VALVULAR HEART DISEASE

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CARDIAC RADIOLOGY

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VALVULAR HEART DISEASE Martin J. Lipton, MD, MRCP, FRCPC, and Richard Coulden, MB, ChB, MRCP, FRCPC

years ago, the immunologic effects of the different serologic types are similar: an acute inflammatory illness often producing longterm scarring of the cardiac valves. Rheumatic fever is primarily, but not exclusively, a disease of children occurring in the 5- to 15year age group. It often presents with a sore throat and in 1%to 3% may produce an acute pancarditis, sometimes with heart failure. Arthritis is also a common feature. The prevalence rate is higher in developing countries, notably Latin America, Africa, and the Orient, and the disease process there is often accelerated. Mitral valve prolapse may occur acutely due to stretching of the chordae tendinae causing an audible murmur of regurgitation.I6 Treatment is with salicylates and penicillin. The American Heart Association recomPATHOPHYSIOLOGY AND mends that this be continued prophylactically EPIDEMIOLOGY OF VALVULAR for many years.33If prophylaxis is properly HEART DISEASE followed, then 70% of patients with a murmur of mitral regurgitation (MR) acquired In developing countries, where 60% of the during the acute episode lose it within 5 world's population live, half of all cardiovasyears. cular disease is caused by rheumatic fever. The prognosis of arthritis following the Indeed, in the first five decades of life it is acute episode is excellent; however, this is not the leading cause of death.' In the United the case for the heart. Severe valvular disease States, with the widespread use of antibiotics, may become manifest 20 or more years later, rheumatic heart disease had been on the defrequently requiring surgery. In some councline, but since 1985 there has been a resurgence in the number of new p r e ~ e n t a t i o n s . ~ ~tries , ~ ~ a juvenile form produces severe symptoms of valve disease much earlier, often in Acute rheumatic fever is an infectious disthe teens. The frequency and speed of modease caused by a group A P-hemolytic strepern intercontinental jet travel regularly brings tococcus. Although Lancefield16classified the organism into serologic groups more than 50 new cases to the United States. It is important for radiologists, especially those in training, to understand the clinical basis of valvular heart disease as well as the radiologic features. Only with this background can we participate in the cardiovascular team and provide added diagnostic value to our patients and referring physicians. As the complexity of cardiac imaging grows, new opportunities arise. Developments in CT and MR imaging could have a profound influence on the investigation and management of future cardiac patients, therefore, it is essential that radiologists take an active interest. If we do not, then past experience has shown that we will be excluded.

From the Department of Radiology, University of Chicago (MJL), Chicago, Illinois; and the Department of Radiology, Papworth Hospital (RC), Cambridge, United Kingdom

RADIOLOGIC CLINICS OF NORTH AMERICA VOLUME 37 NUMBER 2 MARCH 1999

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In the developed world, other etiologies of valve disease are more common. These include congenital abnormalities (bicuspid aortic stenosis); infections (bacterial endocarditis); and degenerative conditions (Marfan syndrome). The presentation, investigation, and management depend predominantly on which valve is involved; whether the dominant lesion is stenotic or regurgitant; and whether the disease process is acute or chronic. The underlying disease process is often of secondary importance to the hemodynamic consequences of the valve lesion, although it may affect long-term outcome. AORTIC VALVE DISEASE Aortic Stenosis

Aortic stenosis (AS) is the obstruction of blood flow across the aortic valve during left ventricular (LV) systole. Isolated AS is congenital in over 90% of cases. Bicuspid aortic

valves are seen in 4 per 1000 live births, with a male preponderance of 4:l. There are two forms of presentation: (1) in the young and (2) in adults. In the young, there is congenital fusion of valve cusps resulting in a stenotic orifice and patients present in infancy or childhood with LV obstruction. The valve is either bicuspid with commissure fusion and a slit-like orifice, or monocuspid with a central or eccentric orifice (Figs. 1 and 2). In the adult form of congenital AS, the valve is also bicuspid but initially it is nonobstructive. Over a period of many years it undergoes commissure fusion with calcification, presenting in adult life with stenosis. Aortic regurgitation (AR) may occur at any time if a bicuspid valve becomes infected with endocarditis. A bicuspid valve is not usually associated with two sinuses of Valsalva; indeed, there are normally three but there is loss of the normal pattern of symmetry. The noncoronary sinus becomes larger and extends more posteriorly and inferiorly. Congenital AS may be associated with other abnormalities, nota-

Calcium

Stenosis

AnteriodPosterior

\' Regurgitation

RighULeft

\r

A Infection

B Figure 1. Bicuspid aortic valve. A, Location of cusps. B, Complications. (From Jefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Buttenvorths, 1980; with permission.)

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Rheumatic endocarditis Degenerative (sclerosis in old age) Hypercholesterolemia

A

B

Figure 2. Monocuspid aortic valve, which may have a central orifice (A), or an eccentric, slit-like orifice (6). (From Jefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.)

bly coarctation of the aorta, ductus arteriosus, ventricular septa1 defect, or pulmonary valve stenosis. Isolated pure AS of rheumatic origin is rare because AR is usually coexistent. Other causes of aortic valve stenosis are listed below*: Congenital Turner 's syndrome *FromJefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.

The normal adult valve area is more than 3 cm2. Any reduction in valve area produces obstruction at high flow rates, but when it is reduced to less than 0.6 cm2 a significant pressure gradient develops at resting flow rates. This places an increased pressure load on the LV, which compensates by undergoing hypertrophy. The LV chamber and cardiac silhouette do not enlarge, although the shape of the left heart border on chest radiograph may suggest it. Enlargement only occurs when AR is also present or the LV decompensates as a consequence of ischemic heart disease. Poststenotic dilation of the ascending aorta is variable and depends on the duration and severity of obstruction and the direction of the stenotic jet. Ascending aortic dilatation may be difficult to separate in older patients from typical elongation and unfolding of the normal aorta. Furthermore, it may not be seen in the frontal projection if the dilatation occurs in the sagittal rather than in the coronal plane. Thus, it is vital on plain radiographs to search for aortic valve calcification, which is nearly always present in AS in men over 40 years, and is best seen on the lateral film (Fig. 3). Patients with AS in whom the systolic pressure gradient is less than 40 mm Hg are often asymptomatic, whereas gradients more than 70 mm Hg are associated with exertional dyspnea, syncope, angina pectoris, and even sudden death. Aortic gradients equal to or

Figure 3. A, PA chest radiograph in a patient with predominant aortic stenosis and dilatation of the ascending aorta (arrowheads). The heart is not usually enlarged unless there is either cardiac failure or coexistent aortic regurgitation, as in this patient. B, Lateral projection of the same patient. Note the aortic ring calcification (arrowheads)typical of congenital calcific AS.

