(Circulation. 2009;119:468-478.)
© 2009 American Heart Association, Inc.
Valvular Heart Disease: Changing Concepts in Disease Management |
From the Division of Cardiology (P.J.C., C.M.O.), Department of Medicine, and Department of Radiology (J.H.M.), University of Washington, Seattle, Wash.
Correspondence to Peter J. Cawley, MD, 1959 NE Pacific St, Box 356422, Division of Cardiology, Seattle, WA 98195-6422. E-mail pcawley{at}u.washington.edu
Key Words: echocardiography imaging magnetic resonance imaging regurgitation rheumatic heart disease valves
| Introduction |
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Echocardiography is now the standard tool for initial assessment and longitudinal evaluation of patients with valvular heart disease; however, echocardiography is limited in patients with poor acoustic windows and may be more operator dependent than other modalities, particularly for quantitation of disease severity. In the last 20 years, cardiovascular magnetic resonance (CMR) has emerged as an alternative noninvasive modality without ionizing radiation that is applicable to patients with valvular heart disease. CMR provides images of valve anatomy and allows quantitative evaluation of stenosis and regurgitation. CMR can also discern the consequences of the valvular lesion, including the effects of ventricular volume or pressure overload and alterations in systolic function. The purpose of the present review is to summarize the general principles of CMR and validate CMR as a tool for evaluation of valvular heart disease.
| General Principles |
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Anatomy
CMR has the potential to visualize all parts of the valve (leaflets, chordae tendineae, and papillary muscles) throughout the entire cardiac cycle. Congenitally abnormal valve leaflets (bicuspid), aberrant papillary muscles or aberrant chordal attachments (parachute mitral valve), leaflet thickening, presence and extent of calcification, leaflet redundancy and prolapse, and commissural fusion are all anatomic descriptions that have been reported by CMR. However, 2-dimensional (2D) echocardiography is superior for imaging structures that are thin and highly mobile owing to its greater temporal resolution and the absence of partial volume effects. Although 2D echocardiography remains the primary approach for visualization of valve anatomy, CMR is a reasonable alternative if ultrasound windows are poor.
In addition, CMR can provide visualization of valve masses such as vegetations, thrombi, or tumors, including attachment site and mobility.3–6 For masses of sufficient size, tissue characterization may be helpful when the origin of the mass is unknown.4,6 However, the minimum size of the mass needed for detection by CMR has not been described, and sensitivity and specificity compared with 2D echocardiography have not been evaluated.
The steady-state free precession (SSFP) cine pulse sequence is the most widely used CMR pulse sequence for assessing valve anatomy and motion (Figures 1 and 2
). This pulse sequence has excellent blood-to-myocardium contrast and a high intrinsic signal-to-noise ratio and has largely replaced gradient echo as the preferred pulse sequence for cine imaging of valve anatomy. SSFP produces a 2D image in any prescribed plane having multiple phases (frames) throughout the cardiac cycle, with a typical temporal resolution of 25 to 50 ms. To produce an SSFP cine image throughout all of systole and diastole, image acquisition is gated to the ECG and occurs over several cardiac cycles, easily obtained in a single breath hold (6 to 12 seconds). Non-cine pulse sequences such as turbo spin echo (T1 weighted, T2 weighted, fat saturation) and segmented inversion recovery gradient recalled echo pulse sequences may aid in tissue characterization of valve masses.4,6
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Velocity
SSFP and gradient echo cine pulse sequences can visualize flow turbulence (Figure 3) on the basis of loss of signal (signal void) due to the dephasing of moving protons. This approach can help show the location of "jets" and optimize the location of velocity sampling. Although SSFP provides improved visualization of valve anatomy, it is less sensitive for depicting flow disturbances. This can lead to underestimation or the overlooking of a regurgitant jet. Gradient echo cine pulse sequences, on the other hand, are more sensitive for the detection and sizing of regurgitant jets. With gradient echo sequences, the sensitivity for detecting dephasing (eg, valve regurgitation) is a function of the echo time: the longer the echo time, the larger and more pronounced the regurgitant jet.7
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Phase-contrast pulse sequences (other names include velocity-encoded cine, Q flow, or velocity mapping) are used for velocity measurements and are based on the accumulated phase of moving protons. In this pulse sequence, bipolar gradients oriented in the expected direction of blood flow are applied to each frame of the imaging slice of interest to induce phase shifts.8 Phase refers to the angular position of an individual protons spin vector with respect to a frame of reference. Stationary objects within this slice have a net phase of zero, because all phase induced by the first lobe of the bipolar gradient is reversed by the second lobe. Moving objects (blood) gain a net phase depending on the direction of blood flow, and this net phase (or phase shift) is proportional to the velocity of blood. This net phase can be displayed as a phase map with differences in signal intensity representing different velocities (Figure 4). Pixels depicting flow in the phase-encoding direction appear bright (Figure 4A), and flow opposite to the phase-encoding direction appears dark (Figure 4B). Objects with a phase shift of zero (stationary) are gray or speckled, as can be seen in the lungs or chest wall.
