Published online October 17, 2002, 10.1148/rg.e9
(Radiographics. 2003;23:e9-e9.)
© RSNA, 2003
Evaluation of Cardiac Valvular Disease with MR Imaging: Qualitative and Quantitative Techniques1
James F. Glockner, MD, PhD,
Donald L Johnston, MD and
Kiaran P McGee, PhD
1 From the Departments of Radiology (J.F.G., K.P.M.) and Cardiology (D.L.J.), Mayo Clinic, 200 First St SW, Rochester, MN 55901. Presented as a scientific exhibit at the 2001 RSNA scientific assembly. Received March 25, 2002, revision requested July 11, revision received and accepted September 14. Address correspondence to J.F.G. (e-mail: glockner.james{at}mayo.edu
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Abstract
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Magnetic resonance (MR) imaging is almost never performed as the initial imaging test in cardiac valvular disease; that role is dominated by echocardiography. Nevertheless, MR imaging has much to offer in selected patients. Quantitative information regarding the severity of regurgitant or stenotic lesions can be obtained by using a combination of cine gradient-echo or steady-state free precession and cine phase-contrast sequences. In addition to providing measurements of peak velocity and flow, MR imaging is the standard of reference for evaluation of ventricular function, which can be a critical factor in determining when surgical intervention is indicated. Improvements in cardiac MR imaging technology have been particularly striking in the past few years, and these developments can easily be applied to the examination of cardiac valves. The authors briefly describe the pathophysiology of valvular disease, discuss standard MR techniques for qualitative and quantitative evaluation of valvular lesions, and illustrate these concepts with several case studies.
© RSNA, 2002
Index Terms: Blood, flow dynamics, 53.12142, 53.12144, 56.12142, 56.12144 • Heart, MR, 53.12142, 53.12144 • Heart, valves, 53.172, 53.174, 53.175, 53.83
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Introduction
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The incidence of cardiac valvular disease is relatively low compared with the incidence of ischemic heart disease, but it nevertheless causes considerable morbidity and mortality. In 1999, the total estimated mortality attributable to valve disease in the United States was 19,612 deaths. Aortic valve disease accounted for 12,212 deaths, and mitral valve disease for 2,895 deaths. Valve repair or replacement surgery is commonplace, with approximately 96,000 procedures performed annually in the United States (1).
Echocardiography is the dominant imaging modality for evaluation of patients with valvular heart disease and has a number of inherent advantages: It is cheap, fast, portable, and for the most part highly accurate. The high spatial and temporal resolution achievable with echocardiography is unmatched and allows superb visualization of valve morphology.
The role of magnetic resonance (MR) imaging in valve disease has been limited for a number of reasons, including cost, availability, and relatively difficult, labor-intensive examinations. Recent technologic advances have made evaluation of cardiac valves with MR imaging much more straightforward and reliable. Even so, MR imaging is unlikely to replace echocardiography as the initial imaging test in cases of suspected valvular disease. Nevertheless, MR imaging has much to offer in selected patients. MR imaging generally allows more accurate and reliable quantification of ventricular mass and function, often important parameters clinically, than does echocardiography. Quantitative measurement of velocity and flow can be achieved on a pixel-by-pixel basis. Finally, MR imaging is a useful alternative examination in patients who have undergone limited or nondiagnostic transthoracic echocardiography.
We provide a brief overview of the pathophysiology and clinical aspects of valvular heart disease, describe standard MR techniques for valve-oriented examination of the heart, discuss techniques for quantitation of valvular stenosis and insufficiency, and illustrate these concepts with case studies.
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Anatomy and Physiology
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The four cardiac valves comprise two semilunar (aortic and pulmonic) and two atrioventricular (tricuspid and mitral) valves. Valves consist of a central collagenous core covered by fibroelastic tissue. The fibrous rings of the valves interconnect to form the backbone of the cardiac skeleton (Figs 1, 2).
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Figure 1a. (a) Schematic and (b) pathologic views of the fibrous skeleton of the heart. The aortic valve is wedged between the mitral and tricuspid valves; the pulmonic valve is most anterior.
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Figure 1b. (a) Schematic and (b) pathologic views of the fibrous skeleton of the heart. The aortic valve is wedged between the mitral and tricuspid valves; the pulmonic valve is most anterior.
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Normal cardiac valves allow unidirectional blood flow without stenosis or regurgitation. Stenotic or regurgitant lesions lead to volume or pressure overload of the affected chambers. When lesions occur acutely, there is little time for the heart to adapt to the added stress and symptoms appear immediately. With chronic lesions, however, compensatory mechanisms can often preserve cardiac function for years.
