Noninvasive assessment of mitral stenosis before and after percutaneous balloon mitral valvuloplasty

NoninvasiveAssessmentof Mitral Stenosis Before and After PercutaneousBalloon Mitral Valvuloplasty PATRICIA C. COME, MD, MARILYN F. RILEY, BS, RDMS, DANIEL J. DIVER, MD, JAMES P. MORGAN, MD, PhD, ROBERT D. SAFIAN, MD, and RAYMOND G. MCKAY, MD

Thirty-seven patients with symptomatic mitral stenosis underwent balloon dilatation of the mitral valve. Significant increases (p 1 of 4 grades in only 1 patient. The lateral mitral valve orifice diameter increased more than the anteroposterior diameter, suggesting commissural splitting as the mechanism of successful valvuloplasty. Increases (all p
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he development of successful percutaneous balloon mitral valvuloplastylP5 will undoubtedly increase the number of patients with rheumatic heart disease undergoing invasive diagnostic testing and therapeutic intervention. Imaging and Doppler echocardiography From the Charles A. Dana Research Institute and the HarvardThorndike Laboratory of Beth Israel Hospital, Department of Medicine (Cardiovascular Division), Beth Israel Hospital and Harvard Medical School, Boston, Massachusetts. This study was presented in part at the annual meeting of the American Heart Association, November 1987. Manuscript received September 29, 1987; revised manuscript received and accepted December 10,1987. Address for reprints: Patricia C. Come, MD, Cardiovascular Division, Beth Israel Hospital, 330 Brookline Avenue, Boston, Massachusetts 02215.

(7 f 5 to 18 f 10 mm/s), excursion (11 f 5 to 13 f 4 mm), S2OS interval (0.07 f 0.02 to 0.08 f 0.02 s) and cardiac output (4.2 f 1.3 to 5.3 f 2.0 liters/min). There were significant decreases (all p
have been shown to be reliable noninvasive techniques for detecting rheumatic deformity of the mitral valve and for quantitating the severity of associated mitral stenosis and regurgitation.6-16 The uses and limitations of echocardiography in defining the results of balloon valve dilatation, however, have not been fully defined. Accordingly, this study, including the 15 patients undergoing valvuloplasty at the Beth Israel Hospital in whom valvuloplasty techniques and initial findings have previously been reported,3 was designed with 2 major objectives: to evaluate the accuracy of noninvasive techniques in determining the results of balloon valvuloplasty in patients with mitral stenosis and to determine the changes in valve appearance, mitral regurgitation, left atria1 size and integrity of the interatrial septum following percutaneous mitral valve dilatation.

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Methods Patients: Between October 1985 and March 1987,37 patients underwent balloon dilatation of the mitral valve for mitral stenosis at the Beth Israel Hospital. One of these patients, referred from another hospital for aortic valvuloplasty, was found by echocardiogra; phy to also have significant mitral stenosis. After severe stenosis of both valves was confirmed by hemodynamic measurements made immediately before valvuloplasty, both valves were dilated. Six additional patients considered for balloon valvuloplasty were rejected on the basis of echocardiographic study. In 3, imaging echocardiography detected thrombus in the appendage (2 patients) or the body (1 patient] of the left atrium, confirmed subsequently at operation. Based on echocardiographic studies, it was felt that 3 other patients, with prior catheterization diagnoses of severe mitral stenosis, had either no rheumatic mitral valve disease (2 patients) or insignificant mitral stenosis (1 patient with mitral valve area >l.5 cm2). Repeat diagnostic catheterizations, with pulmonary capillary wedge pressures confirmed by the finding of wedgeposition oxygen saturations equivalent to systemic arterial oxygen saturations, confirmed the echocardiographic findings. One of the 3 patients was found to have pulmonary venous obstruction localized to the right lower lobe. The patients undergoing balloon valvuloplasty included 11 men and 26 women (mean age 55 f 14 years]. All had symptoms of pulmonary venous congestion, most commonly .dyspnea on exertion. Ndninvasive evaluation by imaging and Doppler echocardiography and echo-phonocardiography preceded valvuloplasty by 1 or 2 days. Repeat noninvasive evaluation was performed 2 to 4 days (all patients], 6 weeks (17) and 6 months (8) after valvuloplasty. Normal sinus rhythm, paced rhythm and atria1 fibrillation were present in 22, 1 and 14 patients,, respectively. Phonocardiography: The aortic second sound. to mitral valve opening interval was measured from echo-phonocardiograms obtained on an Irex System II. Valve opening was determined by the presence of an opening snap coinciding with the E point of the mitral valve echogram or from the E point alone when an opening snap could not be recorded. M-mode and two-dimensional echocardiographic studies: M-mode echocardiograms were obtained using Irex System II, ATL Mark 600, or Hewlett-Packard 77020A echocardiographs. Two-dimensional and Doppler echocardiographic studies were performed with the ATL or Hewlett-Packard equipment. Mitral valve excursion was measured (in mm] as the maximal amplitude of the anterior diastolic movement of the anterior mitral leaflet.17 The mitral valve EF slope was measured in mm/s. Maximal systolic left atria1 diameter was measured using the leading edge to leading edge technique l7 from cursor-derived M-mode echocardiograms, with the sound beam oriented perpendicular to the long axis of the left atrium and left ventricle. If the cursor could not be oriented perpendicularly through the left atrium, systolic diameter was measured directly off the X-dimensional screen. The

