Dr. Carabello is a Professor of Medicine at the Medical Uni-
`versity of South Carolina and is an attending physician at
`the Ralph H. Johnson Department ofVeterans Affairs Med-
`ical Center in Charleston. After graduating from Temple
`Medical School, he did his residency at Massachusetts Gen-
`eral Hospital and his fellowship in cardiology at the Peter
`Bent Brigham Hospital. There he developed an interest in
`valvular heart disease. From Brigham Hospital, he became
`an Assistant Professor of Medicine at the University ofVir-
`ginia, where he developed indexes for the outcome of valve
`replacement in mitral regurgitation. From Virginia, he re-
`turned to Temple University, where he and his colleagues
`performed several clinical investigations of left ventricular
`mechanics in the various left-sided valve lesions. At Tem-
`ple, he also developed a canine model of mitral regurgita-
`tion with Dr. Patrick Kleaveland. Investigations pursued in
`this model at the Medical University of South Carolina have
`further elucidated the pathophysiology of mitral regurgita-
`tion and the mechanisms of contractile failure. Dr.
`Carabello is a member of the American Heart Association's
`Council on Clinical Cardiology and Council on Circulation,
`a Fellow of the American College of Cardiology, and a mem-
`ber of the American Society for Clinical Investigation.
`
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`MITRAL VALVE DISEASE
`
`Mitral valve regurgitation, stenosis, and prolapse all impose poten-
`tially life-threatening structural and hemodynamic burdens on the
`heart. Fortunately, the last quarter century has seen remarkable ad-
`vancements in our understanding of the pathophysiology of mitral
`valve disease, which has in tum led to improved therapy. Mainte-
`nance of the integrity of the mitral valve apparatus during mitral valve
`surgery, percutaneous balloon mitral valvotomy for mitral stenosis,
`and refinement of the definition of the mitral valve prolapse syn-
`drome are just three of many advances that will be highlighted in
`this issue of Current Problems in Cardiology. It is my hope to pro-
`vide the reader with a general review of the problems that exist in
`the area of mitral valve disease and to focus on the most important
`advances and the problems that remain.
`
`MITRAL REGURGITATION
`ETIOLOGY
`Primary Mitral Regurgitation
`The mitral valvular apparatus shown in Figure 1 is composed of its
`anterior and posterior leaflets, the chordae tendineae, the papillary
`muscles, and the mitral annulus.1 Abnormalities in any of these struc-
`tures can produce primary mitral regurgitation, i.e., regurgitation due
`to pathology of the valve itself. Common leaflet abnormalities include
`rheumatic valvulitis, in which the leaflets are scarred and retracted;
`endocarditis, in which the leaflets are damaged by infection or in-
`flammation; and myxomatous degeneration of the leaflets, which pro-
`duces failure of coaptation.
`The chordae tendineae comprise primary, secondary, and tertiary
`chordae. Primary chordae attach to the free edges of the leaflet and
`prevent systolic edge eversion. Secondary chordae are the strongest.
`They arise from the papillary muscles and attach to the ventricular
`side of the leaflets, preventing prolapse. Tertiary chordae arise from
`the ventricular wall and attach to only the posterior leaflet. The rup-
`ture of a single secondary chord may cause substantially more mi-
`tral regurgitation than the rupture of several less important tertiary
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`FIG 1.
`The mitral valve apparatus is demonstrated from an Intraventricular view, looking up at the
`valve from its underside. (From Wieting DW, Stripling TE: Dynamics and fluid dynamics of
`the mitral valve, in Duran C. Angell WW, Johnson AD, et al [eds]: Recent Progress in Mitral
`Valve Disease. London, Butterworths, 1984, pp 13·-46. Reproduced by permission.)
`
`chordae tendineae. Abnormalities of the chordae tendineae that
`cause mitral regurgitation include spontaneous chordal rupture,
`myxomatous degeneration producing chordal elongation, and rheu-
`matic chordal scarring and fusion, which alter the closing mechan-
`ics of the valve.
`The papillary muscles are extensions of the endocardium, the myo-
`cardial layer most susceptible to ischemia. Ischemic papillary mus-
`cle dysfunction prevents normal valve closing, allowing for prolapse
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`and regurgitation. Ischemic regurgitation usually improves when the
`ischemia resolves. Infarction with disruption of a papillary muscle
`head produces severe mitral regurgitation. More extensive papillary
`muscle infarction can lead to transection of the entire muscle, which
`produces overwhelming mitral regurgitation incompatible with life.