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Figure 4. A, PA chest radiograph showing cardiomegaly predominantly caused by enlargement of the left ventricle. B, Lateral view of same patient following aortic valve replacement (ball-in-cage). The major lesion is severe AR. Note posterior enlargement of the LV behind the inferior vena cava.

greater than 50 mm Hg should be considered for intervention. Occasionally, the site of obstruction may be above or below the valve. Subvalvular stenosis is either caused by a thin diaphragm, tethered to the valve by fibrous tissue, or by hypertrophic muscle as in certain cardiomyopathies (e.g., hypertrophic obstructive cardiomyopathy [HOCM]). Supravalvular stenosis is usually part of a widespread congenital arteriopathy. The ascending aorta is involved just beyond the upper margins of the sinuses of Valsalva, but there are frequently other stenoses of the thoracic and abdominal aorta. Pulmonary artery stenosis or stenoses of its branches may also be a feature. A number of syndromes have been described in which supravalvular stenosis is a part. The best known of these is Williams syndrome, which comprises hypercalcemia of infancy, abnormal elfin facies, and mental retardation. Aortic Regurgitation The causes of aortic regurgitation (AR) are*:

Lesions of the Aortic Cusps Congenital malformation Rheumatic endocarditis Infective endocarditis “FromJeffersonK, Rees S (eds):Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.

Syphilis Ankylosing spondylitis Reiter’s syndrome Rheumatoid arthritis Mucopolysaccharidoses Spontaneous or traumatic rupture Degenerative Disease of the Aortic Wall Cystic medionecrosis Aortic dissection Syphilis Marfan syndrome Systemic hypertension Osteogenesis imperfecta Pseudoxanthoma elasticum Anomalies of the Aortic Root Aortic sinus of Valsalva aneurysm Aortic sinus fistula to LV Aorto-LV tunnel AR may be acute, as in infective endocarditis, cusp rupture, dissecting aneurysm, and aortic fistula, or chronic. It is usually chronic and may be well tolerated for years, presenting only when LV failure intervenes. AR imposes a volume overload on the LV; stroke volume is increased and the LV dilates. Chronic volume overload leads to an increase in muscle mass. Combined AS and AR may be congenital or acquired. In chronic AR the ascending aorta dilates, which together with enlargement of the LV produces an increase in cardiac silhouette. Figure 4 demonstrates the radiographic appearances of AR.

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Figure 5. Echocardiographic assessment of AS. A, Two-dimensional short axis echocardiogram through the left ventricle of a patient with mild AS showing the line of acquisition for the M mode for left Ventricle function (RV = right ventricle). B,M mode showing vigorous ventricular contraction and normal wall thickening. No significant ventricular hypertrophy. C, Continuous wave Doppler in the same patient who has AS and AR. Peak systolic velocity is 2 m/s, giving a gradient of 16 mm Hg.

Evaluation and Treatment

The natural history of the disease is important; 50% of patients diagnosed clinically with severe AS (with or without symptoms) die within 5 years? Patients with signs of AS presenting with congestive heart failure, angina, or exertional syncope undergo echocardiography together with chest radiography and EKG. Echocardiography demonstrates whether the valve is bicuspid, thus allowing qualitative assessment of valve motion, calcification, and valve area. LV cavity dimensions are easily measured by M-mode, and this technique or two-dimensional imaging is used to assess contractility and LV

muscle mass (Fig. 5). Doppler measurement of peak systolic velocity across the aortic valve is central to the examination; therefore, it is essential that the technologist or physician persists in order to obtain the maximum possible velocity. This requires continuous wave Doppler because peak velocity is likely to exceed the Nyquist limit of pulsed wave Doppler. Under certain circumstances, it may be impossible to align the Doppler beam with the stenotic jet without using suboptimal acoustic windows (i.e., sternal notch or right parasternal position) where two-dimensional imaging is impractical and measurements have to be made blind. This can be time consuming and is very operator-dependent. Re-

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corded systolic flow velocities decrease as the angle of the ultrasound beam deviates from the axis of blood flow. This effect is proportional to the cosine of the angle between the beam and the direction of flow. For angles less than 20 degrees, the true velocity is underestimated by a factor of less than 0.06 and errors can be ignored. For larger angles, however, errors can be considerable (e.g., at 45 degrees velocity is underestimated by a factor of 0.27). The maximum instantaneous gradient across a valve (P) is calculated from the peak velocity (V) using the modified Bernoulli equation:

P (mm Hg) = 4V2(m/s) This equation holds for any situation where the prestenotic velocity is less than 1.5 m/s. Above this, both the velocity in the valve orifice and the prestenotic velocity must be taken into account. Aortic valve area can also be derived from a modified Bernoulli equation, but this is rarely of clinical value. Color flow mapping may be helpful in identifying the direction of a stenotic jet but it is of greatest value in the assessment of AR. Semiquantitative estimates of AR can be made by defining the spatial extent of regurgitant turbulence in the LV cavity in at least two orthogonal planes. It must be remembered that the turbulence detected by color flow mapping is velocity-dependent and not volume-dependent; absolute echocardiographic measurement of regurgitant volumes is impossible." When the aortic gradient is greater than 50 mm Hg, the majority of cardiologists still recommend cardiac catheterization as the next procedure. This is not because of a lack of confidence in the Doppler result, but in postmenopausal women and men over 35 years there is a significant incidence of coronary artery di~ease.~' These patients may require coronary artery revascularization at the same time as valve surgery. The pressure drop across the aortic valve is measured using an end hole hemodynamic catheter by 'pull-back' across the aortic valve. The gradient measured by pull-back is always lower than the Doppler gradient, which measures peak instantaneous gradient (Fig. 6). All catheter pressure measurements should be made before intravascular contrast medium is given, because this alters the hemodynamics to a variable and unknown degree. A supravalvular aortogram is used to evaluate aortic valve disease, not left ventriculography. Su-

P res I su re

Time Figure 6. Simultaneous measurement of pressure in the aortic root (Ao) and left ventricle showing the difference between maximum instantaneous gradient (MIG), as measured by Doppler, and peak to peak or pull back gradient (P-P), as measured by catheter.

pravalvular aortography typically demonstrates an immobile domed aortic valve, which is outlined in ventricular systole. Additionally, the presence and extent of calcification together with a negative jet of blood ejected into a contrast-filled aortic root can usually be seen. Most importantly, this technique estimates the severity of the AR (Table l),which can be difficult by other techniques. Modifications of this system are used to grade regurgitation of other valves, changing the relevant chambers to match the valves concerned (Fig. 7). Several therapeutic approaches to AS are available. Commissurotomy of noncalcified valves in younger patients can be achieved by either surgery or percutaneous balloon valvuloplasty. Balloon valvuloplasty may be possible in some adults, although by the time they present the valve is often calcified and immobile. It is usually reserved for patients who are unfit for surgery. Dilatation is associTable 1. ANGIOGRAPHIC ASSESSMENT OF AR

Trivial Moderate Severe Gross

Regurgitant contrast is cleared from the ventricle during each systole. Regurgitant contrast is incompletely cleared but does not accumulate. Regurgitant contrast is seen to accumulate from one diastole to the next. LV is completely filled with contrast medium in the first diastole.

From Jefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.

VALVULAR HEART DISEASE

Figure 7. Left anterior oblique aortograrn showing a dilated aortic root in a patient with severe AR. Contrast medium refluxes back into the left ventricle, becoming denser than the aorta over several heart beats.

ated with complications, the most important being AR, which if severe may necessitate surgery. The great majority of patients with AS and all of those with significant AR require aortic valve replacement.26

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Typical appearances are shown in Figure 8. Thrombus commonly forms within the left atrial appendage, partly due to cardiac rhythm disturbance, notably atrial fibrillation, and partly due to atrial enlargement and sluggish blood flow. Embolization of thrombotic or calcific material is well recognized; therefore, patients require long-term anticoagulation. Rarer causes of MS include congenital MS; parachute mitral valve; atrial myxoma; thrombus; secondary tumors growing into the mitral orifice (typically hypernephroma or lymphoma); and, occasionally, carcinoid syndrome. Left atrial myxomas usually arise from the interatrial septum and are pedunculated. As the tumor prolapses into the valve orifice, it obstructs flow causing functional stenosis. Even during systole, it can disturb mitral valve function, so it is often associated with the murmur of MR. Myxomas rarely cause identifiable calcification and have no specific radiographic features. Carcinoid valve disease is predominantly right sided and related to hepatic metastases from a primary bowel carcinoid. Mitral and aortic valve lesions are caused by primary bronchial tumors. Causes of MS are summarized below*: *From Jefferson K, Rees S (eds): Clinical Cardiac Radiol-

ogy, ed 2. London, Butterworths, 1980; with permission.

MITRAL VALVE DISEASE

Mitral Stenosis

Mitral stenosis (MS) is more prevalent in women and develops when scarring narrows the valve orifice or some other process obstructs flow through the mitral valve. The most frequent cause, by far, is rheumatic fever. Isolated mitral valve involvement is most common, followed by a combination of mitral and aortic valves. The valve leaflets become thickened, immobile, and encrusted by lumps of calcified fibrous tissue. The process may involve the commissures and eventually the subvalvular apparatus. Standard chest radiographs show dense calcification, but lesser amounts are only detected by other techniques. Typical findings on chest radiographs include left atrial enlargement, pulmonary venous hypertension, pulmonary edema, pulmonary arterial hypertension, and ultimately right heart failure. MS may be pure, although tethering and fibrosis of the chordae often result in varying degrees of regurgitation. The LV is not enlarged in the absence of MR. "

Figure 8. MS with large main pulmonary artery and beneath it the convex bulge of the enlarged left atrial appendage (arrow). The left ventricle is not enlarged. Infiltrate in the right mid-zone abutting the lesser fissure reuresents a oulmonarv infarct.

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Figure 9. A, PA chest radiograph in a patient with rheumatic mitral valve disease and an enlarged left atrium containing extensive curvilinear calcification. 6,Lateral radiograph of the same patient with left atrial enlargement displacing the cardiac outline posteriorly (curved arrows). Left ventricle enlargement is indicated by displacement of the posterior wall of the left ventricle behind the inferior vena cava (black arrow).

Congenital Rheumatic endocarditis Carcinoid syndrome Eosinophilic endocarditis Systemic lupus Rheumatoid arthritis Atrial myxoma Senile calcification involves only the mitral annulus, not the leaflets. It rarely impairs valve function. It is typically C-shaped, being incomplete medially. It must be distinguished from calcification of the left atrium, which is usually heaviest posterolaterally, indicating thrombus and a brittle atrial wall (Fig. 9). The surgeon should be warned of its presence because bleeding may be profuse and suturing can be difficult. Alternative causes of cardiac calcification (e.g., in the pericardium, coronary arteries, and other valves) must be distinguished.22 The normal adult mitral orifice area is 4 to 6 cm2.When narrowed to 2 cm2, there is minor elevation of left atrial pressure and a gradient across the valve during exercise. Further reduction to 1 cm2 produces severe pressure overload leading to an increase in left atrial size, which does not correlate with the degree, severity, or duration of the disease. Enlargement of the left atrial appendage is

more common than in other causes of pulmonary venous hypertension. In untreated pulmonary venous hypertension, there is a broad correlation between left atrial pressure and the radiographic a p p e a r a n ~ e When . ~ ~ left atrial pressure is less than 12 mm Hg, the radiographic appearance may be normal. At 12 to 18 mm Hg, there is upper lobe vascular redistribution. Between 18 and 22 mm Hg, there is interstitial edema, and above 22 mm Hg, alveolar edema develops. These figures are a general guide. They take no account of individual variations in plasma osmotic pressure, the efficiency of lymphatic clearance, or the chronicity of venous hypertension. Interstitial edema occurs when the pressure exceeds the plasma osmotic pressure of 25 mm Hg. Chronic pulmonary venous hypertension eventually leads to passive pulmonary arterial hypertension and dilatation of both main and proximal pulmonary arteries. Pulmonary vascular resistance subsequently increases due to a combination of vasoconstriction and hypertrophy of the muscular layers of the pulmonary arterioles. This varies in degree, but in some patients pulmonary hypertension dominates the appearance of the chest radiograph. Ultimately, the right ventricle fails and the right-sided cardiac chambers dilate.

VALVULAR HEART DISEASE

Mitral Regurgitation

MR develops when there is inadequate closure of the mitral apparatus and blood is ejected into the left atrium during ventricular systole. MR may be either functional or anatomic. Functional lesions are usually related to LV dilatation and disturbance of papillary muscle function. The latter can be due to altered geometry as the ventricle enlarges or the consequence of ischemic heart disease and dyskinesia. Anatomic causes are numerous. Congenital MR may be due to a cleft in one of the leaflets, accessory leaflet tissue, or deficient leaflet tissue. Idiopathic mitral prolapse affects 6% of women and 2% of men, making it the most common cause of regurgitation in the Western world. Rheumatic fever, however, is the most common cause world wide. Myxomatous degeneration of the valve apparatus and chordae leads to elongation of the chordae with enlargement of the leaflets. The process is usually asymmetric, giving rise to eccentric regurgitation, which is rarely severe. As expected, the chest radiograph is normal unless the hemodynamic abnormality is significant. Inherited collagen disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, and osteogenesis imperfecta, may also cause mitral valve prolapse, but in these cases significant regurgitation is more frequent.17 The causes of MR are*: Chronic regurgitation Congenital heart disease Rheumatic endocarditis Mitral leaflet prolapse (myxomatous, inflammatory) Any cause of LV dilatation Papillary muscle dysfunction (infarction or ischemia) Calcified mitral annulus Heritable disorders of connective tissue (Marfan syndrome) Ehlers-Danlos syndrome, osteogenesis (imperfecta) Left atrial myxoma Acute regurgitation Rupture of chordae tendinae (myxomatous, trauma, endocarditis) Rupture of papillary muscle (infarction, trauma) Papillary muscle dysfunction Valve perforation (endocarditis) *From Jefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.