left atrium, including the appendage, was carefully scanned for echogenic densities suggestive of thrombus.18 Both M-mode and 2-dimensional echocardiograms were assessedfor abnormalities of mitral valve movement typical of rheumatic deformity.7~g-11The degree of thickening of the valve and chordae tendineae was estimated from the &dimensional scans. Findings suggestive of a flail mitral leaflet, including highfrequency systolic fluttering or projection of a leaflet into the left atrium, were evaluated.7 Attempts were made to visualize the mitral valve orifice in short axis.+11 To do so, the 2-dimensional transducer was placed in the second or third left intercostal space and angled to provide a parasternal long axis view. It was then rotated and angled inferiorly to provide a short axis view at the level of the papillary muscles. With slow superior transducer angulation, the mitral valve orifice at the tips of the mitral leaflets, where the area is generally smallest, was visualized. Transducer orientation was maximized to provide, when possible, true transverse rather than oblique views of the mitral orifice. The anteroposterior and lateral diameters of the mitral valve orifice were measured in the 30 patients in whom definition of anterior, posterior and lateral borders was possible both before and after valvuloplasty. In some patients, the edges of the mi-tral valve orifice could not be adequately visualized throughout all 360’ of its circumference to permit optimal planimetry for determination of areas. In others, with severe pulmonary hypertension and resultant sizeable right heart dilation, the sound beam could not be directed perpendicularly through the left ventricle or mitral orifice. In addition, among those patients with marked chordal thickening, it was apparent that the limitation of leaflet separation might not be the only contributor to mitral inflow obstruction. Finally, prior echocardiographic studies had demonstrated that Doppler assessment of mitral valve area provides a reliable means of assessing the severity of mitral stenosis relative to catheterization6JsJ6J9 and may be the preferable technique in patients after surgica1 commissurotomy.lg For these reasons, mitral valve areas were not planimetered from 2-dimensional short axis images. Doppler echocardiographic studies: The magnitude of mitral regurgitation and stenosis was assessed using pulsed Doppler echocardiography. The left atrium was interrogated for regurgitation using parasternal long axis and apical 4- and a-chamber views.lsJ6 Trace to mild regurgitation was diagnosed if regurgitation could be recorded only at leaflet level or within the first third of the left atrium; moderate regurgitation was diagnosed if the signals extended to one-third to two-thirds of the length of the left atrium, generally over at least two-thirds of its width; and severe regurgitation was diagnosed when signals were obtained from even wider areas of the atrium. For evaluation of mitral stenosis, the pulsed Doppler transducer was positioned at the apex to obtain 4or a-chamber apical views and the,sample volume was placed on the ventricular side of the mitral valve. Using both audio and visual output, transducer position