In general, patients with stenotic lesions can be monitored clinically until symptoms appear. On the other hand, patients with regurgitant lesions require careful monitoring for signs of left ventricular (LV) dysfunction and may require surgery even while asymptomatic. There is little effective medical therapy for valvular disease; treatment is surgical.
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Valve Diseases
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Aortic Stenosis
Aortic stenosis can occur above, below, or at the valve. The most common cause in adults is idiopathic degeneration of a normal valve, followed by degeneration of a congenital bicuspid valve, which typically occurs with earlier onset (Fig 3). Rheumatic heart disease is the third most frequent cause. Subvalvular and supravalvular stenoses are usually congenital lesions, but subvalvular stenosis can also be due to hypertrophic cardiomyopathy.
Classic symptoms are dyspnea on exertion, exertional syncope, and angina. Signs include a holosystolic murmur with weakened peripheral pulses. Symptoms usually appear after an extended asymptomatic period of 20–30 years. Once symptoms appear, however, there is a rapid downhill course and 75% of patients die within 3 years if the valve is not replaced (2). The pathophysiology of aortic stenosis involves obstruction of LV outflow, which leads to elevated LV pressures during systole and diminished cardiac output. The primary compensatory mechanism for this is LV hypertrophy, which helps maintain cardiac output and reduce LV wall stress (Fig 4).
The compensatory mechanisms are often effective for many years but can eventually cause additional problems: LV hypertrophy decreases ventricular compliance and increases end-diastolic pressure. These factors may limit coronary perfusion in the face of increased oxygen demand due to hypertrophic myocardium, a situation made worse by coexisting coronary atherosclerotic disease. Eventually ischemia, angina, and LV failure occur in the decompensated patient.
MR imaging can directly demonstrate LV hypertrophy and poststenotic dilatation of the ascending aorta. Calcification of the aortic valve is frequent and can be seen as foci of signal void within the valve on bright-blood images. This technique is not especially reliable, however; the extent of the signal void depends on the pulse sequence used and its specific parameters and on the placement of cine sections. In addition, signal voids caused by valvular calcification may be difficult to distinguish from flow jets through stenotic or regurgitant valves. CT is a much more effective modality for detecting calcification.
Aortic stenosis can be graded in several ways. Echocardiographic evaluation involves Doppler measurement of peak systolic velocities across the valve. These can be converted into a pressure gradient by using the modified Bernoulli equation. The aortic valve area is calculated indirectly by measuring the time-velocity integral across the valve and in the aortic outflow tract and then assuming conservation of flow. MR imaging can also be used to measure peak velocity directly and to determine pressure gradients (Table 1).
Aortic Insufficiency
Aortic insufficiency can be due to primary valve disease or aortic root dilatation. The most common cause is idiopathic degeneration of a normal valve. In patients younger than 40 years, Marfan syndrome with aortic root dilatation is the most frequent cause. Additional causes include endocarditis, aneurysm, bicuspid valve, syphilis, trauma, rheumatic disease, ankylosing spondylitis, and dissection. Combined insufficiency and stenosis is fairly common. Infective endocarditis, acute dissection, and trauma usually cause acute insufficiecy resulting in rapid elevation of LV filling pressures and reduced cardiac output. Other causes produce chronic aortic insufficiency. Classic symptoms include shortness of breath, angina, and palpitations. A diastolic murmur and low diastolic blood pressure may be noted at physical examination. Patients are often asymptomatic despite severe LV volume overload, and by the time symptoms occur, they may be unable to benefit from surgical repair because of irreversible LV dysfunction. For this reason, close monitoring of patients with aortic insufficiency is recommended. Some authors advocate valve replacement in asymptomatic patients when there are indications that LV function may be compromised (3,4).
The pathophysiology of aortic insufficiency involves volume overload of the left ventricle, resulting in increased LV diastolic pressure and reduced aortic diastolic pressure. Ventricular dilatation and increased LV compliance are compensatory mechanisms that allow increased stroke volume and preservation of cardiac output despite large regurgitant volumes. When LV function begins to deteriorate, both end-systolic and end-diastolic volumes increase, end-diastolic pressure rises, and myocardial perfusion is diminished, resulting in ischemia and further compromise of function.
Secondary signs of aortic insufficiency demonstrated with MR imaging include LV dilatation and variable dilatation of the aorta. Aortic insufficiency is usually graded by regurgitant volume (volume of regurgitant flow across the valve per heartbeat) or regurgitant fraction (regurgitant volume divided by forward stroke volume) (Table 2).