`Severe mitral annular calcification may also interrupt the normal
`mechanics of mitral valve closing, producing mitral regurgitation.
`
`Secondary Mitral Regurgitation
`The term secondary mitral regurgitation indicates that the mitral
`valvular apparatus itself is relatively normal, but other pathology has
`led to valvular incompetence. The major cause of secondary mitral
`regurgitation is left ventricular dysfunction and dilatation. Left ven-
`tricular dilatation and asymmetry caused by a variety of cardiac dis-
`eases lead to malalignment of the papillary muscles and annular di-
`latation, causing failure of the mitral valve leaflets to coapt.'~· 3 Typi-
`cally, secondary mitral regurgitation is only mild to moderate in se-
`verity.
`Secondary mitral regurgitation also occurs in idiopathic hypertro-
`phic subaortic stenosis. In this disease, systolic anterior motion of
`the mitral valve causes the regurgitation. One explanation for systolic
`anterior motion is that the anterior leaflet is drawn forward by a Ven-
`turi effect as blood accelerates between the valve and the outflow
`tract.4
`A third type of secondary mitral regurgitation occurs in severe val-
`vular aortic stenosis, in which high left ventricular intercavitary pres-
`sure combined with muscle dysfunction and chamber dilatation
`cause mitral incompetence. Although this type of secondary mitral
`regurgitation is usually mild, it suggests that the aortic stenosis is se-
`vere and long-standing, and it indicates a poorer prognosis than
`when mitral regurgitation is absent.5
`.... S.H. RAHIMTOOLA: I am uncertain whether mitral regurgitation that results from
`left ventricular dilatation and dysfunction caused by aortic stenosis is a sepa-
`rate type of secondary mitral regurgitation. Idiopathic hypertrophic subaortic
`stenosis is now commonly called hypertrophic cardiomyopathy.
`
`PATHOPHYSIOLOGY
`Mitral valve incompetence causes a portion of the left ventricular
`stroke volume to be ejected back into the left atrium. This portion of
`the stroke volume (the regurgitant volume) is both ineffective and del-
`eterious because it does not nourish the body tissues but adds to
`the total volume burden that the left ventricle must pump. The vol-
`ume overload of mitral regurgitation differs from most other left ven-
`tricular volume overloads because the extra volume is pumped into
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`the relatively low pressure zone of the left atrium.6• 7 In other types
`of left ventricular volume overload, such as aortic regurgitation, ane-
`mia, thyrotoxicosis, and complete heart block, the excess volume is
`pumped into the relatively high pressure zone of the aorta. Thus,
`these latter types of volume overload represent combined volume and
`pressure overload, in which both preload and afterload are increased.
`In aortic regurgitation, for instance, the large stroke volume produces
`high systolic pressure; these combine to produce systolic wall stress
`(stress = [pressure x radius)lthickness) as high as that found in the
`9
`pressure overload of aortic stenosis.6
`'
`•
`~ S.H. RAHIMTOOlA: In ventricular septal defect, which is also a form of left ven-
`tricular volume overload, the left ventricle empties into a high- or low-pressure
`chamber depending on the size of the septal defect, resistance to right ventric-
`ular outflow, and the pulmonruy vascular resistance.
`Pathophysiologically, mitral. regurgitation can be divided into three
`stages: acute mitral regurgitation, chronic compensated mitral regur-
`gitation, and chronic decompensated mitral regurgitation?0
`11
`•
`
`8
`
`Acute Mitral Regurgitation
`In acute mitral regurgitation, such as might occur with spontane-
`ous chordal rupture, there is a sudden volume overload on a previ-
`ously unprepared left ventricle and left atrium. The consequences of
`this overload for the classic components of left ventricular mechan-
`ics and hemodynamics are demonstrated in Figure 2A. The volume
`overload on the left ventricle increases left ventricular sarcomere
`stretch (increased preloadl.12 This compensatory mechanism aug-
`ments total left ventricular stroke volume by increasing end-diastolic
`volume and at the same time increases left ventricular stroke work
`by use of the Frank-Starling mechanism. However, the use of preload
`compensation has the negative consequence of moving the left ven-
`tricle up along its pressure-volume curve, thereby increasing left ven-
`tricular filling pressure. Increased left ventricular filling pressure,
`combined with the active transfer of blood from the left ventricle to
`the left atrium during systole, elevates left atrial pressure, which is
`referred to the lungs, where it creates pulmonary congestion and
`causes the symptom of dyspnea.
