slice thickness, FOV 30 cm or less, 128 x 256 matrix, temporal resolution < 25-30 ms.  End-diastolic, end-systolic volumes and LV mass are calculated as the product of slice thickness, number of pixels, and absolute pixel size  For LV mass, multiply derived LV area inscribed by endocardial and epicardial contours by the specific gravity of LV myocardium (1.0055).

Evaluation of LV Systolic Function  Ejection Fraction:  SV/EDV=Total EF  Systolic Wall Thickening (% Thickening):  ES thickness- ED thickness / ED thickness  Centerline Analysis:  Circumferential Segmental Analysis  Systolic Strain (%S)  ED length-ES length/ED Length

Impact of Regurgitation on EF  Effective EF in Mitral Regurgitation:  SV/EDV (SV derived from Aortic PVM)  Effective EF in Aortic Regurgitation:  SV/EDV (SV derived from Aortic PVM)  Regurgitant volume = 3DSV- Forward PVMSV  Regurgitant fraction = 3DSV- F-PVMSV/3DSV

Acquisition of Standard 3D Short Axis Images Non-triggered axial (transverse) scout 4 Chamber Short Axis Triggered axial (transverse) scout 2 Chamber

3D Short-Axis Scans are Integrated 2D Multiple Slices

Evaluation of LV & RV Morphology and Function; Semi-automated Endocardial and Epicardial Contours

Complicated Myocardial Infarction 58 YO GI Physician with LHCath with EF= 51%

Evaluation of Cardiomyopathy; Part of an Integrated Approach First Pass Perfusion Delayed Hyperenhancement

LV Aneurysm, LV Pseudoaneurysm or LV Diverticulum? None of the above: Myocardial Hamartoma

PRE -AVR PRE -AVR PRE -AVR POST-Aortic Valve Replacement PRE-Aortic Valve Replacement Biederman RWW et al, submitted to Circulation

Hypertrophic Cardiomyopathy

Post Dor Procedure for Ischemic Cardiomyopathy Pre-Dor

RV Function  Not quite the same as for the LV but remains the ‘gold standard’ due to resolution, FOV and 3D  Acquired in same manner; SA is best with acquisition starting above the pulmonic valve (3-4 slices above MV plane)  RV mass quantification possible, best with SSFP.  RV function: RWMA, qualitative, or quantitative.  RF tissues tagging is challenging  Excellent for congenital heart disease and ARVD. Lorenz C et al. JCMR 1998;1:7-21 Fogel MA et al. Circulation 1995;15:219-230.

Myocardial Function Problems Solutions  Breathhold  Real time imaging or dynamic sampling  Time  Dynamic sampling  Valve plane motion  Floating MV plane  Diastolic function  Phase velocity mapping/ torsion recovery  RF tagging  Regional wall motion  RF tagging  Inability to track discrete material Points  Tethered motion  RF tagging  Distinguish between  RF tagging chamber function and myocardial performance

Myocardial Function: Radio-Frequency Tissue Tagging  Based on the deposition of presaturation planes intersecting the myocardium  Typically, systolic deformation (tags)are assessed following the ‘R’ wave  Tracked through time, the property of underlying myocardium (T1) and rate of imaging determine the survival of tags  Quantified mathematically  Interrogation of strain as a measure of deformation  Allows for the deconvolution of bulk cardiac motion (rotational and translational) [This may be greater in magnitude than the local myocardial deformation].  Provides a measurement of regional wall function in terms of a tensor.  Can be expressed as vector or color schema

Myocardial Strain Diagram illustrating the calculation of circumferential and longitudinal strains from long- and short-axis tagged data. Though not shown in this diagram, principal strains and fiber and cross-fiber direction strains can subsequently be calculated from the circumferential and longitudinal strains. MacGowan G. et al. Noninvasive Measurement of Shortening in the Fiber and Cross-Fiber Directions in the Normal Human Left Ventricle and in Idiopathic Dilated Cardiomyopathy. Circulation 1997; 96: 535-541.

How are LV MR Images Acquired?

Short Axis Scans are Multiple Slices

Echocardiography vs MRI: detection of LVH  With an alpha set at 0.05, beta at 0.80, the question was asked “ How many patients would it take to detect a 10g decrease in LVH following pharmacological therapy by Echo and by MRI?”  Answer: 550 patients by echo and 17 patients by MRI  The precision of LVM by MRI (11 g) was over twice that observed with ECHO (26 g).  The reliability of MRI LVM estimates was more consistent (+/- 8 g) than that for ECHO (+/- 49 g). Bottini PB et al Magnetic resonance imaging compared to echocardiography to assess left ventricular mass in the hypertensive patient Am J Hypertens 1995 Mar;8(3):221-8

Pharmogologic Applications  A pharmaceutical company (using its brains ,  not its brawn ) could capitalize and convert such knowledge into faster return on their R&D expenses, more rapid submission to the FDA, and likewise, sooner FDA approval  For example: if it takes 500 pts to demonstrate efficacy in LV mass regression over 5 years (it took 9,194 in the LIFE trial), using echocardiographic techniques @ $500/echo and 100 patients@$1000/ MRI over 9 months (4E-Eplerenone) and the average amount per patient for FU/expenses is $1000/year, THEN…