Mitral Stenosis
Mitral stenosis is usually secondary to rheumatic heart disease. At least 60% of patients with mitral stenosis have a remote history of rheumatic fever, and nearly all valve specimens have evidence of rheumatic deformities (5). Symptoms are typically those of left heart failure: shortness of breath and fatigue. Symptoms can be exacerbated by exercise or any condition associated with an increased heart rate. Of patients with symptomatic mitral stenosis, 30%–40% develop atrial fibrillation. This is problematic for quantitative analysis with MR imaging, which relies on reliable and reproducible electrocardiographic gating. Mitral stenosis is a continuous progressive disease with a slow, stable course early and progressive acceleration later in life. Once symptoms develop, the 10-year survival in untreated patients is 50%–60% (5).
The pathophysiology of mitral stenosis involves development of a pressure gradient across the mitral valve. Left atrial pressure rises to maintain flow across the valve, and this in turn leads to increased pulmonary venous and capillary pressures, resulting in interstitial and eventually alveolar pulmonary edema. Pulmonary hypertension can develop as a response to chronic elevated left atrial pressure, leading to increased pressure loads on the right ventricle and eventual right ventricular failure. MR imaging may demonstrate increased signal intensity within the lungs, corresponding to pulmonary edema. The left atrium and left atrial appendage are dilated, and right ventricular dilatation and hypertrophy may also be seen.
Mitral stenosis is typically graded by valve area and transvalvular pressure gradient (Table 3).
Mitral Insufficiency
There are many causes of mitral insufficiency, including ischemia and papillary muscle rupture, infective endocarditis, mitral valve prolapse syndrome, collagen vascular disease, and rheumatic fever. Patients with acute mitral insufficiency may present with pulmonary edema and low cardiac output. Chronic mitral insufficiency is likely to manifest as fatigue and weakness. A holosystolic murmur may be noted at physical examination.
Regurgitant blood in the left atrium increases left atrial pressure, and a volume stress is placed on the left ventricle as the regurgitant volume returns during diastole. The left ventricle dilates to maintain cardiac output, and the left atrium enlarges as well. Chronic decompensation usually presents as low cardiac output manifesting as fatigue and weakness. MR imaging reveals left atrial and LV dilatation.
Mitral insufficiency is usually graded by regurgitant volume (Table 4).
Tricuspid and Pulmonic Valve Disease
Tricuspid stenosis is almost always related to rheumatic heart disease and is rarely an isolated finding; the aortic and mitral valves are usually also involved. Other causes of tricuspid stenosis include congenital atresia and carcinoid syndrome. Patients typically present with signs and symptoms of right heart failure: fatigue, abdominal pain, and lower-extremity swelling.
Tricuspid insufficiency is most commonly the result of dilatation of the right ventricle and tricuspid annulus rather than intrinsic valvular disease. This is also the most common valvular lesion in intravenous drug abusers with infectious endocarditis, since left-side valves are protected by the lungs, which act as a filter.
Pulmonic stenosis is almost always due to congenital deformity of the valve. A pressure gradient develops across the valve, eventually resulting in right heart failure.
Pulmonic regurgitation is most commonly caused by dilatation of the valve ring secondary to pulmonary hypertension. Infective endocarditis is the second leading cause of pulmonic insufficiency.
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Valve Examination with MR Imaging
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It is important to have a clear idea of what needs to be accomplished during the MR examination and to prioritize this list in the event that the patient does not last as long as the ideal examination dictates. We usually begin with a series of scout sequences to locate the valve of interest. Once this is accomplished, cine images and sometimes black-blood images through the valve plane are obtained to evaluate valve morphology; bicuspid aortic valves, thickened leaflets, and heavily calcified valves can be appreciated. Cine images through the valve plane and perpendicular to the valve are obtained for visualization and qualitative evaluation of flow jets. Quantitative analysis of regurgitant flow or peak velocities is then performed by means of cine phase-contrast sequences. Evaluation of cardiac function is a second and equally important aspect of the examination. Long- and short-axis cine images of the ventricles are acquired, and these can be used to measure mass, ejection fraction, end-systolic and end-diastolic volume, and stroke volume.