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Velocity mapping requires that the appropriate maximum velocity be programmed into the pulse sequence. Aliasing occurs if the angular phase shift is >180°, and the velocity within that pixel is then misregistered. This occurs if the programmed maximum velocity is less than the sampled velocities of blood flow in the imaging slice. The closer the programmed maximum velocity is to the maximum velocity present, the greater the sensitivity and accuracy of this technique to detect lower velocities within the region of interest.
Velocity mapping produces 2 sets of images: magnitude image and phase velocity maps (Figure 4). The magnitude image is used for anatomic orientation of the imaging slice and to identify the boundaries of the vessel imaged. Blood has an increased signal, whereas turbulent flow is depicted with signal loss within the magnitude image. The phase map encodes the velocities within each pixel. Using both images, a region of interest can be traced on each time frame of the data set. The region of interest must be drawn for each frame of the cardiac cycle carefully because of movement and deformation of the vessel. Within each region of interest, the peak instantaneous velocity (Vmax) for each time frame can also be obtained. With the simplified Bernoulli equation (4V2max), the peak instantaneous gradient can be estimated by substituting in the peak instantaneous velocity. Mean pressure gradients are obtained by averaging all of the instantaneous velocities over systole. With flow phantoms, phase velocity mapping has been shown to accurately measure velocities over 5 m/s.9
Flow Volume
Velocity maps can also be used to determine flow volume throughout the cardiac cycle. With the same magnitude and phase velocity maps, a region of interest is traced around the vessel lumen to determine the area of the vessel, frame by frame. By multiplying the velocity (cm/s) of each pixel by the area (cm2) of the region of interest, the instantaneous flow volume (cm3/s) is obtained for each frame of the cardiac cycle. The instantaneous flow volume of each frame (y-axis) can be plotted against the time of the cardiac cycle (x-axis) to show bulk flow as it relates to the cardiac cycle (Figure 5). When the area under the curve is integrated for systole and diastole, forward and regurgitant volumes can be generated. Stroke-volume measurements by velocity mapping in the ascending aorta have been shown to have a strong correlation to in vivo stroke-volume measurements by cine CMR pulse sequences of the left ventricle in subjects without significant mitral regurgitation, in vivo stroke volume by the Fick principle and by thermodilution, in vivo stroke-volume measurements by Doppler, and in vitro stroke-volume measurements within continual and pulsatile flow phantoms.10–14
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Potential Pitfalls for Phase-Contrast Imaging
Although the "in-plane" pixel size for phase-contrast imaging may be on the order of 1.5 to 2.0 mm, the slice thickness (volume of tissue) is typically 6 to 8 mm. Thus, vena contracta velocities may be underestimated owing to averaging of flow velocities from inside and outside the actual vena contracta (partial volume averaging). In these circumstances, velocity measurements for each pixel may be lower than actual velocities. Furthermore, the smaller the structure of interest, the fewer pixels are fully within this region, which amplifies the effects of partial volume averaging. Limited temporal resolution reduces the accuracy of CMR velocity measurements. Lower frame rates may not be able to capture high velocities of short duration, which results in underestimation of peak velocities. In addition, it is very important for the imaging slice to be oriented perpendicular to the flow of blood. If the angle of intercept is not 90°, an increased likelihood exists of inaccurate velocity measurements.
Ventricular Volumes and Function
Left ventricular volume assessment by CMR has been performed in several ways. In 1 method, the same formula used for biplane left ventriculography can be applied to the 2- and 4-chamber CMR views.15 However, these types of formulas depend on left ventricular geometric assumptions that may not apply to any individual patient. Left and right ventricular volume assessment is optimally performed with multislice 2D SSFP cine imaging covering both ventricles. A parallel stack of serial images (short-axis or 4-chamber) is acquired from base to apex of the left ventricle (Figure 6) with a 6- to 8-mm slice thickness. Most commonly, an imaging "gap" of 2 to 4 mm is used to balance the accurate assessment of ventricular volumes against excessive prolongation of total scan time. Volume for each image plane is calculated as the area of the endocardial tracing multiplied by the addition of the image slice thickness and interslice gap. End-diastolic and -systolic volumes are calculated by summing all slices, which allows for calculation of stroke volume, cardiac output, and ejection fraction with standard equations.