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and angulation were altered to record mitral inflow signals of highest velocity and narrowest spectral bandwidth (characteristics suggesting orientation of the sound beam in line with blood flow]. Hard-copy recordings were made and digitized with a graphics tablet (GTCO) and microcomputer (IBM PC] using custom-written software (Datastat). Digitization consisted of tracing the velocity curves; from these velocity points for calculation of instantaneous pressures were obtained every 4 ms, permitting calculation of the mean pressure gradient. The pressure half-time was also calculated from the hard-copy recordings and mitral valve area (MVA] was estimated from the formula: MVA (cm21= 220/pressure half-time (ms).13The values reported for mean gradients and valve areas represent the average of values obtained from 10 beats. Special care was necessary to analyze the tracings from patients with atria1 flutter” because increases in flow velocity are frequently seen after flutter waves on the ECG. If the slope of velocity decay was to be drawn to include velocity peaks caused by atria1 contraction, underestimation of mitral valve area would have resulted. In such patients, therefore, only the initial slope was used to calculate valve area (Figure 1). In patients with atria1 fibrillation or normal sinus rhythm, the downslope of the flow velocity signal was generally linear throughout diastole or until atria1 contraction, respectively. Color Doppler imaging was performed in 2 patients using a Toshiba SSH-65A phased array scanner. After mitral regurgitant area was visually assessed,both the width of the diastolic mitral inflow signal and the presence or absence of aliasing and of marked color variegation, typical of turbulent flow, were assessedbefore and after valvuloplasty. Atria1 septal defect flow was determined using pulsed Doppler, contrast echocardiography, or both.13J0-22For pulsed Doppler echocardiography, the sample volume was placed on the right atria1 side of the interatrial septum, in the subcostal and parasternal right ventricular inflow tract views. Shunt flow from the left atrium to the right atrium was recognized by the presence of a continuous flow disturbance, usually maximal during late systole and late diastole, and directed toward the right atrium.13J0 Contrast echocardiography was performed after the injection of agitated saline mixed with the patient’s own blood into an antecubital vein. Imaging was performed during quiet respiration and during and after release of a Valsalva maneuver. A communication between right and left atria was diagnosed if there was a subsequent negative contrast effect in the right atrium or a positive contrast appearance in the left heart, or both.21,22All echocardiographic recordings were made by the senior technologist or the laboratory director. The measurements were made by a senior echocardiographer, unaware of results of any prior hemodynamic assessment. Cardiac catheterization and valvuloplasty: Left and right heart catheterizations using a 7 Fr pigtail catheter and a 7 Fr balloon flotation catheter, respectively, were performed via the left femoral artery and left femoral vein. During right heart catheterization, a

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diagnostic oxygen saturation series was obtained. After placement of left and right heart catheters, measurements were made of systemic arterial, left ventricular, pulmonary capillary wedge and pulmonary arterial pressures. Pulmonary arterial and left ventricular oxygen saturations were determined. The pulmonary arterial catheter was then advanced to the pulmonary capillary wedge position, under hemodynamic monitoring. The presence of the catheter in the wedge position was confirmed by aspiration of blood with oxygen saturation equivalent to that of systemic arterial blood. Oxygen consumption was measured using a metabolic rate meter (Waters Instrument], and cardiac output was calculated using the Fick technique. In the patients undergoing valvuloplasty, transseptal catheterization was performed following baseline hemodynamic measurements. After dilatation of the interatrial septum, balloon dilatation of the mitral valve was carried out using techniques described previously.3 The balloon was inflated for 10 to 15 seconds; saline and a radiographic contrast agent [Angiovist) were used. Repeated inflations were performed until a waist in the balloon, created by the mitral valve, disappeared. Maximal balloon sizes were 23 mm (1 patient] and 25 mm (21 patients]. Simultaneous inflations of 18 mm and 20 mm balloons were performed in 15 patients. Immediately after balloon valvuloplasty, all hemodynamic recordings and oximetric analyses were repeated. Mitral valve gradients were calculated from recordings of simultaneous pulmonary capillary wedge or left atria1 and left ventricular pressures. The mitral valve areas before and after valvuloplasty were calculated according to the Gorlin formula. Left ven-

MITRAL

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2.6 cm2

FIGURE 1. Pulsed Doppler recordings of mitral valve inflow patterns in a patient with atrial flutter (FL) indicate the increases in flow velocity (V) produced by atrial contractions. Reliable noninvasive estimation of mitral valve area was possible using the initial rapid diastolic slope. The atrial contributions to flow velocity are clearly seen in this patient, whereas in others’it may be more difficult to separate the initial slope from intermittent flutter waves. An underestimation Of valve area would occur if the slope of velocity decay was drawn to include the V peaks due to atrial contractions.