Several methods have been described for localizing cardiac and valve planes, and all are effective. We have been most successful by choosing one or two localization methods and practicing them often enough so that localization becomes fast and reproducible. As an example, we illustrate the localization series for the aortic valve examination. Initially a sagittal breath-hold-gated fast gradient-echo sequence is performed. From these images, a breath-hold steady-state free precession (SSFP) cine sequence (commercially known as FIESTA [GE Medical Systems, Milwaukee, Wis), true FISP [fast imaging with steady-state precession] [Siemens Medical Systems, Iselin, NJ], or balanced FFE [fast field echo] [Philips Medical Systems, Best, The Netherlands] is prescribed in a plane that passes through the LV apex and the mitral valve. This generates a horizontal long axis or four-chamber view (Fig 5). Next, a series of short-axis cine sections are prescribed from the four-chamber view perpendicular to the long axis of the left ventricle (Fig 6). Short-axis sections near the base of the left ventricle demonstrate the LV outflow tract, and one of these images is used to prescribe a cine sequence oriented through the LV outflow tract—the three-chamber view (Fig 7). The three-chamber view is then used to prescribe sections in the valve plane and, if desired, additional coronal oblique cine sequences perpendicular to the valve plane and the three-chamber view (Fig 8).
Other valves can be approached in a similar fashion: mitral and tricuspid valves can be localized from the four-chamber view. The pulmonic valve is often well seen on sagittal images.
MR Imaging Technique
MR imaging technology is constantly evolving, and this is nowhere better illustrated than in cardiac MR imaging, in which "conventional" technique seems to change on a yearly basis. Nevertheless, two widely available standard sequences can be used for nearly all valve examinations: cine gradient-echo or SSFP sequences to demonstrate wall motion, ventricular function, valve morphology, and visualization of flow jets, and cine phase contrast sequences for flow quantitation.
Cine sequences come in several varieties. The first widely available version consisted of a gradient-echo electrocardiograph-gated sequence in which the cardiac cycle was divided into an arbitrary number of phases, and one phase-encoding gradient step was acquired for each cardiac phase per heartbeat (6). This necessitated fairly long imaging times, and motion artifacts could pose an important problem. The next advance was the introduction of fast gradient-echo segmented k-space acquisitions, in which multiple phase-encoding gradient steps were acquired for each cardiac phase per heartbeat (7). This technique allows acquisition of a complete data set within a single breath hold and thereby eliminates or greatly reduces motion artifact. Recently, breath-hold cine acquisitions using an SSFP sequence have been introduced (8). The advantage of this sequence lies in the greater signal-to-noise ratio and blood-myocardium contrast. Acquisition times are also somewhat shorter. SSFP sequences are gradually replacing fast gradient-echo cine sequences for routine cardiac MR imaging. Fast gradient-echo sequences do have some advantages in valve examinations, however. SSFP sequences are technically more demanding, requiring repetition times less than 7 msec and minimal magnetic field inhomogeneity. The short echo times of SSFP sequences may actually be a disadvantage in visualizing flow jets, which result from dephasing of complex or turbulently flowing blood. Fast gradient-echo sequences generally produce fewer artifacts in regions of pulsatile flow and sometimes allow better visualization of valves. Occasionally, a stenotic or regurgitant jet may be better seen with the fast cine sequence, but sometimes it is better seen with the SSFP sequence and there is nothing wrong with trying both sequences. An alternative to breath-hold cine sequences is the navigator-gated technique, in which breathing motion is monitored by exciting a small column of tissue perpendicular to the diaphragm (9). These navigator echoes are usually interleaved with the cine sequence. With use of an edge-detection algorithm, the position of the diaphragm-lung interface can be determined with a high degree of accuracy, and then one of several strategies can be employed to limit the data used in reconstruction to that acquired within a specified window of diaphragm position. This is a robust technique that effectively limits motion artifact. The major advantage is that breath holding is no longer necessary, an important consideration for many patients. The disadvantage is that acquisition times are longer, and the total examination time often increases. These sequences are not widely available from all vendors but probably will be within 1–2 years.
The second standard technique for valve evaluation is the cine phase-contrast sequence used for quantitative velocity and flow measurement (Fig 9). Velocity information can be encoded by adding additional gradient lobes to a fast gradient-echo sequence: moving spins accumulate a net phase proportional to velocity. Both phase and magnitude images are generated. Velocity data are contained within the phase images, and magnitude images allow accurate definition of vessel borders. Cine phase-contrast sequences incorporate cardiac gating and again divide the cardiac cycle into an arbitrary number of phases. Segmented k-space techniques allow breath-hold acquisitions; however, these pulse sequences are not universally available. Time-velocity and time-flow curves can be generated from these data by drawing a region of interest around a vessel or flow jet. Flow is obtained by multiplying the velocity of a pixel by its area and adding up the contributions of all pixels in the region of interest, or alternatively by multiplying the area of the region of interest by the average velocity of the spins within it.