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The accuracy of CMR-calculated LV volumes has been validated both in vitro and in vivo. In vitro, a close correlation has been shown between CMR ventricular volumes and fluid-filled phantoms, wax casts of porcine ventricular cavities, latex casts of cadaveric hearts, and dynamic (pulsatile-flow) phantoms.16,17 In vivo, a close correlation between left and right ventricular stroke volumes has been shown in normal subjects with excellent reproducibility.16,18 Right ventricular volumes have also been validated in vitro to casts of cadaveric hearts.19
Areas of delayed gadolinium enhancement of the left ventricular myocardium correlate histopathologically with infarction20 but have also been described in patients with hypertrophic, dilated, and infiltrative cardiomyopathies. Several patterns of delayed gadolinium enhancement have been reported in adults with severe aortic stenosis,21,22 although the clinical implications of these findings in terms of prognosis and timing of intervention have not been fully elucidated.
| Evaluation of Valve Stenosis |
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Peak Antegrade Velocity and Pressure Gradient
Validation studies in human subjects have been published as early as the 1990s showing that antegrade velocity correlates well with continuous-wave Doppler echocardiography in adults with aortic stenosis. A trend can be identified for CMR to underestimate the peak velocity, most likely because of partial volume averaging within the vena contracta (Table 2).23–31 In patients with mitral stenosis, inflow velocities as assessed by Doppler echocardiography and CMR phase-contrast imaging correlate well (Table 3).23,32–37
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Valve Area
In aortic stenosis, the valve area can be defined in 2 different ways: anatomic valve area and physiological valve area. An anatomic valve area is defined as the planimetered area of maximal opening of the aortic valve leaflets. CMR planimetry for the assessment of anatomic aortic valve area is based on direct visualization of the valve orifice, made possible by the excellent blood-to-myocardium contrast and high signal-to-noise ratio provided by SSFP (Table 2).23–31 SSFP planimetry has been shown to correlate better with planimetry using transesophageal echocardiography than does gradient echo cine imaging.31 Some of these studies have included patients with bicuspid aortic valves. Planimetry, however, is a less than optimal approach in patients with calcific stenosis. This is because leaflet calcification and jet turbulence can make accurate visualization of the true orifice difficult and because of the complex, 3-dimensional shape of the stenotic orifice. Tomographic measurements assume a planar orifice that lies entirely within the image plane. In addition, physiological valve area, which correlates better with clinical outcome, is smaller than anatomic valve area owing to contraction of the flow stream as it passes through the narrowed orifice.38
Few data are available comparing physiological (continuity equation) valve area between CMR and echocardiography, although this approach is feasible on the basis of CMR velocity mapping of the velocity-time integral in the left ventricular outflow tract and aortic valve orifice.26 The different concepts underlying anatomic and physiological valve areas may explain some of the apparent discrepancies in comparisons of diagnostic approaches. These comparisons are most appropriate when measurements based on similar concepts are compared (Tables 2 and 3
).23–37
For evaluation of mitral stenosis, 2 methods are commonly used to determine valve area: planimetry and pressure half-time.39 A trend can be identified for CMR to overestimate the pressure half-time valve area compared with echocardiography; however, a close correlation is seen between CMR and echocardiographic planimetered valve areas (Table 3).23,32–37 Planimetry of the mitral valve is a well-validated echocardiographic approach, because anatomy of the stenotic mitral valve results in a planar elliptical orifice in diastole.39 To find the minimal mitral or aortic valve orifice on CMR images, thin (preferably 4 mm or less) overlapping slices are used as opposed to the usual 6- to 8-mm slices used for ventricular imaging. Reproducibility rates, as measured by interstudy, interobserver, and intraobserver variability of CMR for both aortic and mitral stenosis, are acceptable for clinical use (Tables 2 and 3
).23–37
| Evaluation of Valve Regurgitation |
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Regurgitant Jet Area
The presence of a regurgitant jet can be visualized with cine pulse sequences, either SSFP or gradient echo. Flow turbulence across valves produces a loss of net signal (signal void) on cine pulse sequences due to dephasing of protons43; however, correlation of the degree of signal void with the severity of regurgitation can be problematic, because the appearance of the signal void is highly dependent on pulse-sequence parameters.7,43,44 Early studies using CMR to evaluate valve regurgitation (aortic or mitral) focused on visualizing the signal void, with validations based on qualitative assessment or measurement of jet length or area compared with color Doppler or angiography (Tables 4 and 5
).45,45–58 Evaluation of regurgitant severity based on jet area or length is no longer recommended, because this method is not a reliable indicator of disease severity. Nevertheless, visualization of distal flow disturbance by CMR, echocardiography, or angiography remains useful for detection of regurgitation and evaluation of jet direction and origin. Quantitation now focuses on proximal jet geometry, including vena contracta width and regurgitant orifice area.