Costs Number Costs Years Total Costs Echo 500 $ 500 5 $2,750,000 MRI 100 $1000 0.75 $ 175,000 Difference $2,575,000 % Difference 6.8% Note; this does not include the average amount of dollars lost once NDA is applied for and approved by the FDA: $1,000,000/day)

Myocardial tagging technique Problems Solution  Material tagged points  Addressed by are not necessarily registration with an those points that are orthogonally acquired associated with that image image at end systole  Tag persistence  Common k-space technique  tracking algorithm for mathematical strain  Semi-automated-Finite representation Element Modeling  Cuboidal heterogeneity  Limited by physiological deformation approaching image

Rotational Patterns in the Heart-HARP Biederman, RWW et al, Circulation 2005

MRI Radio-frequency tagging ®MRI RF tissue tagging is an optimal tool for the evaluation of ventricular function; ®improved contrast ®spatial resolution ®signal to noise ratio ®transmural nature ®reproducibility ®validated ®inherent 3D nature

HARP Analysis for Rapid RF - Tag Analysis Biederman et al, Circulation 2005 A B HARP LV end -diastolic (A) and end-systolic (B) images demonstrating Tags overlaid by epi, endo and mid - wall contours (Semiautomatic). A strain map is then generated demonstrating intramyocardial deformation. 30 30 30 25 25 25 20 20 20 15 15 15 Torsion (° ) 10 10 10 5 5 5 0 0 0 1 2 3 4 5 6 7 8 9 10 11 12 1314 15 16 1718 1920 1 2 3 4 5 6 7 8 9 10 11 1213 1415 16 17 1819 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 -5 -5 -5 -10 -10 -10 A B C HARP offline analysis of base to apex torsion in a patient with aortic stenosis. A is pre Aortic Valve Replacement (AVR), B is 6 month post AVR and C is 14 months post AVR. Y axis = Torsion (°), X axis = time (ms)

Is ‘Exuberant Hypertrophy’ Hype, Hyperbole or History? Male Aortic Stenosis- pre AVR Diastole Systole Female Diastole Systole 2D CVMRI images of geometry in A) 65 YO female with a small thick LV and B) 68 YO male with a larger, thinner LV, both with similar mean gradient (52±4mmHg), BSA (2.1±1), and LVMI corrected for EDV (1.33±0.10) but with dissimilar LVMI

LV Reconstruction (Dor Procedure) Pre Post (1mo) Late (1yr) LVEDV: 300 ml, LVEDV: 158 ml, LVEDV: 194 ml, LVEDV 223ml, LVEDV 118ml, LVEDV 137ml, LVSV 77ml, LVSV 40ml, LVSV 57ml, LVEF 24% LVEF 25% LVEF 30% MR 2-3+ MR 1-2+ MR 2+

Diastole

Diastolic Function -Restrictive Pattern; What Precision is Achievable? Rathi VR, Biederman RW. J of Cardiovasc Mag Res 2008; 11;205-215.

But can CMR Duplicate More Sophisticated Measurements? TTE MRI Myocardial velocities at mitral annulus (septum) by Tissue Doppler Imaging (TDI) vs. PVM

Velocity Measure Measurements Mark Doyle, Ph D MRI ‘Doppler’

What can’t Cardiac MRI do?  It can’t spin your wheels…but it can spin your protons.  It can’t image all…but all can imagine being imaged  It can’t enhance your heart…but it can hyperenhance your patients heart  It can’t turn an unclear image into nuclear!  But it can make your heart beat faster…if you see Dr. Rathi.

4D Stream Lines for Aortic Flow Markl R, et al, Circulation 2006

What is the difference in body vs. cardiovascular MRI (CMR)? Function Anatomy Myocardial strain

Virtual Luminal Angiography; Complex aortic dissection The Fantastic Voyage…Aldous Huxley, PhD

Surface Rendering Volume Rendering

Can your Daddy’s MRI Machine do this? Virtual Luminal AKA: Angiography The Fantastic Voyage by Aldous Huxley, PhD

AGH Surface Rendered MRA …in 9 seconds AGH

Why is Maria Sharapova like MRI?  They both serve up excellent images  They both are both sensational (to look at too)  They both keep you up at night  They both have a lot of heart  When they are good, they are very, very good  But they are only good to a select few  Only one looks good in a pair of jeans  But only one can be my mistress!

Why is CV MRI like Shania Twain?  They both are both sensational (to look at too)  They both keep you up at night  They both have a lot of heart  When they are good, they are very, very good  But they are only good to a select few  Only one looks good in a pair of jeans  But only one can be my mistress!