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Figure 9a. (a) Magnitude and (b) phase images from a cine phase-contrast sequence through the proximal main pulmonary artery. Magnitude images are used to trace the vessel contour for each phase (there are good software programs that have automated this process to a large extent). The velocity information in the phase images can then be used to generate plots of (c) velocity versus time and (d) flow versus time.
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Figure 9b. (a) Magnitude and (b) phase images from a cine phase-contrast sequence through the proximal main pulmonary artery. Magnitude images are used to trace the vessel contour for each phase (there are good software programs that have automated this process to a large extent). The velocity information in the phase images can then be used to generate plots of (c) velocity versus time and (d) flow versus time.
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Figure 9c. (a) Magnitude and (b) phase images from a cine phase-contrast sequence through the proximal main pulmonary artery. Magnitude images are used to trace the vessel contour for each phase (there are good software programs that have automated this process to a large extent). The velocity information in the phase images can then be used to generate plots of (c) velocity versus time and (d) flow versus time.
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Figure 9d. (a) Magnitude and (b) phase images from a cine phase-contrast sequence through the proximal main pulmonary artery. Magnitude images are used to trace the vessel contour for each phase (there are good software programs that have automated this process to a large extent). The velocity information in the phase images can then be used to generate plots of (c) velocity versus time and (d) flow versus time.
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Table 5 lists specific parameters used in our practice (we use GE Medical Systems equipment) for the pulse sequences described above.
Quantitative Analysis with MR Imaging
Early investigators demonstrated good correlation between the size and volume of flow jets and the severity of valvular lesions as revealed by angiography and Doppler echocardiography (10–12). This method is semiquantitative at best, however, and the size of the observed jet depends strongly on the orientation of the image and imaging parameters.
Quantitative analysis of valve disease with MR imaging most often consists of calculation of regurgitant volume and fraction (Fig 10) in patients with regurgitant valves and measurement of peak or time-average velocities and pressure gradients in patients with stenotic valves. Numerous studies have documented the accuracy and reliability of these methods (13-20).
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Figure 10. Flow curve through the proximal aorta in patient with aortic insufficiency. Regurgitant volume (RV) is the area under the time-flow curve below zero (A). Regurgitant fraction (RF) represents the ratio of regurgitant flow to forward flow (A/B).
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These measurements are performed most often for aortic insufficiency, and in this case slice positioning is fairly important: the phase contrast slice should be positioned above the valve at the level of the coronary ostia (Fig 11).
Sections positioned in a more distal location (for instance at the level of the right pulmonary artery) tend to underestimate the amount of regurgitant flow.
Quantification of stenotic valves with either echocardiography or MR imaging involves measuring peak and average velocities across the valve and converting these into pressure gradients with the modified Bernoulli equation:
P = 4vmax2 ,
where P is pressure in millimeters of mercury and v is velocity in meters per second. The technique for measurement of peak velocity is slightly different from that used for flow measurement in regurgitant valves. Several phase-contrast sections are oriented perpendicular to the flow jet rather than perpendicular to the vessel; this assures that the error in velocity caused by oblique positioning is minimized. Phase-contrast sections can also be positioned parallel to the flow jet, although they must be very thin to avoid volume averaging errors. It is important to set the velocity-encoding gradient to a fairly high value, since peak velocities across stenotic valves can reach 4–6 m/sec. When the phase-contrast images have been obtained, the next step is to find the pixels within the vessel with the highest velocities (Fig 12).
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Figure 12. Phase (left) and magnitude images from section just above stenotic valve. Red region of interest depicts entire aorta. Green pixels represent the peak velocity of the flow jet.
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The maximum velocity is then used to calculate the peak pressure gradient (Fig 13). The time-velocity curve of these pixels can also be used to determine the average pressure gradient during systole.
Additional parameters can be obtained using echocardiography to quantify valvular lesions. Effective valve area and effective regurgitant orifice are frequently measured. These are quantities determined indirectly by obtaining time-velocity integrals at the valve and at an adjacent site with an easily measurable diameter (for example the aortic outflow tract). Assuming conservation of flow, the product of the time-velocity integral and area should be constant. Effective valve area or effective regurgitant orifice can be determined, since the remaining parameters can all be measured (21).