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Secondary distortion of the mitral valve may also be produced by enlargement of the left atrium, impairing motion of the posterior mitral valve leaflet. When the left atrium is large and compliant, the effects of MR on the pulmonary circulation can be minimal. Many patients with compensated MR have little or no evidence of pulmonary venous hypertension. Increased pulmonary vascular resistance is rare unless regurgitation is severe or longstanding. A giant left atrium may arise in both MS and MR, but is more common in the latter. Acute MR, as seen with a ruptured chorda, is characterized by severe pulmonary venous hypertension, pulmonary edema, and little or no cardiomegaly. The left atrium is not compliant and is rarely enlarged. HOCM may be associated with mitral valve dysfunction due to systolic anterior motion of the fibrosed anterior mitral valve leaflet, although asymmetric hypertrophy with a mid-LV cavity gradient is generally more clinically important. Bacterial endocarditis causes MR by a destructive process, which may perforate a leaflet. Sometimes this is secondary to spread from the aortic valve, but also occurs in isolation. The diagnosis of endocarditis rests almost entirely with echocardiography. High frame rates are needed to identify small, mobile vegetations and nodules. Other imaging techniques are usually inadequate. Add to this the benefits of being able to image a sick patient by the bedside, and the choice of technique is clear. Transesophageal echocardiography provides even greater clarity of valve leaflet morphology, and although invasive, should be used whenever there is doubt about the diagnosis. Evaluation and Treatment

As with aortic valve disease, accurate assessment and treatment are essential. Untreated, only 60% of patients presenting with rheumatic MS survive 5 years compared with 80% for patients with MR. Combined MS and MR is associated with an intermediate survivorship of approximately 70?'0.~The chest radiograph allows crude assessment of heart size, chamber enlargement, and the degree of pulmonary venous hypertension, but echocardiography is the basic tool of diagnosis and management planning. M-mode and two-dimensional echocardiography demonstrate valve leaflet mobility,

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Figure 10. Echocardiographassessment of mitral stenosis (MS).A, Two-dimensionalechocardiogram showing the vertical long axis through the aortic and mitral valves of a patient with MS. The mitral valve leaflets are thickened and open poorly. Arrowheads show anterior leaflet. Arrow shows posterior leaflet. LA = Left atrium. f3, M mode through the mitral valve showing very poor motion. Anterior and posterior leaflets move together anteriorly in diastole because of commissural fusion. C, Doppler color flow map in the same plane as A showing the turbulent MS jet (arrows) during diastole. See also Color Plate 1, Fig. 3.

calcification, and the involvement of subvalvular apparatus. As with the aortic valve, MS is characterized by doming of the valve leaflets in diastole with the mitral inflow becoming funnel-like as the chordae become progressively shorter. This in turn leads to MR (Fig. 10 and Color Plate 1, Fig. 3). Using color flow mapping to identify the stenotic jet, pulsed wave or continuous Doppler is used to assess the severity of stenosis. Unlike AS, however, measurement of the Doppler gradient is less valuable than an estimate of valve area. According to the principles of Bernoulli hemodynamics, the relationship be-

tween the pressure drop across a stenosis and the velocity of flow is quadratic. In other words, pressure half time (PHT), the time taken for the pressure gradient across the valve to fall by half, can be calculated from the mitral inflow velocity profile by dividing the peak velocity (V) by .\/2 and measuring the time from peak velocity to V/.\/2 (Fig. 11).Hatle et all1 have since calculated an empirical constant that relates PHT in milliseconds to mitral valve area (MVA): MVA (cm') = 220/pressure half-time (milliseconds). Although this method is widely used, care must be taken under certain conditions. In

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procedure and there is no reliable means of predicting which patients will do well and at what stage in the disease process surgery should be performed. LV deterioration appears to be related to loss of the subvalvular apparatus resulting from valve replacement. The chordae and their valvular attachments help to brace the LV during systole and under normal conditions prevent globular dilatation. There are two possible solutions: (1) to preserve the subvalvular apparatus if valve replacement is unavoidable, and (2) to conserve the valve by leaflet reconstruction and repair in cases of pure MR. Successful repair depends entirely on the skill of the surgeon. Accurate shortening of chordae or excision of redundant leaflet tissue relies on detailed preoperative assessment, but this has been made easier with the use of preoperative and intraoperative transesophageal ultrasound. Figure 11. Continuous wave Doppler of mitral diastolic flow showing calculation of pressure half time (PHT) from which mitral valve area can be calculated.

atrial fibrillation, an average of five beats should be used to estimate PHT. When LV diastolic pressure rises rapidly, as in AR or with a noncompliant ventricle (as found in cases of LV hypertrophy or ischemic heart disease), PHT may be inappropriately short, giving an overestimate of valve area. Mitral valve prolapse of any degree is easily identified by two-dimensional echocardiography. The presence of MR can be determined by color flow mapping, and as with AR can be semiquantitatively assessed. More recently, peak mitral in-flow velocity has been shown to predict the severity of MR.” Cardiac catheterization is reserved for those patients likely to require intervention. In MS this may be by balloon valvuloplasty or by surgery. Valvuloplasty is most successful when the mitral valve leaflets are mobile and uncalcified but can also be used when the patient is unfit for surgery. Valve area may increase by 50% to 100% with a concomitant fall in pressure gradient, but results are generally less satisfactory than with valve replacement. A left ventriculogram outlines the mitral valve in systole providing qualitative assessment of regurgitation. Catheterization should include coronary angiography in patients over 35 years old. The surgical treatment of MR has been valve replacement for many years. Unfortunately, LV function often deteriorates after the

RIGHT-SIDED VALVULAR HEART DISEASE Tricuspid Valve The causes of tricuspid stenosis (TS) are the same as those of the mitral valve. Congenital lesions are rare. They occur in isolation or in combination with right ventricular (RV) hypoplasia. Acquired TS is nearly always rheumatic and associated with mitral disease.32Its importance lies in the fact that it may reduce the pulmonary vascular effects of MS. The right atrium enlarges, but it is often impossible on chest radiograph to distinguish enlargement due to TS from the consequences of pulmonary hypertension. When TS is isolated, carcinoid syndrome, endocardia1 fibrosis, or lupus erythematosus should be suspected. Mechanical obstruction of the valve by thrombus or tumors, such as atrial myxoma or hypernephroma, may also occur. Acquired tricuspid regurgitation (TR) is usually functional but this does not occur in the absence of pulmonary hypertension. Anatomic causes of TR duplicate those of MR but carcinoid and infective endocarditis are more common. Tricuspid endocarditis, frequently complicating intravenous drug abuse, may present with fever, pulmonary abscesses, or infarction. Valvular involvement may only manifest itself at a later stage. Causes of TR are*: *FromJefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.