The Holy Grail

APPROPRIATENESS CRITERIA 90 minutes in a smoke filled bar and a blood alcohol of 0.06

67 YO Attorney +FH, Father MI at 48, and no CP Wants to know, “Am I next?” Courtesy of Ronald Mikolich, MD

Coronary Imaging

Coronary Artery Imaging Today in a perfect world  SENSE reduces acquisition time by a factor of 2  Balanced TFE increases resolution  RCA and LCA can be acquired in the same time  Exam time: 5 min

Three-Dimensional Breath-Hold, Non-gadolinium Coronary Arteries (Courtesy of Melind Desai, MD Johns Hopkins, former AGH CV Fellow)

3D Breath hold, Non-Gadolinium Coronary Arteries Courtesy of Melind Desai, MD Johns Hopkins, former AGH CV Fellow

How about the coronaries?

Coronary Artery Imaging Free breathing: works in progress

Is this CT or CMR?

The ARBITER Study Kent S. M., et al, AHA 11/2002

It would matter little if there were a rupture in the plaque's fibrous cap were it not for the ensuing thrombus!

Visualization of Ruptured Plaque by CV MRI Magnetic resonance T2-weighted turbo-spin-echo images in transverse orientation revealing increased wall thickness of the carotid and vertebral arteries. A, Note the pronounced thickening of the posterior arterial wall in both the right and left internal carotid artery. B, Significantly thickened vessel wall in the left carotid bifurcation (LCAbif). Also shown are two arteriosclerotic lesions in the right common carotid artery (RCCA) with dark lipid core and thin fibrous cap. C, Close-up of right common carotid artery suggestive of plaque rupture with discontinuity of the thin fibrous cap (arrow). ECG-gated MRI (double-inversion recovery turbo-spin echo) was performed on a 1.5-T clinical scanner by use of a paired surface coil phase array for signal reception. Imaging parameters were the following: TR, 2 cardiac cycles; TE, 81 ms; field of view, 12 cm; in-plane resolution, 0.47x0.47 mm2; and slice thickness, 3 mm. RECA indicates right external carotid artery; RICA, right internal carotid artery; LECA, left external carotid artery; LICA, left internal carotid artery; RVA, right vertebral artery; and LVA, left vertebral artery. Visualization of the Ruptured Plaque by Magnetic Resonance Imaging Frank Wiesmann, Matthew D. Robson, Jane Francis, Steffen E. Petersen, C. Paul Leeson, Keith M.

Vertebral Artery Plaque

Introduction  Atheroma vulnerability to rupture is hightened in the presence of a large lipid core and further raised in setting of a thin fibrous cap on the plaque.  Morphologic characteristics of plaque composition have been proposed to explain the apparent paradox of improved clinical events despite no or minimal reduction in % stenosis with statins. CMR can distinguish underlying features that determine plaque ‘vulnerability’.  Coronary lesions demonstrate that rupture of the fibrous cap overlying the lipid core typically occurs where it is thinnest and most heavily infiltrated by inflammatory cells  MRI can non-invasively characterize human carotid atheroma composition delineating lipid admixtures in vivo. Falk E.Coronary thrombosis: pathogenesis and clincial manifestations. Am J Cardiol.1991; 68:28B-35B.

Hypothesis  We hypothesize that in statin-naive patients with high-grade carotid artery stenosis, there will be a high degree of correlation in the relationship between the ‘unstable’ lipid pool and ‘stable’ fibrous plaque by 3D CMR, yet may be independent of 2D percent stenosis.

Methods  Symptomatic patients were recruited who were referred for imaging who demonstrated ≥50% stenosis by any technique (MRA, carotid Dopplers [range] or x-ray angiography) representing 530-two mm contiguous CMR (1.5T GE) in vivo slices of advanced (mean 61±24% stenosis) carotid disease.  26 complete bilateral human (age: 66±14yrs) plaques were analyzed for 3D volumetric extent of vascular wall: lipid pool, fibrous cap, matrix and minima/maxima of each.  All were related to fasting lipid levels relative to %stenosis as a function of underlying lipid fractions, subfraction and component ratios.

Methods, cont  3D MRI imaging (1.5T GE, EXCITE, Milwaukee, WI)  Serial 2mm, contiguous images using T1/PD/T2 imaging guided by non-MRA prior imaging aimed at the area of region of greatest stenosis, generally in viscinty of carotid bulb. Baseline images were triangulated for use in one-year.  No gadolinium was used.  In all, 25/26 in vivo plaques were imaged.  Mean resolution: 0.7x 0.7x 2mm with 256x256 matrix, FOV 18 and sl thickness 2mm interleaved with blood suppression and pulse gating.

Methods, cont  3 plane high resolution localizer: Sequence parameters: Fiesta scout, 13images in each direction (Z,X,Y), 384 x384 matrix, NEX =2, PFOV=1, TE=Min, FA=45, Band=125,Fov=37  Cervical spine is used as the landmark because it is the most stationary structure and most reproducible in a 1 year time span. Breathing, swallowing, head positioning such as tilting can change but the cervical spine will remain the stable structure.  Utilize sagital image and center to the top of C3 or C4 disc. Center images to make sure bifurcation will be captured on images. Centering is crucial and must be reproduced for 2nd scan.  Transverse T1 black blood sequence from the top of C3 disc to about C7. TE=15ms. Sat band is used to suppress respiratory motion. Blood suppression is essential for this protocol and pulse (peripheral) gating.  Sequence Parameters: TE=15, BSP=Auto, ET=12, Bandwidth=11.9, FOV=18,sl=2, Matrix 256x256, Nex=1,FOV=1, SAT=I/S  Transverse T2 black blood sequence from the top of C3 disc to about C7. TE=100 Make sure SAT band is used to suppress respiratory motion. All other parameters are the same as the T1.