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Regurgitant Volume and Fraction
Regurgitant volume is defined as the amount of blood that flows in a retrograde direction across the valve with each heartbeat. Regurgitant fraction is the regurgitant volume expressed as a percentage of total stroke volume. CMR allows calculation of regurgitant volume by calculating the differences between right and left ventricular volumes, either by cine assessment of ventricular volumes or by velocity mapping and flow quantitation in the pulmonary artery and aorta. In the absence of cardiac disease, right and left ventricular stroke volumes are equal. With valve regurgitation, assuming only 1 valve is affected and no intracardiac shunt is present, the difference in stroke volumes reflects the regurgitant volume. Most adults with chronic valve regurgitation have significant regurgitation of only a single valve, which makes this approach widely applicable (Tables 4 and 5
).45–58
Phase contrast can directly quantify antegrade and retrograde flow volume across semilunar valves (Figures 4 and 5
). To evaluate aortic regurgitation, phase-contrast imaging is performed in the aortic root, and total stroke volume and regurgitant volume are measured directly as the antegrade and retrograde transaortic volume flow rates.47–50 The same approach can be used for the pulmonic valve. Phase-contrast imaging of the mitral valve is more difficult because of the movement of the mitral valve annulus during ventricular systole. An alternative approach for measuring mitral regurgitation is to calculate total left ventricular stroke volume with SSFP imaging and forward stroke volume in the aorta using phase-contrast imaging. The difference between these 2 values represents the regurgitant volume. This technique is useful because in patients without mitral regurgitation, forward stroke volume has a very close correlation with total stroke volume.10,13,14
Limited CMR studies on assessment of regurgitant orifice area (mainly by planimetry with aortic regurgitation) are available, even though this is 1 of the key variables in the assessment of regurgitant severity and the strongest predictor of clinical outcome.59,60 Planimetry of the aortic valve to determine the regurgitant orifice area has the same problem as does planimetry of the aortic valve for stenosis: The orifice does not lie in a single plane, and contraction of blood flow results in a smaller effective regurgitant orifice area than the anatomic area.
| Right-Sided Valve Disease |
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CMR provides visualization of the pulmonic valve and regurgitant jet, quantitation of regurgitant severity, and accurate measurement of right ventricular volumes and ejection fraction. Quantitation of pulmonic regurgitation by phase contrast has been validated against CMR right and left ventricular stroke volumes.61 Other studies are primarily limited to comparisons of quantitative CMR with qualitative echocardiographic measures, although 1 study showed a close correlation between regurgitant fraction by CMR and Doppler pulmonary regurgitant severity defined by the diastolic duration of regurgitant flow on continuous-wave Doppler.62
CMR allows accurate quantitation of right ventricular volumes and ejection fraction because it allows direct visualization of the right ventricle in multiple tomographic planes and does not rely on geometric assumptions about chamber shape. In adults with chronic pulmonic regurgitation after tetralogy of Fallot repair, CMR has been used to measure the reduction in right ventricular volumes after valve replacement.63,64 One retrospective study suggested that right ventricular volumes may be an indicator of the optimal timing of pulmonic valve intervention.64 Prospective studies of this promising approach to the timing of pulmonic valve intervention are needed.
Tricuspid Valve Disease
Tricuspid regurgitation can be visualized on the basis of its signal void with cine imaging. Phase-contrast imaging of the tricuspid valve presents the same challenges as with the mitral valve owing to annular motion with the cardiac cycle. Tricuspid regurgitation can be calculated in terms of regurgitant volume and fraction in similar ways to mitral regurgitation: The forward stroke volume, as measured in the pulmonary artery with phase contrast, is subtracted from the total right ventricular stroke volumes from the SSFP images.
| Other Cardiac Imaging Approaches |
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| Clinical Implications |
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Despite the promise of CMR for evaluation of valve disease, some limitations still exist. Notwithstanding many published validation studies, these methods have not been widely used, and clinical experience is limited. CMR has not been shown to provide reliable information on pulmonary artery pressures or regurgitant orifice area, data that echocardiography does provide. In addition, echocardiographic criteria have been validated and compared with clinical outcomes, data that are not yet available for CMR measures of valve disease. Given the potential strengths of CMR, prospective studies using this approach to define disease progression and the optimal timing of intervention are needed. CMR may also provide a more accurate, precise, and reproducible measure of disease severity for trials of medical therapy in chronic valve disease.
| Acknowledgments |
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Dr Cawley is supported in part by grants from the Society for Cardiovascular Angiography and Interventions and General Electric, as well as by the John L. Locke Jr Charitable Trust.
