Download - Does asymmetric mitral valve disease predict an adverse outcome after percutaneous balloon mitral valvotomy? An echocardiographic study

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Does asymmetric mitral valve disease predict an adverse outcome after percutaneous balloon mitral valvotomy? An echocardiographic study

Leonardo Rodriguez, MD, Victor H. Monterroso, MD, Vivian M. Abascal, MD, Mary Etta King, MD, John P. O’Shea, MD, Igor F. Palacios, MD, and Arthur E. Weyman, MD. Boston, Mass.

Previous studies in our laboratory have shown that morphologic characteristics of the mitral valve are important predictors of outcome after percutaneous mitral valvoto- rny.lp 2 Specifically, the valvular thickness, immobility, calcification, and disease of the subvalvular apparatus are negatively correlated with the increase in valve area. How- ever, there are other morphologic features of mitral valve disease whose relationships to outcome after percutaneous mitral valvotomy remain to be established. For example, excessive thickening and calcification of one commissure may decrease the effectiveness of the procedure by limit- ing the splitting of the involved side of the orifice and pre- disposing the contralateral commissure to rupture or the normal leaflet to tearing. This could also potentially predispose to severe mitral regurgitation after percutaneous mitral valvotomy. Thus the purpose of this study was to evaluate the influence of asymmetric involvement of the mitral valve on the increase in valve area, degree of mitral regurgitation, and pattern of commissural splitting in patients undergoing percutaneous mitral valvotomy.

We studied the first 80 consecutive patients with mitral stenosis who underwent percutaneous mitral valvotomy at Massachusetts General Hospital between January 1986 and September 1988 and in whom two-dimensional and Doppler echocardiographic studies were performed in our laboratory before and within 48 hours after the procedure. There were 65 women and 15 men. The mean age was 56 years (range 21 to 87 years). There were 45 patients in sinus rhythm and 35 in atria1 fibrillation. Sixteen patients were in New York Heart Association functional class II, 50 were in class III, and 14 were in class IV. In each study standard views were obtained from the parasternal, apical, and subcostal windows. In the short-axis view meticulous care was taken to scan the mitral valve from tips to base to obtain the smallest valve orifice in early diastole. Mitral valve area was measured by planimetry. The presence of

From the Cardiac Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School.

Supported by Encyclopaedia Britannica Scholarship 1988 and a grant from Asociacion Cardiovascular Regional Barquisimeto, Venezuela.

Reprint requests: Arthur E. Weyman, MD, Cardiac Ultrasound Laboratory, Phillips House level 8, Massachusetts General Hospital, Boston, MA 02114.

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Table I. Comparison between the asymmetric and symmetric groups

Asymmetric Symmetric p Value

Age (yr) 54 f 16 58 * 14 NS Sex

Male 2 13 NS Female 24 41

Rhythm Sinus 13 32 NS AF 13 22

NYHA II 5 11 NS III 18 32 IV 3 11

LA pressure (mm Hg) Before 25 k 7 24 t 7 NS After 14 + 5 15 * 4 NS

Cardiac output (L/min) Before 3.8 i 0.9 3.7 s 1.0 NS After 4.4 * 1.1 4.2 k 1.2 NS

Echo score 7.1 _t 2 8.4 k 3 NS

AF, Atria1 fibrillation; NYHA, New York Heart Association functional class; LA, left atrium.

mitral regurgitation was assessed with pulsed Doppler and/or color flow mapping. The severity of regurgitation was evaluated in multiple views and graded from 0 to 4+ according to the extent of penetration of the regurgitant jet within the left atrium.3 All patients underwent percutaneous mitral valvotomy with the transseptal approach and either the single- or the double-balloon dilating technique. The single-balloon technique was used for six patients, and the double-balloon was used for 74 patients. The mitral valve area was calculated with the Gorlin formula. Valvu- lar asymmetry was evaluated in the parasternal short-axis view during early diastole in the same frame used to mea- sure the valve area with planimetry. The mitral valve was divided into two parts by a line that passed through the center of the mitral valve orifice and that was perpendic- ular to and bisected a second line that connected the two commissures. The absolute thickening of the leaflet tissue of each half was determined by planimetry of the inner- and outer-orifice echoes, including areas of focal thickening and calcification. The tissue area of each half of the orifice was then expressed as the ratio of the larger to the smaller value. Valvular asymmetry was defined as a ratio >1.5. We assessed the site of commissural splitting in real time by simultaneously comparing the videotape images of the prevalvotomy and postvalvotomy echocardiograms. The short-axis view of the mitral valve was carefully evaluated, particularly for new areas of separation between the leaflets at the commissural level after valvotomy. Variables before and after valvotomy were compared by use of the paired t test. The asymmetric and symmetric groups were compared by use of the unpaired t test. Fisher’s test was

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Fig. 1. Short-axis view of mitral valve in patient with asymmetric valve disease. Medial commissure shows more severe degree of thickening and calcification, but lateral commissure is relatively spared.