This strategy can also be used with MR imaging, although there is little data available regarding the accuracy of this technique. MR imaging also has the potential to measure valve areas directly by means of cine or phase-contrast sequences through the valve plane (Fig 14). This is also a relatively unproven technique, however (22,23).
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Figure 14. Single frame from cine sequence through stenotic aortic valve used to measure valve area. This frame represents the maximal area of the open valve (blue outline). High-resolution images and multiple thin sections are important for accurate and reproducible results. Phase-contrast images can also be used to estimate valve area.
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Quantification: Errors and Pitfalls
Quantitative flow measurement with MR imaging is a reliable and robust technique; however, errors and inaccuracies can easily be introduced without careful attention to detail. Most potential errors are manageable and can be limited by careful attention to technique. Some errors are intrinsic to the method and anatomy and cannot be fixed by using currently available technology. Choosing the correct value for the velocity-encoding gradient is one important detail. The velocity-encoding gradient must be large enough to encompass the expected peak velocities. On the other hand, when the value is set too high, sensitivity for changes in low-flow states is reduced. To limit the length of the phase-contrast cine sequence and to simplify analysis, flow is generally encoded in only one direction, perpendicular to the plane of the section. The implicit assumption is that flow is unidirectional, which is almost never true. The extent to which this assumption affects the accuracy of the results depends on the anatomy and flow characteristics of the region of interest; for example, flow measurement in the ascending aorta is more likely to be accurate than flow measurement within the left ventricle. Complex or turbulent flow is another source of error. This is a problem both in terms of flow direction and flow signal (a voxel with a phase but no magnitude may not be included in the flow measurement). As flow becomes more complex, the individual velocity elements within the voxel are more likely to lose phase coherence during measurement of the MR signal; this is what causes the dark flow jets in cine sequences. While these problems cannot be completely eliminated, small voxels, shortest possible echo times, and improved temporal resolution can help minimize errors caused by complex flow. Adequate spatial resolution is critical for achieving accurate flow measurements. As a general rule, at least 10 pixels should span a vessel to obtain accurate flow data (24–27). Improved resolution can be achieved by decreasing the field of view or increasing the acquisition matrix. Temporal resolution is also important. If temporal resolution is too coarse, peak velocities may not be accurately measured and peak velocity and flow may be underestimated. The number of cardiac phases acquired can be increased up to a point; there are intrinsic limitations based on heart rate and pulse sequence acquisition parameters.
Echocardiography versus MR Imaging
MR imaging is unlikely to replace echocardiography as the primary modality for investigation of valvular heart disease. Echocardiography is fast, cheap, and portable. There is a large literature documenting its efficacy. The superior spatial and temporal resolution of echocardiography are clear advantages over MR imaging in evaluation of valve morphology. The maneuverability of echo cardiography is an advantage in achieving the optimal angulation for measurement of peak velocities. The disadvantage of echo cardiography in this regard is the occasional patient with a poor acoustic window. This can be overcome with a transesophageal examination.
MR imaging is probably more accurate at quantification of ancillary findings in valve disease; it is the standard of reference for measurement of ejection fraction, cardiac volumes, and ventricular mass. Direct measurement of flow is possible with MR imaging but not with echocardiography.
Future Developments
Several investigational techniques will likely become widely available in the next few years. Use of navigator echoes to monitor the position of the diaphragm allows free-breathing acquisition of cine sequences with little if any motion artifact. This technology can also be applied to cine phase-contrast sequences, with the potential for achieving improved spatial and temporal resolution if the limitation of breath holding is no longer a barrier. Navigator echoes have been used to track the position of cardiac valves, so that cine and phase-contrast sections will remain in the valve plane throughout the cardiac cycle (28,29). Parallel imaging techniques can be used to decrease acquisition times by a factor of two or more, again offering possibilities for increased spatial or temporal resolution (30). Combining fast imaging techniques with increased reconstruction speed should allow the MR imaging equivalent of color flow Doppler imaging: superposition of color-coded velocity information over cine images of the heart (31). Velocity and flow information obtained from two- and three-dimensional phase-contrast sequences can be used to study complex flow patterns and calculate shear stress in vessel walls (32–34).
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Conclusions
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MR imaging is not ready to replace echocardiography as the primary test for cardiac valvular disease; however, MR imaging is an excellent alternative or confirmatory examination. MR imaging is probably more accurate in measuring flow (35) and providing accurate and reliable quantification of ventricular function.
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Footnotes
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Abbreviation: LV = left ventricular,
SSFP = steady-state free precession.
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Abstract
Introduction