Carotid Plaque Analysis  Images were acquired in axial projection in a 2D and 3D manner  via QPlaque (Medis, The Netherlands). Plaque morphology determined by T1, T2/PD CMR.  Windows and level settings were set to constant levels to standardize signal intensities for each analyzed image.  Manual contours identified: 1. Fibrous cap 2. Lipid pool 3. Outer and inner wall contours 4. T2 images were reviewed to determine/confirm lipid core determination with the T2 image used to confirm lumen contour. – Fasting lipid profiles drawn on day of MR imaging

Results  Lipid range:  Chol Total 116-262mg/dL (180±40mg/dL)  LDL-C: 63-186mg/dL (116±11mg/dL)  HDL-C: 28-59mg/dL (43±9mg/dL)  TG: 81-213mg/dL (134±48mg/dL)  Lipid pool represented 15±4% while fibrous cap represented 5±15% of total vessel wall.  Total Cholesterol (CholT) and LDL-C were inversely related to minimum vessel wall thickness (r=-0.5 and -0.6, respectively, p<0.05, for both) while only CholT was related to fibrous cap (r=0.6, p<0.01).

Carotid Plaques PRE PRE LEFT RIGHT

Carotid plaques PRE PRE LEFT

Carotid plaque PRE RIGHT

Carotid Analysis

Carotid plaque LEFT

Results, cont  All patients had a lipid core and thus a fibrous cap independent of any cholesterol level.  The greatest amount of lipid pool was generally associated with highest total cholesterol (r=0.5, p<0.05)  The CholT /LDL-C ratio was highly related to minimum fibrous cap thickness (r=0.8, p<0.001).  The 3D lipid pool was the only fraction highly correlated (>0.6) with triglycerides (r=0.6, p<0.01).  A linear regression relating fibrous cap: vessel wall ratio to non-HDL cholesterol and CholT was highly correlated (r=0.6, 0.7, respectively, p<0.01 for both) but was independent of in vivo %stenosis (r=0.1).  Relating %stenosis demonstrated no significant relationship as related to the plaque composition (r=0.19; p=0.54).

Conclusion  Percent stenosis provides relatively little information about vulnerability of de novo, statin-naive carotid plaques.  As most current imaging studies concentrate on plaque stenosis, a more appropriate focus on plaque composition provides a more robust quantifiable volumetric metric and may be more indicative of the underlying pathology by high-resolution 3D CMR.

Much thanks goes to:  Mark Doyle, PhD.  Ronald B. Williams  Saundra B. Grant, RN  Geetha Rayarao, MS  June A. Yamrozik  Vikas K. Rathi, MD  Diane A. Vido, MS  Wadih Nadour, MD  Janice Meister  David R. Neff, DO*  Jeanine Privitera*  *Merck Schering- Plough Research Laboratories, North Wales, PA.

Conclusion  MRI; it’s not just another pretty face  If you need the answer, and the answer matters, think MRI  If in doubt, MRI will help  If you still have questions… that is why it is a 3 year CV fellowship  “…and now you know the rest of the story” Velocity Mapping-Aorta

Thanks to:  Mark Doyle, PhD  Vikas K. Rathi, MD  June Yamrozik, RT  Ronald B. Williams, RT  Geetha Rayarao, MS  Saundra B. Grant, RN  Diane A.Vido, MS  Janice Meister, Sec  None of this is possible without:  Kimberly  Brittani  Addison  Caroline

38 YO presents with “bizarre” cath finding 1) Coronary fistula 3) anomalous pulmonary vein 5) ectatic LIMA graft 2) Cameral fistula 4) persistent LSVC

Cardiovascular Magnetic Resonance Imaging for the Elderly Robert W W Biederman MD, FACC, FASA, FSGC Director of Cardiovascular MRI Department of Medicine Associate Professor of Medicine September 2008 Drexel University College of Medicine Allegheny General Hospital, Pittsburgh, PA Supported in part via an American Heart Association- National Scientist Development Grant

Normal 60 or 17 YO WF?; No history of CV disease

17 YO or 60 WM w Pulmonary Arterial Hypertension referred for CVMRI to exclude secondary causes

The One-Stop Shop: are we there yet? Can we be there for those> 60years old?

Coronary artery-CABG by MRI

Coronaries the AGH Way

Diagnostic Accuracy of Coronary Magnetic Resonance Angiography to Detect Stenoses of >=50 Percent Kim W et al. N Engl J Med 2001;345:1863-1869

Is this CT or CMR?