Disclosures
Dr Maki serves as a consultant and on the speakers bureau for Bracco Diagnostics. The remaining authors report no conflicts.
| Footnotes |
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| References |
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2. Mugler JP III. Overview of MR imaging pulse sequences. Magn Reson Imaging Clin N Am. 1999; 7: 661–697.[Medline] [Order article via Infotrieve]
3. Caduff JH, Hernandez RJ, Ludomirsky A. MR visualization of aortic valve vegetations. J Comput Assist Tomogr. 1996; 20: 613–615.[CrossRef][Medline] [Order article via Infotrieve]
4. Wintersperger BJ, Becker CR, Gulbins H, Knez A, Bruening R, Heuck A, Reiser MF. Tumors of the cardiac valves: imaging findings in magnetic resonance imaging, electron beam computed tomography, and echocardiography. Eur Radiol. 2000; 10: 443–449.[CrossRef][Medline] [Order article via Infotrieve]
5. Pollak Y, Comeau CR, Wolff SD. Staphylococcus aureus endocarditis of the aortic valve diagnosed on MR imaging. AJR Am J Roentgenol. 2002; 179: 1647.
6. Sievers B, Brandts B, Franken U, Trappe HJ. Cardiovascular magnetic resonance imaging demonstrates mitral valve endocarditis. Am J Med. 2003; 115: 681–682.[CrossRef][Medline] [Order article via Infotrieve]
7. Suzuki J, Caputo GR, Kondo C, Higgins CB. Cine MR imaging of valvular heart disease: display and imaging parameters affect the size of the signal void caused by valvular regurgitation. AJR Am J Roentgenol. 1990; 155: 723–727.
8. Saloner D. Flow and motion. Magn Reson Imaging Clin N Am. 1999; 7: 699–715.[Medline] [Order article via Infotrieve]
9. Mostbeck GH, Caputo GR, Higgins CB. MR measurement of blood flow in the cardiovascular system. AJR Am J Roentgenol. 1992; 159: 453–461.
10. Hundley WG, Li HF, Hillis LD, Meshack BM, Lange RA, Willard JE, Landau C, Peshock RM. Quantitation of cardiac output with velocity-encoded, phase-difference magnetic resonance imaging. Am J Cardiol. 1995; 75: 1250–1255.[CrossRef][Medline] [Order article via Infotrieve]
11. Bogren HG, Klipstein RH, Firmin DN, Mohiaddin RH, Underwood SR, Rees RS, Longmore DB. Quantitation of antegrade and retrograde blood flow in the human aorta by magnetic resonance velocity mapping. Am Heart J. 1989; 117: 1214–1222.[CrossRef][Medline] [Order article via Infotrieve]
12. Chatzimavroudis GP, Oshinski JN, Franch RH, Walker PG, Yoganathan AP, Pettigrew RI. Evaluation of the precision of magnetic resonance phase velocity mapping for blood flow measurements. J Cardiovasc Magn Reson. 2001; 3: 11–19.[CrossRef][Medline] [Order article via Infotrieve]
13. Van Rossum AC, Sprenger M, Visser FC, Peels KH, Valk J, Roos JP. An in vivo validation of quantitative blood flow imaging in arteries and veins using magnetic resonance phase-shift techniques. Eur Heart J. 1991; 12: 117–126.
14. Kondo C, Caputo GR, Semelka R, Foster E, Shimakawa A, Higgins CB. Right and left ventricular stroke volume measurements with velocity-encoded cine MR imaging: in vitro and in vivo validation. AJR Am J Roentgenol. 1991; 157: 9–16.
15. Cranney GB, Lotan CS, Dean L, Baxley W, Bouchard A, Pohost GM. Left ventricular volume measurement using cardiac axis nuclear magnetic resonance imaging: validation by calibrated ventricular angiography. Circulation. 1990; 82: 154–163.
16. Longmore DB, Klipstein RH, Underwood SR, Firmin DN, Hounsfield GN, Watanabe M, Bland C, Fox K, Poole-Wilson PA, Rees RS. Dimensional accuracy of magnetic resonance in studies of the heart. Lancet. 1985; 1: 1360–1362.[Medline] [Order article via Infotrieve]
17. Rehr RB, Malloy CR, Filipchuk NG, Peshock RM. Left ventricular volumes measured by MR imaging. Radiology. 1985; 156: 717–719.
18. Sechtem U, Pflugfelder PW, Gould RG, Cassidy MM, Higgins CB. Measurement of right and left ventricular volumes in healthy individuals with cine MR imaging. Radiology. 1987; 163: 697–702.
19. Jauhiainen T, Jarvinen VM, Hekali PE, Poutanen VP, Penttila A, Kupari M. MR gradient echo volumetric analysis of human cardiac casts: focus on the right ventricle. J Comput Assist Tomogr. 1998; 22: 899–903.[CrossRef][Medline] [Order article via Infotrieve]
20. Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O, Bundy J, Finn JP, Klocke FJ, Judd RM. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation. 1999; 100: 1992–2002.