`The sudden opening of a new orifice for ejection lowers left ven-
`tricular a.fterload, permitting more complete ejection from the ven-
`tricle, thus reducing end-systolic volume?8 Reduced end-systolic vol-
`ume further augments total left ventricular stroke volume. However,
`although total stroke volume has been increased by both an increase
`in end-diastolic volume and a decrease in end-systolic volume, for-
`ward stroke volume is reduced because a large portion of the total
`volume is regurgitated back into the left atrium.
`Left ventricular contractile function in the acute phase is probably
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`.....
`
`PYOO
`
`ESS
`FSV
`K4yrk;tn' CF EF RF CC's
`100
`N
`90
`.lfl
`IJ
`.so 70
`.82
`N
`60
`
`p,._ -5L
`
`p
`2.07
`
`2.25
`
`N
`A AMR
`
`Ctyoruc DfOOmDtnll!td MR
`
`.....
`
`Preload AJtonood
`FSV
`ESS
`5L
`Kdyl\'cm' CF Ef 1\F CC's
`p
`.5
`60
`2.2S
`.82
`N
`70
`2.19
`N
`5
`90
`95
`.19
`
`AMA
`B CCI.IR
`
`Prelold Morbod
`FSV
`Sl
`E5S
`KdyNcm Cf EF RF CC's
`p
`.Jt .so 85
`2.19
`10
`N
`L ~ .$1
`2.19
`120
`55
`
`CCMA
`
`c COUA
`
`FIG 2.
`(A) Normal left ventricular mechanics and hemodynamics are compared to those of acute
`mitral regurgitation. (B) Left ventricular hemodynamics and mechanics In acute mitral re-
`gurgitation are compared to those of chronic compensated mitral regurgitation. (C) Left
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`normal or increased, due to sympathetic activation. The combination
`of increased preload, decreased afterload, and normal or increased
`contractile function augments ejection fraction, which is often greater
`than 80% in acute mitral regurgitation .
`• S.H. RAH!Mroo~: In acute left-sided valve regurgitation the obseJVed pathophys-
`iologic changes are also importantly influenced by the left ventricular diastolic
`pressure-volume relationship (Clin Cardio/1992.; 15 [Suppli]:I-ZZ).
`
`Chronic Compensated Mitral Regurgitation
`If the patient can tolerate the acute mitral regurgitation without
`the need for surgery, he or she enters the chronic compensated phase
`!Fig 2BJ. This phase is produced by the development of compensa-
`tory eccentric left ventricular hypertrophy. Grossman and coworkers
`have hypothesized that increased diastolic stress produced by the
`volume overload triggers the replication of sarcomeres in series,
`which in tum elongates individual myo~es producing an increase
`in left ventricular end-diastolic volume.1 If the volume overload re-
`mains severe, end-diastolic sarcomere length remains greater than
`normal, reflecting continued use of the Frank-Starling compensatory
`mechanism.12 Thus, the combination of more sarcomeres in series
`and their being stretched to near maximum length produces a much
`greater increase in end-diastolic volume than was possible during the
`acute phase, when only sarcomere stretch was available to increase
`end-diastolic volume. Increased end-diastolic volume allows for a
`large augmentation of total stroke volume, helping to reset forward
`stroke volume toward normal.
`ln this chronic compensated phase, afterload (wall stress) tends to
`increase toward normal, compared to the acute phase.15' '~6 Greater
`afterload than in the acute phase develops because, although the re-
`gurgitant valve continues to provide an unloading pathway for ejec-
`tion of blood from the left ventricle, increased left ventricular radius
`produced by the eccentric hypertrophy increases the numerator in
`the stress equation (above), thereby increasing stress (afterload).
`In parallel with this mild to moderate increase in afterload, end-
`systolic volume also increases. Contractile function is nearly normal
`
`ventricular hemodynamics and mechanics of chronic compensated mitral regurgitation are
`compared to those of chronic decompensated mitral regurgitation. EDV = end-diastolic
`volume; LA "' left atrium; ESV"' end-systolic volume; MR "' mitral regurgitation; SL = sar-
`comere length; ESS "' end-systolic stress; CF = contractile function; EF "' ejection frac-
`tion; RF "' regurgitant fraction; FSV = forward stroke volume; N = normal; AMR = acute
`mitral regurgitation. CCMR = chronic compensated mitral regurgitation, CDMR = chronic
`decompensated mitral regurgitation. (From Carabello SA: Mitral regurgitation: Basic patho-
`physiologic principles. Part 1. Mod Concepts Cardiovasc Dis 1988; 57:53-58. Reproduced
`by permission.)