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triculography was performed in only 9 patients both before and after valve dilatation. High pulmonary venous pressures or concomitant renal disease, or both, precluded the safe use of 2 doses of contrast in many of the other patients. Twenty of the 37 patients undergoing valvuloplasty had had a diagnostic catheterization 1 to 3 months before valvuloplasty, generally at an outside referral hospital. This afforded the opportunity to assess the reproducibility of catheterization estimates of mitral valve areas. In all cases, cardiac outputs had been assessed using Fick or thermodilution techniques. Statistical evaluation: Mean and standard deviation were determined for all variables. Correlations between variables were determined by the correlation coefficient and linearity was assessedby linear regression. Paired t testing determined the statistical significance of changes in parameters of valve function after valvuloplasty and also compared results of first and second prevalvuloplasty assessments of mitral valve area in patients having 2 catheterizations before valvuloplasty.

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FIGURE 2. Correlation between estimations of mitral valve area made by Doppler pressure half-time techniques and catheterization assessments of mitral valve area before (/en) and after (righf) mitral valve valvuloplasty (V) in the group of 37 patients undergoing valvuloplasty for significant, symptomatic mitral stenosis.

FIGURE 3. Pulsed Doppler recordings of mitral valve inflow before (left) and after (righf) mitral valve dilation. Peak velocity (V) decreased from 2.55 to 2.1 m/s, mean gradient decreased from 16.5 to 9 mm Hg and Doppler-estimated mitral valve area increased from 0.96 to 1.47 cm2. By catheterization, mitral valve area changed from 0.9 to 1.5 cm*. The unlabeledblack arrowsindicate the velocity at pressure half-time. The dark vertical lines represent l-second markers. EKG = electrocardiogram.

Results Mild, mild to moderate and moderate to severe valvular thickening was noted on 2-dimensional echocardiography in 14, 5 and 18 patients, respectively. Moderate or severe subvalvular thickening, thought to represent dense fibrosis and fusion of chordae tendineae, was observed in 2 patients. In the 37 patients undergoing mitral valvuloplasty, prevalvuloplasty measurements of mitral valve area by Doppler and catheterization techniques were 0.9 f 0.2 and 0.9 f 0.3 cm2, respectively (r = 0.51, p <0.002) [Figure 2). After valvuloplasty, mitral valve areas-assessed by catheterization and Doppler techniques-increased in each patient, with group means increasing from 0.9 f 0.3 to 1.8 f 0.8 cm2 and from 0.9 f 0.2 to 1.7 f 0.5 cm2 (both p
FIGURE 4. Short axis views of the diastolic mitral valve (MV) orifice before (left) and after (right) valvuloplasty. The anteroposterior diameter increased from 0.8 to 0.9 cm and the lateral diameter increased from 1.7 to 2.5 cm. Catheterization assessment of the mitral valve area revealed an increase from 0.9 to 3.6 cm*. Markingson the right side of the pictures indicate 1 cm (longer horizontal markings) and 0.5 cm (shorter horizontal markings). LV = left ventricle; RV = rlght ventricle.

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Mitral regurgitation was detected by pulsed Doppler echocardiography in 24 of the 37 patients before balloon valvuloplasty and in 24 patients after it (Figure 51,An increase of >l grade of regurgitation was noted in only 1 patient. Ventriculography performed both before and after valvuloplasty in only 9 patients revealed an increase in mitral regurgitation of >l grade in 2 patients. Seven patients had either no regurgitation on either study (5 patients] or no change from a prevalvuloplasty pattern of mild mitral regurgitation (2).

No patient had an evident atria1 septal defect before valvuloplasty. However, an interatrial communication was detected after valvuloplasty in 12 patients by contrast, Doppler echocardiography, or both (Figure 6) and in 9 patients by oximetry (mean Qp/Qs = 1.6, range 1.1 to 2.31.Echocardiographic and oximetric diagnoses of the presence or absence of an atria1 septal defect were concurrent in 30 patients. One shunt (Qp/ Qs = 1.2) was not detected by noninvasive study and in another patient noninvasive evaluation of the integrity of the interatrial septum was inadvertently omitted from study. Five patients with echocardiographic findings of a left-to-right shunt had no diagnostic oxygen step-up (i.e., <2 volumes %) in the right heart. Following valvuloplasty, there were increases (all p
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tively. There were decreases (all p
FIGURE 6. Pulsed Doppler interrogation of the interatrial septum in the subcostal 4-chamber view (/en) demonstrates a continuous flow disturbance (right) directed toward the transducer and characteristic of left-to-right shunt flow through an atrial septal defect (ASD) created by transseptal catheterization and dilatation of the lnteratrial septum for passage of dilatation catheters. EKG = electrocardiogram; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

AFTER VALVULOPLASTY

NONE

NONE

TRACE

TRACE

MILD

MILD

MODERATE

MODERATE

SEVERE

FIGURE 5. Grade of mitral (right) mitral valvuloplasty.