Selected References  Higgins et al Prediction of Myocardial Viability. Circulation 1999  Rogers et al Early contrast enhancement MRI predicts late functional recovery after reperfused myocardial infarction. Circulation 1999  Sechtem U et al Assessment of myocardial viability in patients with MI using MRI techniques Circulation 1995  Wendland M et al Toward necrotic cell fraction measurements by contrast-enhanced reperfused ischemically injured myocardium Acad Radiol 1998  Ricciardi M et al Visualization of discrete microinfarction after PTCA associated with mild CK-MB elevation Circulation 2001  Rogers W and Biederman R Timing is everything MR Imaging in Med 2001  Klein C et al Assessment of Myocardial viability with contrast enhanced MRI, Comparison with PET Circulation 2002  Doyle M and Biederman R Regions of Delayed Hyperenhancement can demonstrate long term improvement Circulation 2002  Doyle M and Biederman R Predictive value of early delayed hyperenhancement; post revascularization Circulation 2002

Visualization of Ruptured Plaque by CV MRI Magnetic resonance T2-weighted turbo-spin-echo images in transverse orientation revealing increased wall thickness of the carotid and vertebral arteries. A, Note the pronounced thickening of the posterior arterial wall in both the right and left internal carotid artery. B, Significantly thickened vessel wall in the left carotid bifurcation (LCAbif). Also shown are two arteriosclerotic lesions in the right common carotid artery (RCCA) with dark lipid core and thin fibrous cap. C, Close-up of right common carotid artery suggestive of plaque rupture with discontinuity of the thin fibrous cap (arrow). ECG-gated MRI (double-inversion recovery turbo- spin echo) was performed on a 1.5-T clinical scanner by use of a paired surface coil phase array for signal reception. Imaging parameters were the following: TR, 2 cardiac cycles; TE, 81 ms; field of view, 12 cm; in-plane resolution, 0.47x0.47 mm2; and slice thickness, 3 mm. RECA indicates right external carotid artery; RICA, right internal carotid artery; LECA, left external carotid artery; LICA, left internal carotid artery; RVA, right vertebral artery; and LVA, left vertebral artery. Visualization of the Ruptured Plaque by Magnetic Resonance Imaging Frank Wiesmann, Matthew D. Robson, Jane Francis, Steffen E. Petersen, C. Paul Leeson, Keith M. Channon, and Stefan Neubauer Circulation 2003 108: 2542

Vertebral Artery Plaque

Can Plaque Morphology Change? Impact of Vytorin 10/40mg Pre statin One-year Post statin (June 3rd, 2008) Biederman RWW, Grant SB, Doyle M et al, Featured presentation at AHA 2008

CMR for Interrogation of Strain  Radio-frequency Interrogation of strain tissue-tagging Biederman RWW et al. HTN 2008;52(2):279-286 Epub 2008 Jul 7

MRI Radio-frequency tagging ®MRI RF tissue tagging is an optimal tool for the evaluation of ventricular function; ®improved contrast ®spatial resolution ®signal to noise ratio ®transmural nature ®reproducibility ®validated ®inherent 3D nature

HARP Analysis for Rapid RF - Tag Analysis Rathi V et al, submitted to JACC Biederman et al, Circulation 2005 A B HARP LV end -diastolic (A) and end-systolic (B) images demonstrating Tags overlaid by epi, endo and mid - wall contours (Semiautomatic). A strain map is then generated demonstrating intramyocardial deformation. 30 30 30 25 25 25 20 20 20 15 15 15 Torsion (° ) 10 10 10 5 5 5 0 0 0 1 2 3 4 5 6 7 8 9 10 11 12 1314 15 16 1718 1920 1 2 3 4 5 6 7 8 9 10 11 1213 1415 16 17 1819 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 -5 -5 -5 -10 -10 -10 A B C HARP offline analysis of base to apex torsion in a patient with aortic stenosis. A is pre Aortic Valve Replacement (AVR), B is 6 month post AVR and C is 14 months post AVR. Y axis = Torsion (°), X axis = time (ms)

Rotational Patterns in the Heart-HARP Biederman, RWW et al, Circulation. 2005;112(9 Suppl):I429-36

Constrictive Pericarditis the Easy Way: Radio-frequency Tissue Tagging

Example: Dyssynchrnoy

MRI Dyssynchrony Results: Constrained Region Mid Region, Post MI, With Patch  At post MI for the 60 50 108 mid-ventricular 40 region, the absolute 30 20 dyssynchrony index Bin Value 10 Std. Dev = 108.65 Mean = 296.8 0 N = 195.00 was lower in the 15 77 13 20 26 7 32 8 38 9 45 9 51 57 1 63 1 69 2 76 82 3 88 4 1. 3. 5. 7. 0. 0. 2. 4. .5 .6 9. 2. 4. 6. 8. 7 0 3 5 End-Systolic Time (ms) mesh group vs. Mid Region, Post MI, No Patch controls 30  108 ms vs. 123 ms 20 123  F< 0.05 10 Bin Value Std. Dev = 123.36 Mean = 329.9 0 N = 121.00 19 97 17 25 33 41 48 56 64 72 80 88 .6 .8 6. 4. 2. 0. 9. 3. 2. 7. 5. 0. 1 1 3 6 9 4 7 9 2 4 End-Systolic Time (ms)