21. Ochiai K, Ishibashi Y, Shimada T, Murakami Y, Inoue S, Sano K. Subendocardial enhancement in gadolinium-diethylene-triamine-pentaacetic acid-enhanced magnetic resonance imaging in aortic stenosis. Am J Cardiol. 1999; 83: 1443–1446.[CrossRef][Medline] [Order article via Infotrieve]
22. Debl K, Djavidani B, Buchner S, Lipke C, Nitz W, Feuerbach S, Riegger G, Luchner A. Delayed hyperenhancement in magnetic resonance imaging of left ventricular hypertrophy caused by aortic stenosis and hypertrophic cardiomyopathy: visualisation of focal fibrosis. Heart. 2006; 92: 1447–1451.
23. Kilner PJ, Manzara CC, Mohiaddin RH, Pennell DJ, Sutton MG, Firmin DN, Underwood SR, Longmore DB. Magnetic resonance jet velocity mapping in mitral and aortic valve stenosis. Circulation. 1993; 87: 1239–1248.
24. Eichenberger AC, Jenni R, von Schulthess GK. Aortic valve pressure gradients in patients with aortic valve stenosis: quantification with velocity-encoded cine MR imaging. AJR Am J Roentgenol. 1993; 160: 971–977.
25. Sondergaard L, Hildebrandt P, Lindvig K, Thomsen C, Stahlberg F, Kassis E, Henriksen O. Valve area and cardiac output in aortic stenosis: quantification by magnetic resonance velocity mapping. Am Heart J. 1993; 126: 1156–1164.[CrossRef][Medline] [Order article via Infotrieve]
26. Caruthers SD, Lin SJ, Brown P, Watkins MP, Williams TA, Lehr KA, Wickline SA. Practical value of cardiac magnetic resonance imaging for clinical quantification of aortic valve stenosis: comparison with echocardiography. Circulation. 2003; 108: 2236–2243.
27. John AS, Dill T, Brandt RR, Rau M, Ricken W, Bachmann G, Hamm CW. Magnetic resonance to assess the aortic valve area in aortic stenosis: how does it compare to current diagnostic standards? J Am Coll Cardiol. 2003; 42: 519–526.
28. Kupfahl C, Honold M, Meinhardt G, Vogelsberg H, Wagner A, Mahrholdt H, Sechtem U. Evaluation of aortic stenosis by cardiovascular magnetic resonance imaging: comparison with established routine clinical techniques. Heart. 2004; 90: 893–901.
29. Debl K, Djavidani B, Seitz J, Nitz W, Schmid FX, Muders F, Buchner S, Feuerbach S, Riegger G, Luchner A. Planimetry of aortic valve area in aortic stenosis by magnetic resonance imaging. Invest Radiol. 2005; 40: 631–636.[CrossRef][Medline] [Order article via Infotrieve]
30. Reant P, Lederlin M, Lafitte S, Serri K, Montaudon M, Corneloup O, Roudaut R, Laurent F. Absolute assessment of aortic valve stenosis by planimetry using cardiovascular magnetic resonance imaging: comparison with transesophageal echocardiography, transthoracic echocardiography, and cardiac catheterisation. Eur J Radiol. 2006; 59: 276–283.[CrossRef][Medline] [Order article via Infotrieve]
31. Schlosser T, Malyar N, Jochims M, Breuckmann F, Hunold P, Bruder O, Erbel R, Barkhausen J. Quantification of aortic valve stenosis in MRI: comparison of steady-state free precession and fast low-angle shot sequences. Eur Radiol. 2007; 17: 1284–1290.[CrossRef][Medline] [Order article via Infotrieve]
32. Mohiaddin RH, Amanuma M, Kilner PJ, Pennell DJ, Manzara C, Longmore DB. MR phase-shift velocity mapping of mitral and pulmonary venous flow. J Comput Assist Tomogr. 1991; 15: 237–243.[Medline] [Order article via Infotrieve]
33. Hartiala JJ, Mostbeck GH, Foster E, Fujita N, Dulce MC, Chazouilleres AF, Higgins CB. Velocity-encoded cine MRI in the evaluation of left ventricular diastolic function: measurement of mitral valve and pulmonary vein flow velocities and flow volume across the mitral valve. Am Heart J. 1993; 125: 1054–1066.[CrossRef][Medline] [Order article via Infotrieve]
34. Heidenreich PA, Steffens J, Fujita N, O'Sullivan M, Caputo GR, Foster E, Higgins CB. Evaluation of mitral stenosis with velocity-encoded cine-magnetic resonance imaging. Am J Cardiol. 1995; 75: 365–369.[CrossRef][Medline] [Order article via Infotrieve]
35. Lin SJ, Brown PA, Watkins MP, Williams TA, Lehr KA, Liu W, Lanza GM, Wickline SA, Caruthers SD. Quantification of stenotic mitral valve area with magnetic resonance imaging and comparison with Doppler ultrasound. J Am Coll Cardiol. 2004; 44: 133–137.