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`or slightly reduced during the compensated phase. The combination
`of increased preload and eccentric hypertrophy produces increased
`end-diastolic volume, whereas normal afterload and normal contrac-
`tile function produce a normal end-systolic volume. In tandem, these
`conditions cause the ejection fraction to be less than that in the acute
`stage but still in the high normal range. The eccentric hypertrophy
`and high ejection fraction permit a return of forward stroke volume
`to normal. At the same time, the increase in left ventricular and left
`atrial volumes allows the regurgitant volume to be accommodated at
`a lower filling pressure, thereby reducing the symptoms of pulmo-
`nary congestion.
`Chronic Decompensated Mitral Regurgitation
`Although mitral regurgitation may be tolerated by the left ventricle
`for a prolonged period of time, eventually the constant severe over-
`load leads to left ventricular muscle dysfunction.7
`19 As demon-
`17
`•
`-
`strated in Figure 2C, impaired muscle function impairs left ventricu-
`lar ejection and increases end-systolic volume. Reduced emptying
`from the left ventricle-left atrial complex reelevates left ventricular
`filling pressures, resulting in pulmonary congestion. Increased end-
`diastolic pressure, in turn, may cause more eccentric hypertrophy
`and left ventricular dilatation that increases systolic wall stress by in-
`creasing left ventricular radius. Now, despite the left atrial unloading
`pathway, afterload may actually be supernormal, further increasing
`end-systolic volume and impairing ejection performance.15 Although
`ejection fraction may still be in the normal range, "normal" in the face
`of augmented preload in the patient with mitral regurgitation indi-
`cates that left ventricular dysfunction has developed.17.zo Table 1
`summarizes the directional changes in preload, afterload, contractile
`function, ejection performance, and pump performance throughout
`this longitudinal pathophysiologic history of mitral regurgitation.
`
`DIAGNOSIS
`History
`A good history is indispensable in evaluating the patient with mi-
`tral regurgitation. Frequently, in the patient who has a dilated poorly
`functioning left ventricle, the question arises whether the mitral re-
`gurgitation caused the left ventricular dysfunction or whether the left
`ventricular dysfunction caused secondary mitral regurgitation.
`Knowledge of when the murmur of mitral regurgitation first appeared
`in relation to the onset of left ventricular dysfunction can help make
`this distinction. Because secondary mitral regurgitation usually oc-
`curs toward the end stage of diseases that cause ventricular dysfunc-
`tion, the history of the murmur is short, beginning near the time of
`
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`TABLE 1.
`Longitudinal Changes in Left Ventricular Mechanics in Mitral Regurgitation
`Mitral Regurgitation
`Preload Afterload Contractility EDV
`lAP
`SYp
`ESV EF
`j j t
`tt ~~tit
`t
`Acute
`~
`~
`j j t N
`t t N
`t
`t
`Chronic compensated
`N
`t t t j
`j t
`i i t
`i
`Chronic decompensated
`N
`~
`EDV = end-diastolic volume; ESV = end-systolic volume; EF = ejection fraction; SVF = forward stroke
`volume; lAP = left atrial pressure; T = increase; ! = decrease; N = normal. Arrows indicate increase
`or decrease from normal.
`
`the onset of congestive heart failure. Conversely, in primary mitral
`regurgitation that has produced left ventricular dysfunction, the mur-
`mur usually precedes the left ventricular dysfunction by years.
`Patients with mitral regurgitation should be closely questioned
`about chest pain. Pain or pressure typical of angina pectoris may in-
`dicate an ischemic etiology for the mitral regurgitation. On the other
`hand, pain atypical of ischemia is consistent with the mitral valve pro-
`lapse syndrome. The sudden onset of sharp pain of brief duration
`occurs occasionally in spontaneous chordal rupture, although rup-
`ture usually is painless.
`The symptoms of mitral regurgitation are those of left-sided heart
`failure, and in very advanced disease, those of right-sided heart fail-
`ure. Thus, dyspnea on exertion, orthopnea, and paroxysmal noctur-
`nal dyspnea are common. When pulmonary hypertension develops,
`ascites and edema may also appear.