Results: Constrained Region  Comparing change from baseline to post MI in the mid-ventricular region: Dyssynchrony Index Change From Baseline The percentage increase in Dyssynchrony Index Change  60% dyssynchrony was lower in 50% the mesh group vs. controls 40% by a factor of 2 * Mesh (%) 30% Control  23% vs. 50%, p<0.05 20% 10%  Similarly, the percentage 0% increase ES time was lower Mesh Control in the mesh group vs. controls by almost a factor of End-Systolic Time Change From Baseline 2 End-Systolic Time Change (%) 40%  19% vs. 34%, f<0.05 35% Now part of Peerless Trial 30%  25% 20% * Mesh Control 15% 10% 5% 0% Mesh Control

22 sec Breath-hold stem-stern MRAngio

Done Cardiovascular MRI Gone in 60 Seconds… starring Nicholas Cage

Illiac Vessels  Aortic run-off 3D MRA reformatted image with the appearance of a string sign in the left iliac artery (arrow) suggesting a high grade stenosis. The image was initially misinterpreted as a severe stenosis, and this diagnosis was later overturned when it was found that a stent had been placed (a stent serves to “shield” the vessel from the MRI signal).

Safety  MRI is an example of imaging that does not cause lesions in biologic tissues (at Tesla<4.0), ours is 1.5T  No radionuclide imaging, No nephrotoxic contrast or associated anaphalactoid risk* No need for intra-arterial injections and no VF risk  Contraindications arise out of the effect of magnetic fields on magnetic implants  Absolute contraindications:  AICD and pacemakers, (neurostimulators should be added)  Thermodilution catheters (induction of thermal injury)  Certain pre-1994 and rare post 1994 intracerebral clips  Some intraocular implants  Foreign bodies: metal shavings in the eye, lodged missiles and extra MRI metal

Safety, cont  Relative contraindications:  Claustrophobic patients (<1.5%)  Pregnancy  Critically ill patients-monitoring (magnetohydrodynamic effect)

First rule… Safety first

Second rule… Safety First Hospital Nightmare Boy, 6, Killed in Freak MRI Accident July 31 — A 6-year-old boy died after undergoing an MRI exam at a New York-area hospital when the machine's powerful magnetic field jerked a metal oxygen tank across the room, crushing the child's head. The force of the device's 10-ton magnet is about 30,000 times as powerful as Earth’s magnetic field, and 200 times stronger than a common refrigerator magnet. The canister fractured the skull and injured the brain of the young patient, Michael Colombini, of Croton-On-Hudson, N.Y., during the procedure Friday. He died of the injuries on Sunday, the hospital said. The routine imaging procedure was performed after Colombini underwent surgery for a benign brain tumor last week. Westchester Medical Center officials said he was under sedation at the time of the deadly accident. Hospital Takes ‘Full Responsibility’

Safety is Paramount

What is that fuzzy Radiologist doing in my MRI machine?

Virtual Luminal Angiography

CMR in Cardiac Amyloidosis ROC curve for subendocardial T1 (left) and the difference in subendocardial and blood T1 (right) at 4 minutes after gadolinium injection for identifying cardiac amyloid. As a result of the abnormal blood and myocardium gadolinium kinetics, the difference between subendocardial T1 and blood T1 is substantially lower in the amyloidosis group than in controls.  CMR in a patient with systemic AL amyloidosis. Top row shows diastolic frames from cines (vertical long axis, horizontal long axis, and short axis, respectively) showing a thickened LV and pleural effusions (Pl eff) and pericardial effusions (Pc eff) associated with heart failure. Bottom row shows late gadolinium enhancement images in the same planes. The CMR sequence forces myocardium remote from the pathology to be nulled (black) such that the abnormal region is enhanced. In cardiac amyloidosis, however, the region of greatest abnormality is enhanced as the entire myocardium is affected with amyloid infiltration, and the result is diffuse global subendocardial enhancement (straight arrows). The endocardium of the right ventricle (RV) is also heavily loaded with amyloid, and therefore the septum in the horizontal long axis view shows biventricular subendocardial enhancement with a dark midwall (zebra appearance; dotted arrows). The right ventricular free wall is also enhanced (curved arrow). Note that the blood pool is dark, which does not occur in other reported conditions, indicating abnormal gadolinium handling in these patients. LA indicates left atrium; RA, right atrium. Alicia Maria Maceira, MD; Jayshree Joshi, BSc; Sanjay Kumar Prasad, MD, MRCP; James Charles Moon, MB, MRCP; Enrica Perugini, MD; Idris Harding, BSc; Mary Noelle Sheppard, MD, FRCPath; Philip Alexander Poole-Wilson, MD, FRCP; Philip Nigel Hawkins, PhD, FRCP; Dudley John Pennell, MD, FRCP. Circulation 2005