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Figure 12. A, Anterior projection right ventricular angiogram in a patient with Ebstein’s anomaly. The cavernous right atrium (RA) is seen with a notch inferiorly (arrow) at the attachment of the congenitally displaced and incompetent tricuspid valve. Note the relatively small right ventricle (rv). €3, Transaxial spin echo MR through the tricuspid valve in another patient with Ebstein’s anomaly showing tricuspid valve (arrow) displaced towards the apex and a massive right atrium.

Chronic regurgitation Congenital (Ebstein’s anomaly) Any cause of RV dilatation Tricuspid leaflet prolapse (myxomatous, inflammatory) Rheumatic endocarditis Ehlers-Danlos syndrome Endomyocardial fibrosis Carcinoid syndrome Right atrial myxoma Acute regurgitation Infective endocarditis Trauma Rupture of papillary muscle (infarction, trauma)

Ebstein’s anomaly is the most frequent primary cause of isolated tricuspid valve disease. Ebstein, a pathologist, recognized the disorder that now bears his name in 1886. In this condition, the inferior and septa1 leaflets are displaced into the body of the ventricle, leaving only the anterior leaflet attached to the valve ring. The degree of right atrial dilatation depends on the severity of regurgitation, but this is usually severe. The pulmonary trunk and aorta are small. Plain chest radiograph shows globular cardiomegaly, which may mimic a pericardial effusion or cardiomyopathy (Fig. 12). The pulmonary artery segment appears decreased in size.

VALWLAR HEART DISEASE

Malignant carcinoid tumors usually originate in the ileum and metastasize to the liver. Relatively few are hormonally active (secrete serotonin) and only those with liver metastases produce the carcinoid syndrome (flushing, diarrhea, and edema). Valve lesions are caused by fibrous plaques forming on the endocardia1 surface of the valve, leading to commissural fusion and valve stenosis. Both tricuspid and pulmonary valves may be involved. The right heart dilates, but there is no poststenotic dilatation of the pulmonary artery trunk. Left-sided valve lesions can occur but are rare in the absence of pulmonary metastases or primary bronchial carcinoid. In right-sided valve disease, the chest radiograph findings are usually those of pulmonary arterial or venous hypertension. When TR is secondary to MS with pulmonary hypertension, pulmonary edema may be surprisingly absent. Right heart failure lowers right-sided cardiac output so that there may be insufficient flow to elevate left atrial pressure. Pulmonary edema therefore resolves. This is an important observation because it is an indicator of severe decompensation. Cardiomegaly is marked with elevated right atrial pressure inferred by a dilated azygos vein. If right heart failure is severe, ascites may elevate the right hemidiaphragm. Echocardiography identifies TS if present and allows assessment of the severity of TR. As with mitral valve prolapse, floppy tricuspid leaflets are readily identified on two-dimensional imaging. Measurement of the peak systolic velocity of the TR jet is frequently used to calculate the pressure gradient across the tricuspid valve. When this value is added to right atrial pressure, this gives a reliable noninvasive estimate of RV systolic pressure and in the absence of pulmonary stenosis, pulmonary artery pressure. In severe pulmonary hypertension, the RV may compress the LV and cause paradoxical interventricular septal motion. This can only be appreciated on crosssectional imaging. Pulmonary Valve Disease The causes of pulmonary valve stenosis (PS) are‘: Congenital Maternal rubella ‘From Jefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Butterworths, 1980; with permission.

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Figure 13. Classical pulmonary valve stenosis causes poststenotic dilatation of the main pulmonary artery (open arrow). This occasionally extends into the left pulmonary artery but does not involve the right.

Noonan’s syndrome Carcinoid syndrome Rheumatic endocarditis

PS with an intact ventricular septum is nearly always congenital. It may be associated with maternal rubella, and occurs in Noonan’s syndrome. The cusps are thickened and poorly mobile, creating a domed valve with either a small central or eccentric orifice. The plain chest radiograph is characterized by a localized dilatation of the main pulmonary trunk with poststenotic dilatation (Fig. 13). Dilatation may extend into the proximal left pulmonary artery and occasionally into the right, but this depends on the angulation of the turbulent jet. Secondary and more distal pulmonary branches are normal. This is in contrast to cases of pulmonary arterial hypertension or plethora, where peripheral vessels are abnormal. Subvalvular stenosis may occur and is due to hypertrophy of the muscular ventricular infundibulum. It is usually associated with other congenital heart defects, and may be distinguishable from PS by absence of central and left pulmonary arterial dilatation. As with AS, the heart does not enlarge on chest radiograph until the RV decompensates and RV dilatation ensues. If the foramen ovale is patent or if there is a coexisting atrial septal defect, then a right-to-left shunt occurs, resulting in clinical cyanosis. Acquired causes of PS include aneurysms of the ascending aorta and masses or tumors of the mediasti-

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Figure 14. Massive dilatation of the pulmonary artery (PA) in a patient with congenital absence of the pulmonary valve. Radiography is alarming, but a pulmonary valve is not essential, and has been used in the past as an autograft for replacing a diseased aortic valve. RA = right atrium.

num. A complete diagnosis requires estimating the severity of PS and excluding other lesions. Echocardiography usually provides this information, but cardiac catheterization may be necessary for a full hemodynamic assessment, particularly in congenital heart disease, or as a precursor to intervention. The lower pressures in the pulmonary circulation make balloon valvuloplasty the technique of choice in PS. After the procedure the pulmonary trunk may reduce in size, but seldom returns to normal. Similarly, heart size decreases little because pathologic changes in a dilated RV myocardium are rarely reversible. Significant congenital pulmonary regurgitation (PR) is rare. Recent Doppler studies, however, have shown that minor degrees of PR are common.'2 Figure 14 illustrates the classic appearance of congenital absence of the pulmonary valve. Acquired PR is frequently iatrogenic and due to dilatation of the valve ring following valvotomy. Functional regurgitation occurs in association with processes that stretch the valve ring as part of right heart failure. It is therefore common in pulmonary hypertension. Idiopathic dilatation of the pulmonary trunk, considered to be a "forme fruste" of Marfan syndrome, may also give rise to PR. Rarer causes include bacterial endocarditis and rheumatic endocarditis. Clinically significant PR is rare. Little radiographic change is seen in PR unless TR intervenes. When this happens, the features

are of cardiomegaly and right-sided chamber enlargement. Causes of PR are*: Congenital Postvalvuloplasty Infective endocarditis Rheumatic endocarditis Carcinoid syndrome Rubella syndrome Trauma Any cause of RV dilatation MULTIVALVE DISEASE