`
`Physical Examination
`Palpation of the precordium demonstrates a displaced and diffuse
`left ventricular impulse in chronic mitral regurgitation but may be
`normal in acute mitral regurgitation. Intensity of the first heart sound
`is reduced. The second heart sound may be widely split due to the
`aortic valve closing early because forward stroke volume is reduced
`in acute or decompensated mitral regurgitation. Intensity of the pul-
`monic component is increased if pulmonary hypertension has de-
`veloped. The presence of a mid systolic click and late systolic mur-
`mur indicates the diagnosis of mitral valve prolapse. In other forms
`of mitral regurgitation, there is a holosystolic murmur, which often
`ractiates to the axilla. The loudness of the murmur does not corre-
`late with the magnitude of the regurgitation. However, if the mitral
`regurgitation is severe, a third heart sound should be audible. In mi-
`tral regurgitation, the presence of an S3 does not necessarily indicate
`overt left ventricular failure. Rather, a third heart sound is indicative
`of a large left ventricular filling volume propelled into the left ventri-
`cle under higher than normal pressure.
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`..... S.H. IWuMrooiA: Recent data from the VA Cooperative Study on Valvular Heart
`Disease indicates that an S3 is common in patients with mitral regurgitation but
`does not necessarily reflect left ventricular systolic dysfunction or increased fill-
`ing pressure. The prevalence of S3 increases with severity of mitral regurgitation
`(Folland ED, et al, N Engl J Med 1992; 327:458).
`
`..... PM. SHAH: A careful bedside examination often yields valuable clues in a pa-
`tient with mitral regurgitation. Signs of advanced pulmonary hypertension with
`parasternal lift and accentuated pulmonary component of the second heart
`sound are more often seen in acute mitral regurgitation with a relatively short
`history of symptoms. On the other hand, severe pulmonary hypertension is un-
`common in chronic mitral regurgitation, and, when present, it occurs at a late
`is a feature of
`stage in course of the disease. Similarly, the presence of an S4
`acute mitral regurgitation since contraction of the nondilated left atrium is quite
`forceful. However, as Dr. Carabello has pointed out, the presence of an 53 is a
`feature of severe chronic mitral regurgitation and does not imply left ventricular
`decompensation. Indeed, the absence of S3 over a palpable left ventricular api-
`cal impulse in left lateral decubitus argues against severe degrees of mitral re-
`gurgitation. The first heart sound intensity is also variable based on the etiology
`of mitral regurgitation. In chronic rheumatic cases or with dilated cardiomyop-
`athy, the S, is often soft. However, many patients with mitral valve prolapse may
`have normal or even accentuated 51 • The latter may represent an early click in a
`patient with holosystolic prolapse.
`
`Laboratory Tests
`The electrocardiogram in acute mitral regurgitation is usually nor-
`mal except for sinus tachycardia. In chronic mitral regurgitation, left
`atrial abnormality, left ventricular hypertrophy, and nonspecific ST -·
`segment and T-wave abnormalities are common. However, there are
`no electrocardiographic findings that are diagnostic of mitral regur-
`gitation.
`The chest radiograph demonstrates cardiac enlargement and pul-
`monary vascular redistribution. A double density may be seen at the
`right heart border when the left atrium expands outside the normal
`silhouette of the right atrium. However, as with electrocardiography
`there are no chest radiograph findings diagnostic of mitral regurgita-
`tion .
`..... S.H. IWuMTOOIA: In acute severe mitral regurgitation, the chest x-ray film may
`show near normal heart size with pulmonary congestion or pulmonary edema.
`Echocardiographic examination with Doppler interrogation of the
`mitral valve usually establishes the diagnosis of mitral regurgitation
`and helps quantify its severity.ln acute mitral regurgitation, the echo-
`cardiographic portion of the examination may be remarkably normal.
`Both the left ventricle and left atrium are only slightly enlarged. Left
`ventricular ejection perl'ormance is hyperdynamic. Notching of the
`mitral valve closure pattern during M-mode examination indicates
`that left ventricular filling pressure is elevated. Doppler examination
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`of the mitral valve shows systolic flow into the left atrium. In acute
`mitral regurgitation, transthoracic echocardiography may underesti-
`mate the severity of mitral regurgitation; transesophageal echocardi-
`ography gives a better estimation of severity.