Thalassemia, Hemochromatosis and Hemosiderosis  A cardiac T2* MRI image shows myocardial iron stores. The lighter ventricle walls in left image indicate heavy iron loading. (38)  Reductions in cardiac iron assessed by MRI correlate with improvements in cardiac function (41, 47). Direct correlation between myocardial iron concentrations (MICs) assessed by MRI and LICs assessed by biopsy is lacking. Importantly, patients with “acceptable” levels of iron in the liver may have increased concentrations of iron in the heart (38).  Assessment of hepatic iron overload  MRI measures tissue iron concentration by detecting the paramagnetic influences of storage iron (ferritin and hemosiderin) on the proton resonance behavior of tissue water (37). This effect can be detected by calculating the longitudinal (R1) and transverse (R2) nuclear magnetic relaxation rates of nearby solvent water protons. Ferritin enhances both R1 and R2 relaxation, but hemosiderin only has a strong R2 relaxation accelerating effect. For this reason, R2 is favored over R1 for determining liver iron concentration (LIC).  MRI has been calibrated to liver biopsy results (38–40). However, the quantitative accuracy of MRI varies with the equipment and, more importantly, the diagnostic protocols used. MRI can be used to monitor reductions in hepatic iron after chelation therapy (41).  Anderson et al, 2004

Hemochromatosis of the Heart? 62 YO M s/p 25 yrs of chelation/transfusion therapy General model: LIVER f(TE) = K*exp(-TE/T2h) Coefficients (with 95% confidence bounds): K= 192.1 (155.8, 228.4) T2h = 16.94 (11.52, 22.37) Goodness of fit: SSE: 1487 R-square: 0.8802 Adjusted R-square: 0.8652 RMSE: 13.63 General model: Heart f(TE) = K*exp(-TE/T2li) Coefficients (with 95% confidence bounds): K = 1.456e+004 (-2.404e+005, 2.695e+005) T2li = 0.4651 (-0.7186, 1.649) Goodness of fit: SSE: 7.443 R-square: 0.965 Adjusted R-square: 0.9606 RMSE: 0.9646

Is there such a Beast as Fatty Transformation of the Myocardium post MI? 76 YO WM 2XIR 3XIR PERFUSION

DHE in same pt with myocardium replaced with fat

Flow Sensitive 4D MRI at 3T Methods Data Acquisition ECG gating & respiration control • Navigator gating • Adaptive k-space ordering • spatial resolution (2.5 x 2 x 3.5)mm3 • TRes = ~48ms, TAcq=15 - 20min 3D Blood Flow M. Markl Diagnostic Rediology Visualization Medical Physics A. Frydrychowicz UNIVERSITY J. Hennig FREIBURG HOSPITAL

Flow Sensitive 4D MRI Mild Aortic Aneurysm • Local flow acceleration high flow along outer AAo • Complex & vortical flow systole: moving flow vortex AAo DAo M. Markl Diagnostic Rediology Medical Physics A. Frydrychowicz UNIVERSITY J. Hennig FREIBURG HOSPITAL

Flow Sensitive 4D MRI at 3T Normal Aorta • Complex 3D flow in entire Ao - helical out-flow - early diastolic retrograde flow • Path of particles in time-resolved 3D velocity vector field • Color-coding = abs. local velocity M. Markl Diagnostic Rediology Medical Physics A. Frydrychowicz UNIVERSITY J. Hennig FREIBURG HOSPITAL

Why is Maria Sharapova like MRI?  They both serve up excellent images  They both are both sensational (to look at too)  They both keep you up at night  They both have a lot of heart  When they are good, they are very, very good  But they are only good to a select few  Only one looks good in a pair of jeans  But only one can be my mistress!

How about in non-infarct settings? Can we detect cardiac sarcoidosis ? 57YO WF

Dr. Biederman, “Can I lose weight by getting a CMR scan with fat suppression imaging?” Fat suppression in CMR describes a pulse sequence feature (=imaging acquisition mode), which allows to selectively suppress the signal from fat (unfortunately it does not burn fat). This CMR technique yields additional information e.g. in the evaluation of arrthythmogenic right ventricular cardiomyopathy (ARVD), where fat can infiltrate the right ventricular myocardium. CMR pulse sequences with and without fat suppression applied to the RV myocardium can objectify this SSFP sequence (dynamic) TIR (fat suppression) pathological process in ARVC. So, fat suppression in CMR does not reduce fat mass in patients. Of course in obesity, the success of a diet e.g. can be accurately quantified by MR (in units of gram). MR allows to selectively image the fat and thus, to quantify subcutaneous as well as intra-abdominal fat, and its reduction caused e.g. by a lifestyle change.