Mitral valve area (crn2)

PRE D~o.001

POST

- ASYMMETRIC @@ SYMMETRIC

Fig. 2. Mean mitral valve area for asymmetric and symmetric groups. There was no significant difference between groups before or after procedure.

used to compare the splitting site between the two groups, For the entire group percutaneous mitral valvotomy and the analysis of variance was used to compare the produced a significant increase in mitral valve area from change in mitral regurgitation. Data are expressed as 0.9 t 0.3 cm2 before valvotomy to 1.7 + 0.6 cm2 after val- mean + standard deviation. Results were considered sig- votomy (p < 0.0001). Mean left atrial pressure decreased nificant when p < 0.05. from 25 + 7.0 mm Hg to 15 + 5 mm Hg 0, < O.OOOl), and

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% Datients /

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p=NS

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June 1992 American Heal Journal

BILATERAL UNILATERAL

- ASYMMETRIC SYMMETRIC

Fig. 3. Site of commissural splitting in both groups, expressed in percentage for each group. Although there was trend for asymmetric group to split unilaterally, this was not statistically significant.

Fig. 4. Short-axis view at mitral valve level of patient with asymmetric commissural deformity before and after mitral valvotomy. At left echo before valvotomy shows severe thickening of lateral commissure. At right echo after valvotomy shows splitting of most involved commissure (arrows).

cardiac output increased from 3.7 f 1.0 L/min to 4.3 f 1.2 L/min (p < 0.0001). Planimetry of the mitral valve was possible in 76 (95%) patients. Severe calcification pre- cluded accurate measurement in the other four patients. Mitral valve area measured by planimetry increased sig- nificantly after valvotomy from 1.0 rt 0.3 cm2 to 1.7 + 0.5 cm2 (p < 0.0001). Mean transmitral Doppler gradient decreased from 9.4 f 4.8 mm Hg to 5.2 + 2.5 mm Hg after the procedure. There were 26 (33 % ) patients with asymmetric disease and 54 (67%) with symmetric disease (Fig. 1). There were no statistically significant differences between

the two groups in sex, age, functional class, or any of the hemodynamic or echocardiographic parameters before or after valvotomy (Table I). The mean valve area after percutaneous valvotomy was 1.6 f 0.4 cm2 in the symmetric group and 1.7 + 0.5 cm2 in the asymmetric group (p = NS) (Fig. 2). The absolute increase in mean valve area was 0.6 & 0.4 cm2 and 0.8 f 0.6 cm2 for the symmetric and asymmetric groups, respectively (p = NS). The site of commissural splitting could be determined by echocardiography in 72 (91%) patients; in the other eight patients the visualization of the commissures was not adequate to de-

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% Patients 60

2+ 3+ 4+

Mitral Regurgitation

m ASYMMETRIC F%%# SYMMETRIC

Fig. 5. Degree of change in mitral regurgitation after percutaneous mitral valvotomy in both symmetric and asymmetric groups.

fine the cleavage site. Bilateral commissural splitting occurred in 42 (57.5%) patients: 13 in the asymmetric group and 29 in the symmetric group (p = NS). Unilateral splitting occurred in 10 patients in the asymmetric group and in 11 patients in the symmetric group (Fig. 3). In the asymmetric group six (54.5 % ) patients experienced splitting along the most severely involved commissure (Fig. 4). There was no significant difference in the mean postvalvotomy valve area in patients in whom one commissure was split when compared with those in whom two commissures were split. In nine patients the mitral valve area increased less than 10% after the procedure, and there was no evidence of commissural splitting. Of these patients, eight were in the symmetric group. Before valvotomy 26 (32%) patients had no mitral regurgitation by pulsed Doppler or color flow mapping. Of this group 17 (61%) experienced regurgitation after valvotomy. Mitral regurgitation did not change in 39 (52%) patients, decreased by one degree in four (5%), patients, and increased in 32 (42.6%) patients (Fig. 5). Of the 12 patients who experienced more significant degrees of mitral regurgitation after valvotomy (increase by two or more degrees), four had asymmetric commissural disease, and eight had symmetric involvement (p = NS). We did not find any case of ruptured chordae or torn leaflets in our patient sample.