Multivalve involvement is common in rheumatic heart disease. Clinical diagnosis can be difficult because the signs of the proximal lesion frequently mask those due to other valves. The mitral and aortic valves are the two valves usually involved and the combination of MS and AR is most frequent. All other combinations may occur, but that of AS and MR is particularly hazardous. The AS increases the degree of MR and the MR reduces the ventricular pressure preload needed to overcome the AS. Cardiac output is reduced and pulmonary venous hypertension is severe. Interpretation of the chest radiograph in multivalve disease is as difficult as clinical diagnosis. The features are dominated by the effects of the proximal valve *FromJefferson K, Rees S (eds): Clinical Cardiac Radiology, ed 2. London, Buttenvorths, 1980; with permission.

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Figure 15. A, Triple valve replacement and generalized cardiomegaly. Braunwald-Cutter prostheses in the aortic (A), mitral (M) and tricuspid (T) positions. All four chambers are enlarged with left atrial enlargement suggested by splaying of the carina (arrows). B, Lateral radiograph in the same patient. Aortic prosthesis lies anterosuperior to mitral. Enlargement of right-sided chambers is indicated by filling in of the anterior mediastinal window. (From Coulden R, Lipton MJ: Radiological examination in valvular heart disease. In Zaibag MA, Duran C (eds): Valvular Heart Disease. New York, Marcel Dekker, 1989; with permission.)

lesion so that involvement of other valves is often missed. Echocardiography is essential. When combined with Doppler and color flow mapping, cardiac catheterization can be avoided in many patients. ARTIFICIAL VALVE DISEASE

There are now over 40 different prosthetic valves being placed in approximately 40,000 patients in the United States annually. They fall into two main categories: (1) mechanical (ball-in-cage and tilting disc), and (2) bioprostheses. The former require lifelong anticoagulation but are highly durable; the latter are nonthrombogenic, thus avoiding the need for anticoagulation, but undergo degeneration and calcification. After 10 to 15 years, this is often so severe that repeat surgery is needed. The choice of valve depends on the patient’s age, associated conditions, and the relative risk of anticoagulation. All prosthetic valves produce an element of stenosis when compared with a normal native valve. This is rarely important in the mitral position, but in the aortic position valve replacement represents conversion of a severe stenosis to a mild one. It is not a cure. For bioprostheses, stenosis increases as degeneration occurs and one of the main aims of imaging postsurgery is to monitor progression. Other complications

include endocarditis, structural failure, and paraprosthetic leaks, all of which result in regurgitation. A paraprosthetic leak occurs when one or more of the valve ring sutures fail and can in severe cases be identified by rocking of the valve ring on fluoroscopy. The mortality associated with valve prostheses is of the order of 5% per year, although this is greater when more than one valve has been r e p l a ~ e d .lo ~ ,Figure 15 shows a patient in whom three prosthetic valves have been placed. ALTERNATIVE CARDIAC IMAGING MODALITIES

Echocardiography, angiography, and radionuclide imaging have well-established and defined roles in cardiac imaging. Cardiac CT and MR imaging are relatively new but have many potential advantages. The next section gives an overview of current technology and outlines areas where each of these modalities could be integrated into mainstream cardiac diagnosis. CT

Conventional CT is of limited value in the diagnosis of heart disease. Even with slip-

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ring systems, scan times are long compared with the length of the cardiac cycle and motion artifact severely degrades image quality. Electron beam CT (EBCT) was developed to overcome this. With scan times as short as 50 milliseconds, cardiac and respiratory motion are frozen and using the range of operating modes available all aspects of cardiac function can be assessed. In addition to freedom from respiratory artifacts, no EKG gating is necessary. Image acquisitions can be triggered by the R wave of the EKG, but without the need for EKG gating and averaging data from multiple cardiac cycles. This is an advantage compared with MR imaging and nuclear cardiology where arrhythmias are a major problem. Short- and long-axis cardiac planes can be imaged directly because the wide EBCT gantry allows table angulation and tilt. The need for reformatting is largely eliminated, although multislice acquisition and multiplanar reconstruction are possible as with conventional systems.6 EBCT is the most sensitive modality for identifying cardiac calcification, and no contrast medium is needed. Calcification can be localized, characterized, and quantified in valves, cardiac chamber walls, pericardium, and coronary arteries. With the widespread use of echocardiography, cardiac catheterization has been largely replaced in the diagnosis of valvular heart disease. It is, however, still used for the preoperative evaluation of middle-aged to elderly patients with a risk of concomitant myocardial ischemia. Patients with severe AS, for example, may have angina either from coronary occlusive disease or from a mismatch of coronary perfusion to muscle mass resulting from LV hypertrophy. A negative EBCT used to assess coronary calcification has a strong negative predictive value of 98% and excludes the need for coronary angiography (Fig. 16).27 Contrast enhancement is needed to evaluate the cardiac chambers and valves (Fig. 17). Relatively small boluses of intravenous contrast agent (20 to 60 mL) can be injected via a peripheral vein. The current rate of image acquisition (frame rate) for EBCT is approximately 17 frames per second depending on the heart rate. This is considerably slower than echocardiography or angiography (30 to 60 frames per second), although it may increase as the technology advances. Cardiac chamber volume and shape, wall thickening and thickness, and myocardial mass can all be measured by EBCT.l, * If only one valve

Figure 16. EKG triggered partial reconstruction axial CT using a conventional scanner showing calcification in the left main stem and anterior descending coronary arteries (arrows). Image quality is very similar to EBCT and allows quantification.

is incompetent, the regurgitant volume may be calculated by comparing the RV and LV stroke v01umes.~The relatively slow frame rate of EBCT limits its value in assessing na-

Figure 17. EBCT through a normal aortic valve showing three aortic cusps in diastole. Image quality compares favorably with echocardiography. Right coronary artery can be seen rising from the anterior coronary sinus (arrowhead).