36. Djavidani B, Debl K, Lenhart M, Seitz J, Paetzel C, Schmid FX, Nitz WR, Feuerbach S, Riegger G, Luchner A. Planimetry of mitral valve stenosis by magnetic resonance imaging. J Am Coll Cardiol. 2005; 45: 2048–2053.
37. Djavidani B, Debl K, Buchner S, Lipke C, Nitz W, Feuerbach S, Riegger G, Luchner A. MRI planimetry for diagnosis and follow-up of valve area in mitral stenosis treated with valvuloplasty. Rofo. 2006; 178: 781–786.[Medline] [Order article via Infotrieve]
38. Otto CM. Valvular aortic stenosis: disease severity and timing of intervention. J Am Coll Cardiol. 2006; 47: 2141–2151.
39. Vahanian A, Baumgartner H, Bax J, Butchart E, Dion R, Filippatos G, Flachskampf F, Hall R, Iung B, Kasprzak J, Nataf P, Tornos P, Torracca L, Wenink A. Guidelines on the management of valvular heart disease: the Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J. 2007; 28: 230–268.
40. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Antman EM, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Lytle BW, Nishimura R, Page RL, Riegel B. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease), developed in collaboration with the Society of Cardiovascular Anesthesiologists, endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2006; 48: e1–148.
41. Quinones MA, Otto CM, Stoddard M, Waggoner A, Zoghbi WA. Recommendations for quantification of Doppler echocardiography: a report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. J Am Soc Echocardiogr. 2002; 15: 167–184.[CrossRef][Medline] [Order article via Infotrieve]
42. Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto CM, Quinones MA, Rakowski H, Stewart WJ, Waggoner A, Weissman NJ. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003; 16: 777–802.[CrossRef][Medline] [Order article via Infotrieve]
43. Sondergaard L, Stahlberg F, Thomsen C. Magnetic resonance imaging of valvular heart disease. J Magn Reson Imaging. 1999; 10: 627–638.[CrossRef][Medline] [Order article via Infotrieve]
44. Spielmann RP, Schneider O, Thiele F, Heller M, Bucheler E. Appearance of poststenotic jets in MRI: dependence on flow velocity and on imaging parameters. Magn Reson Imaging. 1991; 9: 67–72.[CrossRef][Medline] [Order article via Infotrieve]
45. Globits S, Mayr H, Frank H, Neuhold A, Glogar D. Quantification of regurgitant lesions by MRI. Int J Card Imaging. 1990; 6: 109–116.[CrossRef][Medline] [Order article via Infotrieve]
46. Aurigemma G, Reichek N, Schiebler M, Axel L. Evaluation of aortic regurgitation by cardiac cine magnetic resonance imaging: planar analysis and comparison to Doppler echocardiography. Cardiology. 1991; 78: 340–347.[Medline] [Order article via Infotrieve]
47. Dulce MC, Mostbeck GH, O'Sullivan M, Cheitlin M, Caputo GR, Higgins CB. Severity of aortic regurgitation: interstudy reproducibility of measurements with velocity-encoded cine MR imaging. Radiology. 1992; 185: 235–240.
48. Honda N, Machida K, Hashimoto M, Mamiya T, Takahashi T, Kamano T, Kashimada A, Inoue Y, Tanaka S, Yoshimoto N. Aortic regurgitation: quantitation with MR imaging velocity mapping. Radiology. 1993; 186: 189–194.
49. Sondergaard L, Lindvig K, Hildebrandt P, Thomsen C, Stahlberg F, Joen T, Henriksen O. Quantification of aortic regurgitation by magnetic resonance velocity mapping. Am Heart J. 1993; 125: 1081–1090.[CrossRef][Medline] [Order article via Infotrieve]
50. Ley S, Eichhorn J, Ley-Zaporozhan J, Ulmer H, Schenk JP, Kauczor HU, Arnold R. Evaluation of aortic regurgitation in congenital heart disease: value of MR imaging in comparison to echocardiography. Pediatr Radiol. 2007; 37: 426–436.[CrossRef][Medline] [Order article via Infotrieve]
51. Sechtem U, Pflugfelder PW, Cassidy MM, White RD, Cheitlin MD, Schiller NB, Higgins CB. Mitral or aortic regurgitation: quantification of regurgitant volumes with cine MR imaging. Radiology. 1988; 167: 425–430.
52. Nishimura T, Yamada N, Itoh A, Miyatake K. Cine MR imaging in mitral regurgitation: comparison with color Doppler flow imaging. AJR Am J Roentgenol. 1989; 153: 721–724.