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FIGURE 7. Combined M-mode echocardiogram and phonocardiogram in a patient before (left) and after (right) valvuloplasty. The catheterizationand Doppler-estimated mitral valve area increased from 1.4 to 2.4 and from 1.4 to 2.3 cm*, respectively. The excursion of the anterior mitral valve (MV) leaflet did not change but the EF slope increased from 10 to 40 mm/s. The aortic second sound to opening snap (S2OS) increased from 0.04 to 0.07 seconds. The paper speeds in the 2 recordings differ; the distance between the vertical calibration dots denotes 1 second. EKG = electrocardiogram; LV = left ventricle; PW = posterior wall; RV = right ventricle.

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lation between the first and the second measurements (I = 0.74, p
Discussion Because of its initial success and low complication rate,2-5 balloon mitral valve dilatation will likely become widely used for the treatment of symptomatic patients with mitral stenosis. Because diagnostic catheterization is costly and has a definite, albeit small, associated morbidity and mortality, there is a need for noninvasive techniques permitting accurate quantitation of the severity of mitral stenosis and assessment of short- and long-term results of valve dilatation.

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FIGURE 8. Correlation between 2 prevalvuloplasty values for catheterization mitral valve areas in the 23 patients in whom a diagnostic catheterization preceded the catheterization performed’ for purpose of valvuloplasty (V) by less than 3 months. Excluded from the figure are those patients referred with a catheterization diagnosis of severe mitral stenosis but found to have mild mitral stenosis.

A previous study from our institution of 59 consecutive patients with rheumatic mitral valve disease8indicated a close correlation (r = 0.84, p
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percutaneous mitral valve dilatation need not be restricted to those patients with only mild valve fibrosis. They, however, contrast with findings suggesting reduced efficacy of surgical commissurotomy in patients with highly fibrotic and calcific mitral valve disease27-31and with studies from other institutions suggesting lesser short- and long-term efficacy of percutaneous valve dilation in patients with severe leaflet fibrosis and calcification.32-34 The predictive role of echocardiography in identifying optimal patients for valvuloplasty requires further study. Another major role for noninvasive testing in centers performing percutaneous valvuloplasty will be

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confirmation of the presence and severity of mitral stenosis in patients referred for valvuloplasty. In this regard, our echo findings of either no rheumatic disease or of mild mitral stenosis [valve area >l.5 cm2), confirmed by repeat catheterization in our laboratory, in 3 patients referred with catheterization diagnoses of severe mitral stenosis are disturbing in that they suggest that some patients may be undergoing unindicated, aggressive therapy, including valvuloplasty and mitral valve replacement. Another role of echocardiography reflects its ability to define intracardiac pathology in addition to mitral stenosis. The presence and severity of aortic stenosis

FIGURE 9. Color-coded pulsed Doppler recordings obtained with transducer placement at the left ventricular apex before valvuloplasty In systole (upper left) and dlastole (upper right) and after valvuloplasty in systole (lower left) and diastole (lower righf). The magnitude of mltral regurgitation (MR) In the left atrium during systole appears unchanged. Before valvuloplasty, the mitral valve inflow jet had a variegated color pattern (indicating turbulent flow) and aliasing (pointing to high flow velocity). After valvuloplasty, the width of the inflow signal at the level of the mitral valve orifice is far wider and the signal has a fairly homogeneous color spectrum, indicating both lower flow velocity and a lesser degree of turbulence.