VALWLAR HEART DISEASE

tive valve motion, although there may be a role when examining mechanical prostheses. In this situation the most important criteria relate to the degree of valve opening and whether it "rocks." Only echocardiography can provide the detail required to assess valve motion prior to valvuloplasty or identify vegetations in endocarditis. Intracardiac thrombus can be difficult to identify by transthoracic echocardiography and may be difficult to distinguish from tumor. EBCT has a role in this setting in that the absence of enhancement following intravenous contrast medium often indicates thrombus. Chronic thrombus in the atrial appendage is an exception and may enhance when organized. Tumors in this site are exceedingly rare. Despite its potential, the impact of EBCT on cardiac diagnosis has been disappointing. Poor reliability and high cost compared with conventional systems have reduced uptake and only 65 units are installed worldwide. The current hope is that new developments with EKG-triggered acquisition and partial rotation reconstruction will give a conventional scanner some of the functionality of EBCT (Fig. 18).30Whether this approach has a role in the investigation of valvular heart disease has yet to be established. MR Imaging

Cardiac MR imaging provides the opportunity to image structure and function with one

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modality. It does not have the constraints of CT or echocardiography with regard to image plane or acoustic window, and as such has distinct advantages over both. The most useful pulse sequences in cardiac imaging are accelerated versions of the spin echo (SE) and gradient refocused echo (GRE) sequences. All imaging sequences require multiple radiofrequency excitations (pulses) and echo acquisitions. The number of excitations-acquisitions needed to create an image depends on the spatial and contrast resolution required; for most cardiac purposes this is 256 or 512. Conventional SE imaging uses a combination of 90 degree and 180 degree radiofrequency pulses to generate the echo, which is collected at a time TE. Before another excitation pulse can be given, the tissues have to recover their original magnetization, introducing a delay between excitations (TR).With routine MR imaging the values of TE and TR are adjusted to alter the T1 or T2 properties of the final image. To eliminate cardiac motion, EKG gating is needed, removing flexibility over the choice of TR. With cardiac gating the TR must be equal to the R-R interval of the patients EKG or a multiple of the R-R interval. Although several slices can be acquired simultaneously, it takes 256 or 512 heartbeats to generate a set of T1-weighted, cardiac-gated SE images (i.e., 3 to 7 minutes, depending on heart rate). Because each image is a composite of numerous similar cardiac cycles, patients with arrhythmias and fluctu-

Figure 18. Conventional CT images through the same plane of a normal mitral valve (arrowheads) with (A) and without (B) EKG triggering and partial rotation reconstruction. This new approach successfully freezes cardiac motion, allowing valve and subvalve detail to be shown. Note poor definition of the endocardium and star artifact caused by motion around the aortic valve on the nontriggered image. RA = right atrium; LA = left atrium; RV = right ventricle.

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Figure 19. A, Double inversion prepared fast spin echo MR image (IPFSE) through the short axis of the left ventricle giving clear anatomic detail. The blood pool signal has been completely nulled and appears black. B, Segmented K-space cine fast GRE image of the left ventricle in the same plane (Fastcard, GE Medical Systems). The blood pool is of high signal and the image generally is a little noisier. Both acquisitions are completed in a breath-hold.

ating R-R intervals give poor images. Respiratory motion also needs to be addressed and most manufacturers provide a method of motion compensation that can be used in conjunction with EKG gating. The GRE sequence uses a smaller excitation pulse (<90 degree) and may have very much shorter TR times (i.e., TE around 10 millisecond and TR 25 milliseconds for magnets operating at 1.5 T). Multiple repetitions can be performed in a single R-R interval. GRE still requires EKG gating, but multiple images can be obtained at the same level throughout the cardiac cycle. Combining these images into a cine loop gives an accurate demonstration of cardiac motion at that level. The difficulties of imaging patients with irregular rhythms still apply. Over recent years, faster versions of both these sequences have been developed and should be used if available. Images with the same character as a T1-weighted SE sequence can be obtained with a breath-hold double inversion prepared fast SE (IPFSE). This sequence acquires up to 32 echoes in an echo train similar to that in a standard FSE. A very short interecho time allows the whole echo train to be performed in less than 200 milliseconds and this is timed to occur in middiastole, the quietest period of the cardiac cycle in terms of motion. The double inversion preparation pulses are designed to null all signal from blood and are positioned in the preceding heartbeat. The whole acquisi-

tion for a single slice is completed in 8 to 16 heartbeats depending on resolution and parameters of the field of view.5 A similar approach using very fast TR times (< 10 milliseconds) has been applied to the cine GRE sequence. By acquiring multiple data lines (6 to 12) in each time frame of the cine loop, the whole sequence is shortened by the same factor (i.e., if 8 lines of data are obtained in each time frame instead of 1, the sequence can be completed in a breath-hold of 16 heartbeats [8 X 161 rather than 128 heartbeats over 2 to 3 minutes). Image character remains very similar to a routine cine GRE sequence. SE and GRE sequences appear very different (Fig. 19). SE images have a high level of contrast between fast-flowing blood (which appears black) and the surrounding soft tissues. Slow-flowing blood or flow within the imaging plane gives a variable signal making it difficult to distinguish slow flow from adjacent endocardium or thrombus. In most situations this is not a problem and the SE sequence remains the sequence of choice for demonstrating anatomy. On GRE images, flowing blood is of high signal, providing contrast between the vascular spaces and surrounding myocardium. GRE images are generally noisier than SE images and are reserved for functional studies (i.e., cine imaging and examining flow). Like ultrafast CT, MR imaging is well established as an accurate technique for quantifying a range of cardiac parameters: LV and RV

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mass,14 LV and RV volumes,2° ejection fraction, cardiac output, and wall motion abnorm a l i t i e ~The . ~ ~ accuracy of these values, just as for ultrafast CT, has allowed reliable quantitation of univalvar regurgitation. Valve anatomy may be demonstrated by MR imaging, but in general temporal resolution continues to be inferior to echocardiography (Fig. 20). Multiplanar imaging makes MR imaging the ideal modality for imaging the thoracic aorta: hence, its utility in patients with aortic valve disease and ascending aortic dilatation (Fig. 21). The major advantage of MR imaging over ultrafast CT or EBCT is the ability to image and quantitate flow. GRE images are sensitive to flow; as flow velocity increases, the development of turbulence leads to loss of signal. This signal loss correlates with the extent of turbulence and has been used to estimate pressure gradients across stenotic valves. Areas of signal loss are also seen in regurgitant jets but they have proved less valuable in determining the severity of regurgitation (Fig. 22). Modifying the GRE sequence to make signal intensity proportional to the velocity of moving blood, it has been possible to quantitate flow in absolute terms.8Sz9Unlike Doppler echocardiography, the cross-sectional area of the vessel under investigation can be accurately measured and volume flow calculated. There are no restrictions as to imaging plane

and assumptions about the angle of flow relative to the imaging plane are unnecessary. In addition, MR imaging velocity mapping has the advantage of being able to evaluate flow in regions inaccessible to the Doppler beam. When prosthetic valves are studied, they usually cause local signal loss and are not

Figure 20. IPFSE MR image through a normal aortic valve showing three valve cusps. Compare this with the EBCT image in the same plane, Fig. 17. The two modalities give very similar anatomic detail but with different advantages and disadvantages. (Courtesy of A. Arai, MD, and R. Balaban, PhD, Bethesda, MD.)