`In chronic mitral regurgitation, both the left ventricle and left
`atrium should be enlarged. If not either the histol)' of chronicity is
`incorrect, the amount of regurgitation is mild, or some alternative
`process such as concentric hypertrophy has prevented appropriate
`dilatation. Doppler examination of the heart in chronic mitral regur-
`gitation helps quantify the severity of the disease. However, the quan-
`tification is not precise.zt. z.z The color flow Doppler signal is repre-
`sentative of increased flow velocity of the el)'throcytes as they pass
`through the relatively small regurgitant orifice into the left atrium.
`Thus, the Doppler technique measures velocity, not flow.
`It is reasoned that high-velocity jets that entrain a large disturbance
`of el)'throcytes throughout the atrium indicate that the regurgitant
`flow is large.23 In confirmation, jet size, normalized for left atrial size,
`provided a reasonable estimate of severity of mitral regurgitation
`when compared to angiographic quantification.2 1 In another study,
`a maximum jet area of 8 cmz virtually always indicated severe regur-
`gitation confirmed angiographically, but the correlation between an-
`giographic grade and jet area was only modest.24 However, angio-
`graphic quantification itself is an imperfect gold standard against
`which to compare the Doppler results.25
`Generally, vel)' mild and very severe regurgitation can be distin-
`guished accurately by Doppler examination. However, the middle
`grades of moderate and moderately severe mitral regurgitation may
`be very difficult to separate with either this technique or contrast ven-
`triculography.
`Although transthoracic echocardiography is usually diagnostic in
`mitral regurgitation,
`transesophageal echocardiography, which
`brings the transducer closer to the left atrium, produces remarkably
`clear images of the left ventricle, left atrium, and mitral valve and usu-
`ally adds additional information to the transthoracic study. Trans-
`esophageal echocardiography is particularly helpful preoperatively in
`deciding whether the mitral valve can be repaired or will require re-
`placement, an important determinant of surgical outcome. In my
`view, almost all patients who are to undergo mitral valve surgery for
`mitral regurgitation should have a trans esophageal study prior to sur-
`gery to provide all possible anatomic information to the operating
`surgeon .
`Although transesophageal echocardiography is an invasive proce-
`dure with a small but finite risk, the information gained outweighs
`this risk.2 6 The exception might be the patient in whom the trans-
`thoracic echo clearly demonstrates that the cause of the mitral re-
`gurgitation is a flail posterior leaflet due to chordal rupture. Because
`
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`this circumstance lends itself well to valve repair, further informa-
`tion may be unnecessary. However, even in this case, transesopha-
`geal echocardiography will probably be employed intraoperatively to
`gauge the success of the repair .
`... S.H. RAHIMTOOlA: Echo/Doppler often shows a false-positive diagnosis of mitral
`regurgitation; in such instances, the regurgitation is minimal to mild. The find-
`ings of mitral regurgitation on echo/Doppler are also at times interpreted as se-
`ve•-e when the regurgitation is mild to moderate because the diagnosis is based
`on the velocity jet, and the sizes of the left ventricular and left atrial chambers
`are not taken into account.
`
`... P.M. SHAH: Echocardiography in a patient with suspected mitral regurgitation
`provides importan~ clues in regard to the etiology and functional pathology of
`the mitral apparatus. Assessment of severity in a patient with a central regurgi-
`tant jet is indicated by planimetered area of the maximum jet visualized in any
`plane. A maximum jet area of <4 cm2 indicates mild, 4 to 8 em" moderate, and
`>8 cm2 severe degree of regurgita1ion. A correction for the left atrial size is un-
`necessaty and often unreliable. In the presence of an eccentric regurgitant jet,
`the assessment of severity is more problematic. Several additional clues include
`superior extension of the jet, penetration into the atrial appendage and a puJ-
`monary vein, and evidence of systolic reversal of pulmonary venous flow. Trans-
`esophageal echocardiography is especially helpful in patients with eccentric jets
`and uncertain severity and in patients with pool' visual.ization of the left atrium
`by transthoracic approach either from heavy calcifi.cation of the valve and/or an-
`nulus, or from poor penetration of the ultrasound beam from noncardi.ac fac-
`tors. As the author points out, transesophageal echocardiography is frequently
`perlbrmed in preparation fo•· surgical treatment and should be routinely carried
`out intraoperatively to evaluate competence after repair or replacement of the
`valve.