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can be quite accurately defined using the continuity equation.35r36In addition, the presence and relative magnitude of aortic insufficiency and mitral regurgitation and the status of left ventricular systolic performance can be evaluated. While color Doppler echocardiography may be preferable to routine pulsed Doppler echocardiography in estimating the severity of regurgitation, especially if regurgitant jets are eccentric, careful pulsed mapping of the entire left atrium in several planes (as performed in our study] permits detection and gross quantitation of regurgitant severity and, most importantly, allows comparison with prevalvuloplasty assessments.The number of patients undergoing both pre- and postvalvuloplasty ventriculography was small. However, the limited results from our institution suggest that sizable increases in mitral regurgitation are uncommon. In the present study, Doppler estimates of severity of regurgitation were very similar to the ventriculographic assessments. Full noninvasive definition of other pathology is particularly important in patients with high baseline pulmonary capillary wedge pressures, in whom the use of hyperosmolar contrast agents for ventriculography or aortography, or both, may precipitate pulmonary edema, and in patients with renal dysfunction. Echocardiography can also be used to detect left atria1 thrombi within the body or appendage of the left atrium? Their presence, as in the 3 patients denied valvuloplasty, is considered a relative contraindication to valvuloplasty using the transseptal approach. Finally, echocardiography promises to be a useful technique for defining both the short- and long-term results of percutaneous mitral valve dilatation.. Chordal and leaflet tears were not apparent in our study, as assessed by abnormalities of leaflet movement, and the greater increase in lateral rather than in anteroposterior dimension of the diastolic valve orifice was compatible with pathologic findings indicating that successful valvuloplasty involves splitting of previously fused commissures.3J6J7 Doppler mapping of mitral regurgitant jets provides evidence that successful dilatation may usually be accomplished without appreciable increases in mitral regurgitation. Contrast and 2-dimensional echocardiography are sensitive techniques for detection of left-to-right shunting through the hole created in the interatrial septum for passage of the dilatation catheter. Serial studies should permit analysis of whether these defects close over time, and, in appropriate patients such as those without pulmonary or aortic regurgitation, may permit serial quantitation of the Qp/Qs ratio over time. Because right ventricular and, therefore, pulmonary arterial systolic pressure (in the absence of pulmonary stenosis] can be estimated from flow velocities in tricuspid regurgitant jets, Doppler echocardiography may additionally permit study of the rate of regression of pulmonary hypertension in patients after successful dilation. Obviously, the most important parameter to be evaluated is that of mitral valve area. In our study mitral valve area measured by both catheterization and Doppler techniques increased in each patient after valvuloplasty, indicating the ability of echocardiog-

raphy to detect a reduction of the severity of mitral stenosis. It is disappointing, however, that the coefficients of correlation for the relation between Doppler mitral valve areas and catheterization mitral valve areas were lower than that of 0.84 noted in our larger, unselected series of 59 patients previously reported.8 In the group before valvuloplasty, the r value of only 0.51 may reflect the fact that the range of valve areas was very small, with each patient having severe mitral stenosis. Reasons for the discrepancy between catheterization and Doppler assessmentsof mitral valve area after valvuloplasty probably include the following: lower accuracy of catheterization-planimetered gradients when gradients are small; inaccuracies in using the Fick cardiac output in the Gorlin determination of mitral valve area in patients with mitral regurgitation or left-to-right shunts across the created atria1 septal defects: and decreased accuracy of Doppler calculation of mitral valve area in the setting of relatively large mitral areas, probably related to the steep rates of velocity fall-off. Wilkins38 and Reid et a13gnoted very poor correlations between Doppler and catheterization determinations of mitral valve area when measurements were made immediately after or within the first 24 hours after balloon valvuloplasty. Thomas et a140suggested that alterations after valvuloplasty in left atria1 pressure and compliance may adversely affect this correlation. Their studies, performed within the first 24 hours after valvuloplasty, reported pressure half-time measurements based on an average of only 1 to 3 beats. The greater accuracy of postvalvuloplasty pressure half-time valve areas relative to catheterization in our study could reflect a longer delay (48 to 96 hours] between valvuloplasty and echocardiographic evaluation, or the fact that our reported Doppler areas represent mean areas calculated from 10 different beats in normal sinus rhythm or in atria1 fibrillation. The longer delay time may be of importance, since Reid et a13gdemonstrated a much closer correIation between catheterization and Doppler areas 3 months after valvuloplasty .39The lack of planimetered mitral valve areas in our study is an obvious weakness and further work will be necessary to determine if the planimetry technique or the pressure half-time assessment provides more accurate determination of mitral valve area in short- and long-term follow-up. The limitations of catheterization techniques in area determination also must be emphasized. In the presence of mitral regurgitation, the Gorlin formula will underestimate valve area if Fick determinations of cardiac output are used. Although angiographic stroke volume would be preferable, it would be of limited use in mitral stenosis patients who also have aortic insufficiency or in whom high wedge pressures may contraindicate the use of relatively large amounts of contrast. Finally, significant directional changes in left atria1 size, mitral valve gradient, EF slope, mitral valve excursion and second sound to opening snap interval accompany successful valvuloplasty. In patients in whom valve area calculations via planimetry and Doppler techniques are not feasible, serial changes in

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a combination of these parameters may permit a gross means of follow-up to supplement history, physical examination and routine roentgenographic and electrocardiographic evaluations.