Figure 22. Cine GRE image showing the horizontal long axis of the left ventricle in a patient with MS. Signal void caused by the MS jet in diastole is seen within the high signal (white) of the LV blood pool (arrows) RA = Right atrium; LA = left atrium; RV = right ventricle.

Figure 21. Coronal IPFSE MR image showing a dilated aortic root and ascending aorta in a patient with aortic stenosis. Note the small left ventricle in the absence of AR and the left ventricle hypertrophy.

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well seen. Early concerns regarding radiofrequency energy deposition and heating have, to date, been unfounded. The constant drive to shorten imaging times, however, means faster and stronger gradients. Modern machines with rise times of the order of 180 ~s and gradient amplitude of 25 mT/m are available. This is close to the physiologic threshold for muscle and nerve stimulation approaching the limits set by the Food and Drug Administration. Despite this, there are no reports of MR imaging complications related to valve prostheses. Valves that are strongly ferromagnetic (i.e., Starr-Edwards pre-6000 series valves), however, should not be scanned.28 The tools for investigating heart disease by MR imaging have never been more sophisticated. Yet, it has still to be shown whether more accurate diagnosis and assessment will bring improved patient outcome or reduced health care costs. With so many noninvasive modalities available and capabilities changing so fast, it is important to be familiar with the strengths and weaknesses of each. Table 2 compares the relative merits of echocardiography, EBCT, and MR imaging in the evaluation of valvular heart disease. CONCLUSION

Valvular heart disease remains a significant problem for diagnosis and management world wide. Rheumatic fever is responsible for considerable morbidity and mortality and even in the United States it is showing a resurgence. In the Western world, congenital heart disease is the primary cause of isolated AS and PS, whereas heart failure is the most common cause for atrioventricular valve dysfunction. Echocardiography and Doppler are the main tools of diagnosis. The equipment is cheap, the skills to perform and interpret the examination are widely available, and it can be performed at the bedside. Angiography and cardiac catheterization have been virtually replaced except as precursors to intravascular or surgical intervention. MR imaging and EBCT have an established track record in the literature for the investigation of heart disease, but technical limitations and high cost have restricted widespread use. New pulse sequences and faster gradient sets have overcome many of the problems of MR imaging and new developments with cardiac-

Table 2. RELATIVE VALUE OF ECHOCARDIOGRAPHY, EBCT AND MR IMAGING IN VALVULAR HEART DISEASE Echo ~~~

~~~

~~~~

EBCT

MR Imaging

*I

**

~

Evaluation of atrioventricular valves Evaluation of semilunar valves Evaluation of aorta Evaluation of valve prostheses Quantitation of LV and RV mass Quantitation of LV and RV volumes Quantitation of ejection fraction Quantitation of regurgitant volumes Quantitation of valve gradients Evaluation of intracardiac thrombus Evaluation of segmental wall motion abnormalities

*** *** ** **

** *I*

** ***

***

-

*** ***

***

***

***

**

**‘I

***

***

***

***

***

**

***

**1

From Coulden R, Lipton MJ: Radiological examination in valvular heart disease. In Zaibag MA, Duran C (eds): Valvular Heart Disease. New York, Marcel Dekker, 1989; with permission.

triggered, short scan time conventional CT are in the pipeline. In many respects the technology is ahead of the medical community’s capacity to use it. Interspecialty rivalry and unjustified patterns of self-referral and reimbursement continue to plague cardiac imaging.18 Only time will tell whether the new modalities will be fully embraced so that patients will experience the benefit of improved and less invasive diagnostic procedures. ACKNOWLEDGMENT We thank Bernadette Brogan for preparing this manuscript and for her never-ending administrative support.

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VALVULAR HEART DISEASE Advances in CT IV. Heidelberg, Springer-Verlag, 1998, pp 126-136 6. Coulden R, Lipton MJ: Radiological examination in valvular heart disease. In Zaibag MA, Duran C (eds): Valvular Heart Disease. New York, Marcel Dekker Publications, 1989, p 131 7. Diethelm L, Simonsen JS, Dery R, et al: Measurement of LV mass by ultrafast CT and 2-D echocardiography. Radiology 171:213, 1989 8. Firmin DN, Naylor GL, Kilner PJ, et a1 The applications of phase shifts in NMR for flow measurements. Magnetic Resonance in Medicine 14:230, 1990 9. Hall R Other valve disorders: Tricuspid pulmonary and mixed lesions. In Julian DG, et a1 (eds): Diseases of the Heart. London, Balliere Tindall, 1989 10. Hancock WE: Artificial valve disease. In Schlant RC, Alexander RW, Fusten V (eds): Hurst’s The Heart, ed 8. New York, McGraw-Hill, 1994, p 1539 11. Hatle L, Angelson 8,Tromsdal A: Non-invasive assessment of atrio-ventricular pressure half-time by Doppler ultrasound. Circulation 601096, 1979 12. Jefferson K, Rees S Clinical Cardiac Radiology, ed 2. London, Buttenvorths, 1980 13. Kaplan EL Acute rheumatic fever. In Schlant RC, AIexander RW, Fusten V (eds): Hurst’s The Heart, ed 9. New York, McGraw-Hill, 1998, p 1753 14. Katz J, Milken MC, Stray-Gunderson J, et al: Estimation of human myocardial mass with MR imaging. Radiology 169:495, 1988 15. Kavey RW, Kaplan EL: Resurgence of rheumatic fever. Pediatrics 84585, 1989 16. Lancefield RC: A serologic differentiation of human and other groups of hemolytic streptococci. J Exp Med 57571,1933 17. Lavender JP, Doppman J, Shawdon H, et al: The pulmonary veins in left ventricular failure and mitral stenosis. Br J Radio1 35293, 1962 18. Levin DC, Spettell CM, Rao VM, et al: Impact of MR imaging on nationwide costs of health care and comparison with costs of other imaging procedures. AJR 170:557, 1998 19. Lipton MJ, Rumberger J A Exercise EB-CT for the detection of coronary artery disease [editorial]. J Am Coll Cardiol 131082, 1989 20. Longmore DB, Klipstein RH, Underwood SR, et al: Dimensional accuracy of magnetic resonance in studies of the heart. Lancet i:1360, 1985 21. Markowitz M, Taranta A Rheumatic Fever: A Guide to Its Recognition, Prevention and Cure with Special

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Address reprint requests to Martin J. Lipton, MD University of Chicago Department of Radiology MC-2026 5841 South Maryland Avenue Chicago, IL 60637