Is ‘Exuberant Hypertrophy’ in the Elderly Hype, Hyperbole or History? Subtitle: can Blase Carabello and Beverly Lorell be wrong? AGH Female 65 YO Aortic Stenosis- pre AVR Diastole Systole Male 68 YO Diastole Systole 2D CVMRI images of geometry in A) 65 YO female with a small thick LV and B) 68 YO male with a larger, thinner LV, both with similar mean gradient (52±4mmHg), BSA (2.1±1), LVMI and LVM corrected for EDVI (1.33±0.10) but with dissimilar RWT . Biederman, RWW. J Cardiovasc Mag Res. 2005;8:4;234

RV Perforation: 85 YO Unrestrained WM Curiosity seen on TTE- Life threatening rupture on CMR

 But can we estimate velocities well? By using VTI in the continuity equation approach, functional aortic valve dimensions can be calculated. Valve orifice dimensions calculated by velocity-encoded MRI data correlate well with those calculated by Doppler ultrasound (A). Bland- Altman analysis (B) also confirms that the methods agree, exhibiting a mean difference near zero. Shelton D. Caruthers, PhD; Shiow Jiuan Lin, MS; Peggy Brown, RDCS; Mary P. Watkins, RT; Todd A. Williams, RT; Katherine A. Lehr, ADN; Samuel A. Wickline, MD Practical Value of Cardiac Magnetic Resonance Imaging for Clinical Quantification of Aortic Valve Stenosis Comparison With Echocardiography. Circulation. 2003;108:2236.

Are pacemakers and ICDs safe for MR imaging?  Pacemakers (PM) and ICDs are a contraindication for MR imaging, since leads may heat during rf pulsing in the scanner and the magnetic field and gradient switching can cause malfunctioning of the device (see overview by Shinbane et al, J. Cardiovasc. Magn. Reson., 2007:9;5-13).  Reports on incidental imaging of PM and ICD patients with severe and even deadly complications are published. However, in smaller studies patients with PM and ICDs have been imaged without major adverse effects. Since sufficient evidence on safety is missing, PM and ICDs are regarded as contraindicated for MR imaging.  In individual cases and with adequate patient preparation (e.g. device programming), corresponding monitoring and expert knowledge available, and follow-up control visits, MR imaging in selected cases may be justified weighting the need for MR information against risk.  During the past 10 years, MR-compatible PMs were under development. The first specifically designed MR-compatible PM underwent successful MR imaging as a world-premiere on April 10, 2007 (University Hospital Zurich, Switzerland, in cooperation with the Federal Institute of Technology, and Medtronic, EnRhythm MRI Study).

65 YO M s/p CABG x 3, equivocal echo and cath. He is hypotensive, intubated and in great extremis. He is referred for high clinical pre-test probability constrictive Pericarditis but…he has a pacemaker. What to do?

Can there be a worse prognosticator for SCD then EF? Effect of ejection fraction on mortality between days 0 through 30, after 30 days through 2 years, and cumulative. (Probability determined by logistic regression analysis.) MI indicates myocardial infarction. Two- year survival curves for patients with last available ejection fraction (EF) >40% vs 40%: A, all enrolled patients; B, only patients who survived to 30 days. Vertical lines denote censored cases. MI indicates myocardial infarction.

The Paradox of EF in SCD NEJM 2003

 Ngoc Tsai, Michael Dishart, Brian Veynovich, Kosum Tom, Jose Oliva, Anil Singh, Saundra B Grant, June A Yamrozik, Ronald B Williams, Vikas Rathi, Mark Doyle, Robert W W Biederman Background Peri-operative (PO) cardiac complications of liver transplantation (LTX) are devastating. Classical PO evaluation involves echocardiography and stress nuclear imaging to define risk, prognosticate and to provide cardiac clearance. However, over the last decade cardiovascular MRI (CMR) has emerged as the 'gold standard' for many important CV metrics used to define such risk due to its unparalleled spatial resolution, lack of ionizing radiation and intrinsic 3D capabilities. Hypothesis We hypothesize that a CMR PO evaluation of pts being considered for LTX could be performed in a 'One-Stop-Shop' manner more efficiently, effectively and in more detail, obviating several days of work-up; all more inexpensively. Methods Standard 1.5T CMR (GE, Milwaukee WI) was performed using a combination of SSFP, DIR, FSPGR, DHE [post- contrast (MultiHance, Bracco, NJ)] and flow sequences to evaluate LV/RV size, systolic function, valvular and structural pathology. A standard CMR Adenosine stress test was then performed with a myocardial viability assessment. Thoracic and abdominal imaging was also performed with a LAVA sequence as a HCC screen. Results Eleven PO LTX pts (7M; 48±12yrs) underwent complete 3D CMR without complications with image time of 73±26min. One pt had mild treatable claustrophobia. One pt was too large negating the abdominal CMR. A total of 6 and 2 abnormal CV and extra-hepatic exams, respectively, were abnormal impacting surgical decision making. CV examples were: abnormal perfusion exams and dilated RV's while a right replaced hepatic artery and celiac stenosis were also seen. No patients required additional echocardiographic, nuclear imaging or CTS. A cardiac catheterization was performed in one pt to confirm CMR. One pt in whom a history of prior MI was known was demonstrated not to have had an MI granting him LTX consideration. The average length of time saved (not including transportation) was >6hrs. Average cost saving was >$1000. Conclusion 3D CMR has emerged as an important tool in the risk stratification of CV pts and, in limited fashion, we herein show that it can efficiently, effectively and inexpensively negate repetitive, low-yield, lower resolution CV imaging modalities accomplishing a One-Stop-Shop evaluation for pts being considered for Liver transplantation. We propose that CMR may become the new paradigm for effective LTX PO risk stratification.

Cardiovascular Magnetic Resonance; Imaging for the Echocardiographer

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