`
`Cardiac Catheterization
`In the young, otherwise healthy, symptomatic patient in whom
`echo-Doppler examination demonstrates chamber dilatation and se-
`vere mitral regurgitation, cardiac catheterization prior to surgery is
`probably unnecessary. However, this type of patient with mitral re-
`gurgitation is rare. Usually, cardiac catheterization must be per-
`formed to rule out coronary disease as the cause of the mitral regur-
`gitation, to rule out coronary disease as a coexisting secondary dis-
`ease, and to further determine the severity of the mitral regurgita-
`tion.
`If this invasive test is to be employed, it should gamer all possible
`information. Right heart catheterization should be performed care-
`fully, with attention paid to the pulmonary artery and pulmonary
`capillary wedge pressures. The presence of pulmonary hypertension
`may worsen prognosis,27 and its detection is useful in formulating
`preoperative and intraoperative vasodilator strategies. 'I)'pically, a
`large V wave is seen in the pulmonary capillary wedge tracing in mi-
`tral regurgitation as passive filling from the pulmonary veins is cou-
`
`436
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`Curr Probl Cardiol, July 1993
`
`STJUDE1030
`IPR of Patent No. 6,821,297
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`

`

`pled with active filling of the left atrium from the regurgitation itself.
`The increased left atrial blood volume generated from dual filling pro-
`duces an elevation in left atrial pressure during ventricular systole-a
`large V wave. A V wave that is more than twice the mean pulmonary
`capillary wedge pressure often indicates that the mitral regurgitation
`is severe.
`However, several pitfalls exist in the interj,retation of V waves as a
`guide to regurgitation severity. Large V waves also can occur in ven-
`tricular septal defect, in which the increased blood flow returned to
`the left atrium produces the same effect as dual filling in mitral re-
`gurgitation. On the other hand, in the chronic compensated phase
`when the left atrium is dilated and can accommodate the increased
`volume, the V wave may become normal.28 Deficiencies in catheter-
`ization technique can further confuse the issue. Excessive tubing be-
`tween catheter and transducer, small catheter bore, and overdamp-
`ing can obscure a large V wave. Underdamping can exaggerate the V
`wave .
`..... P.M. 51!AH: The statement that amplitude of the left atrial V wave is not a reli-
`able indicator of severity of mitral regurgitation cannot be overemphasized. An
`erroneous notion that a large V wave must accompany severe regurgitation is
`pervasive.
`A major benefit to performing cardiac catheterization is that mitral
`regurgitant flow and regurgitant fraction can be calculated, helping
`to quantify the severity of the regurgitation.25 The regurgitant volume
`is the total stroke volume minus the forward stroke volume (SV p). To-
`tal stroke voiume iS equal to the angiographic stroke volume (end-
`diastolic volume [EDVA), minus end-systolic volume [ESVA)J. Forward
`flow is that flow determined by the standard cardiac output deter-
`mination (Fick or thermodilution techniques). Forward stroke volume
`is this cardiac output divided by the heart rate at the time the stroke
`volume was determined.
`
`- (EDVA - ESVA)- SVF
`.
`.
`Regurgitant fraction -
`(EDV _ ESV 1
`A
`A
`Although the quantitative method adds information to the qualita-
`tive method of ventriculography, the determination of both angio-
`graphic flow and forward flow are subject to errors. Forward flow,
`specifically, should be determined by the Fick technique. The green
`dye technique is inaccurate if either mitral or aortic regurgitation is
`presene9 The thermodilution technique may be satisfactory in mi-
`tral regurgitation but will also become inaccurate if the cardiac in-
`dex is less than 2 Umin/m2 or if tricuspid regurgitation is present.29
`The angiographic portion of the quantification is obviously depen-
`dent on the reliability with which the cardiac catheterization labora-
`
`Curr Probl Cardia(, July 1993
`
`437
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`STJUDE1030
`IPR of Patent No. 6,821,297
`
`

`

`TABLE 2.
`Semiquantitative Angiographic Grading System of Mitral Regurgitation
`o
`No mitral regurgitation.
`1 +
`Contrast enters the left atrium during non ectopic systoles but does not opacify
`the entire chamber; dye clears in 1 or 2 beats after end of injection.
`Left atrium opacities en~irely but not as densely as left ventricle.
`Equal left atrial and left ventricular opacification.
`Dense left atrial opacification with extension to the pulmonary veins.
`
`2 +
`3 +
`4+
`
`tory can generate accurate ventricular volumes. Ac<;urate volume de