53. Glogar D, Globits S, Neuhold A, Mayr H. Assessment of mitral regurgitation by magnetic resonance imaging. Magn Reson Imaging. 1989; 7: 611–617.[CrossRef][Medline] [Order article via Infotrieve]
54. Aurigemma G, Reichek N, Schiebler M, Axel L. Evaluation of mitral regurgitation by cine magnetic resonance imaging. Am J Cardiol. 1990; 66: 621–625.[CrossRef][Medline] [Order article via Infotrieve]
55. Fujita N, Chazouilleres AF, Hartiala JJ, O'Sullivan M, Heidenreich P, Kaplan JD, Sakuma H, Foster E, Caputo GR, Higgins CB. Quantification of mitral regurgitation by velocity-encoded cine nuclear magnetic resonance imaging. J Am Coll Cardiol. 1994; 23: 951–958.[Abstract]
56. Hundley WG, Li HF, Willard JE, Landau C, Lange RA, Meshack BM, Hillis LD, Peshock RM. Magnetic resonance imaging assessment of the severity of mitral regurgitation: comparison with invasive techniques. Circulation. 1995; 92: 1151–1158.
57. Kizilbash AM, Hundley WG, Willett DL, Franco F, Peshock RM, Grayburn PA. Comparison of quantitative Doppler with magnetic resonance imaging for assessment of the severity of mitral regurgitation. Am J Cardiol. 1998; 81: 792–795.[CrossRef][Medline] [Order article via Infotrieve]
58. Kon MW, Myerson SG, Moat NE, Pennell DJ. Quantification of regurgitant fraction in mitral regurgitation by cardiovascular magnetic resonance: comparison of techniques. J Heart Valve Dis. 2004; 13: 600–607.[Medline] [Order article via Infotrieve]
59. Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, Scott C, Schaff HV, Tajik AJ. Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med. 2005; 352: 875–883.
60. Debl K, Djavidani B, Buchner S, Fredersdorf S, Schmid FX, Haimerl J, Poschenrieder F, Feuerbach S, Riegger G, Luchner A. Assessment of the anatomic regurgitant orifice in aortic regurgitation: a clinical magnetic resonance imaging study. Heart. 2008; 94: e8.
61. Rebergen SA, Chin JG, Ottenkamp J, van der Wall EE, de Roos A. Pulmonary regurgitation in the late postoperative follow-up of tetralogy of Fallot: volumetric quantitation by nuclear magnetic resonance velocity mapping. Circulation. 1993; 88: 2257–2266.
62. Li W, Davlouros PA, Kilner PJ, Pennell DJ, Gibson D, Henein MY, Gatzoulis MA. Doppler-echocardiographic assessment of pulmonary regurgitation in adults with repaired tetralogy of Fallot: comparison with cardiovascular magnetic resonance imaging. Am Heart J. 2004; 147: 165–172.[CrossRef][Medline] [Order article via Infotrieve]
63. Vliegen HW, van Straten A, de Roos A, Roest AA, Schoof PH, Zwinderman AH, Ottenkamp J, van der Wall EE, Hazekamp MG. Magnetic resonance imaging to assess the hemodynamic effects of pulmonary valve replacement in adults late after repair of tetralogy of Fallot. Circulation. 2002; 106: 1703–1707.
64. Therrien J, Provost Y, Merchant N, Williams W, Colman J, Webb G. Optimal timing for pulmonary valve replacement in adults after tetralogy of Fallot repair. Am J Cardiol. 2005; 95: 779–782.[CrossRef][Medline] [Order article via Infotrieve]
65. Feuchtner GM, Muller S, Bonatti J, Schachner T, Velik-Salchner C, Pachinger O, Dichtl W. Sixty-four slice CT evaluation of aortic stenosis using planimetry of the aortic valve area. AJR Am J Roentgenol. 2007; 189: 197–203.
66. Habis M, Daoud B, Roger VL, Ghostine S, Caussin C, Ramadan R, Nottin R, Lancelin B, Angel CY, Capderou A, Paul JF. Comparison of 64-slice computed tomography planimetry and Doppler echocardiography in the assessment of aortic valve stenosis. J Heart Valve Dis. 2007; 16: 216–224.[Medline] [Order article via Infotrieve]
67. Alkadhi H, Desbiolles L, Husmann L, Plass A, Leschka S, Scheffel H, Vachenauer R, Schepis T, Gaemperli O, Flohr TG, Genoni M, Marincek B, Jenni R, Kaufmann PA, Frauenfelder T. Aortic regurgitation: assessment with 64-section CT. Radiology. 2007; 245: 111–121.
68. Pouleur AC, le Polain de Waroux JB, Pasquet A, Vanoverschelde JL, Gerber BL. Aortic valve area assessment: multidetector CT compared with cine MR imaging and transthoracic and transesophageal echocardiography. Radiology. 2007; 244: 745–754.
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