References 1. Inoue K, Owaki T, Nakamura T, Kitamura F, Miyamoto N. Clinical apphcation of transvenous mitral commissurotomy by a new balloon catheter. I Thorac Cardiovasc Surg 1984;87:394-402. 2. Lock JE, Khalilullah M, Shrivastava S, Bahl V, Keane JF. Percutaneous catheter commissurotomy in rheumatic mitral stenosis. N EngJ ] Med 19Ll5;313:1515-1518. 3. McKay RG, Lock JE, Safian RD, Come PC, Diver DJ, Bairn DS, Berman AD, Warren SE, Mandell VE, Royal HD, Grossman W. BaIIoon dilatation of mitral stenosis in adult patients: postmortem and percutaneous mitral valvufoplasty studies. IACC 1987;9:723-731. 4. Zaibag MA, Ribeiro PA, Kasab SA, Fagih MRA. Percutaneous doubleballoon mitral valvuloplasty for rheumatic mitral valve stenosis. Lancet 1986;1:757-761. 5. Kveselis DA, Rocchini AP, Beckman R, Snider AR, Crowley D, Dick M, Rosenthal A. Balloon angioplasty for congenital and rheumatic mitral stenosis. Am I CardioJ 1986;57:348-350. 6. Hatle L, Angelsen B, Tromsdal A. Noninvasive assessmentof atrioventricuJar pressure half-time by Doppler ultrasound. Circulation 1979;60:1096-1104. 7. Come PC. Echocardiographic evaluation of valvular heart disease. In: Come PC, ed. Diagnostic Cardiology: Noninvasive Imaging Techniques. Philadelphia: I.B. Lippincott. 1985417-423, 426-428. 8. Come P, Riley M, Carl L, Safian R. Noninvasive assessment of mitral stenosis, including before and after valvuloplasty (abstr). Circulation 1987; 76:IV-23.

9. Martin RP, Rakowski H, Kleiman JH. Beaver W, London E, Popp RL. Reliability and reproducibility of two-dimensional echocardiographic measurements of the stenotic mitral valve orifice area. Am I CardioJ 1979;43:560568.

10. Henry WL, Griffith JM, Michaelis LL, McIntosh CL, Morrow AG, Epstein SE. Measurement of mitral orifice area in patients with mitral valve disease by real-time, two-dimensional echocardiography. Circulation 1975;51:827831. 11. Wann LC, Weyman AE, Feigenbaum H. Dillon JC, Johnston KW, Eggleton RC. Determination of mitral valve area by cross-sectional echocardiography. Ann Intern Med 1978;88:337-341.

12. Hatle L, Brubakk A, Tromsdal A, Angelsen B. Noninvasive assessmentof pressure drop in mitral stenosis by Doppler ultrasound. Br Heart I 1978;40: 131-140.

13. Hatle L, Angelsen B. Doppler Ultrasound in Cardiology. 2nd ed. PhiJadeJphia: Lea and Febiger, 1985:118,228. 14. Stamm RB, Martin RP. Quantification of pressure gradients across stenotic valves by Doppler ultrasound. TACC 1983;2:707-718. 15. Abbasi AS, Allen MW, DeCristofaro D, Ungar I. Detection and estimation of the degree of mitral regurgitation by range-goted pulsed Doppler echocardiography. Circulation 1980;61:143-147. 16. Quinones MA, Young JB, Wagoner AD, Ostojic MC, Ribeiro LGT, Miller RR. Assessment of pulsed Doppler echocardiography in detection and quantification of aortic and mitral regurgitation. Br Heart 1 1980;44:612-620. 17. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey ofechocardiographic measurements. Circulation 1978;58:1072-1083. 18. Herzog CA, Bass D, Kane M, Asinger R. Two-dimensional echocardiographic imaging of left atrial appendage thrombi. JACC 1984;3:1340-1344. 19. Smith M, Handshoe R, Handshoe S, Kwan OL, DeMaria A. Comparative accuracy of two-dimensional echocardiography versus Doppler recordings in

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