In evaluating the first 80 consecutive patients with rheumatic mitral stenosis presenting for percutaneous balloon valvotomy, we found that 33 % had echocardiographic evidence of asymmetry of commissural fibrosis and calcification. This study demonstrates that asymmetric deformity of the mitral valve has no influence on the change in mitral valve’ area, the pattern of commissural splitting, or the development of mitral regurgitation after balloon valvotomy. Previous studies addressing the influence of focal commissural thickening on the result of balloon valvotomy have yielded controversial results. Reid et al4 studied 12

patients by two-dimensional echocardiography, five of whom had calcification more prominent in one of the commissures. In two of those five, there was failure to split the most affected commissure, and two others had the smallest absolute areas after valvotomy. In a subsequent study involving 40 patients, the same authors did not find a significant difference in mitral valve area between patients with no commissural calcium and patients with calcium present in one or both commissures.5 The pathologic studies in ex vivo specimens by Kaplan et a1.6 and Ribeiro et a1.7 have shown a greater tendency for commissural splitting through the most calcified commissure. In our study we found no difference in valve area or in the site of commissural splitting between the symmetric and asymmetric valves. Indeed, an asymmetrically diseased valve was as likely to split along the more involved commissure as it was along the less involved commissure. In addition, eight of the nine patients with an increase of less than 10 % in valve area had symmetric commissural disease. This suggests that the mechanism through which the procedure augments the valve area is not hindered by the asymmetry of the valve, and therefore its presence should not negatively influence the decision to perform the procedure.

The present study also supports the concept that the global involvement of the mitral valve is a more important predicting factor than is focal commissural thickening. In contrast with the lack of correlation of the asymmetric commissural involvement with outcome, analysis of multiple clinical and echocardiographic factors has shown that global morphologic features of the diseased mitral valve such as valvular thickening, immobility, subvalvular disease, and calcification are useful in predicting the outcome of the procedure.2y 5 We have previously reported that 25 % of the patients experienced new mitral regurgitation after balloon valvotomy, and 46 % of those with previous mitral regurgitation had an increase in severity by one grade or

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more.3 Recently Roth et al8 found in a larger sample that effective balloon dilating diameter corrected by body surface area was the only predictor of the increase in mitral regurgitation after valvotomy. In the present study we did not find any relationship between asymmetric commissural involvement and the increase in mitral regurgitation. The absence of these complications reaffirms the safety of per- forming this procedure in patients with asymmetric commissural disease. In conclusion, asymmetric deformity of the mitral valve does not negatively influence the outcome after percutaneous balloon mitral valvotomy.

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Wilkins GT, Weyman AE, Abascal VM, Block PC, Palacios IF. Percutaneous balloon dilatation of the mitral valve: an analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J 1988;60:299-08. Abascal VM, Wilkins GT, O’Shea JP, Choong CY, et al. Pre- diction of successful outcome in 130 patients undergoing percutaneous balloon mitral valvotomy. Circulation 1990;82:448- 56. Abascal VM, Wilkins GT, Choong CY, et al. Mitral regurgitation after percutaneous balloon mitral valvuloplasty in adults: evaluation by pulsed Doppler echocardiography. J Am Co11 Cardiol 1988;11:257-63. Reid CL, McKay CR, Chandraratna PAN, Kawanishi DT, Rahimtoola SH. Mechanism of increase in mitral valve area and influence of anatomic features in double-balloon, catheter balloon valvuloplasty in adults with rheumatic mitral stenosis: a Doppler and two-dimensional echocardiographic study. Cir- culation 1987;76:628-36. Reid CL, Chandraratna PAN, Kawanishi DT, et al. Influence of mitral valve morphology on double-balloon catheter balloon valvuloplasty in patients with mitral stenosis. Circulation 1989;80:515-24. Kaplan JD, Isner JM, Karas RH, et al. In vitro analysis of mechanism of balloon valvuloplasty of stenotic mitral valves. Am J Cardiol 1987;59:318-23. Ribeiro PA, Zaibag M, Rajedran V, et al. Mechanism of mitral valve area increase by in vitro single- and double-balloon mitral valvotomy. Am J Cardiol 1988;62:264-9. Roth RB, Block PC, Palacios IF. Mitral regurgitation after percutaneous mitral valvuloplasty: predictors and follow-up [Abstract]. Circulation 198&78(suppl II):II-488.

Transesophageal echocardiography in the diagnosis of flail tricuspid valve

Timothy Winslow, MD, Rita Redberg, MD, and Nelson B. Schiller, MD. San Francisco, Calif.

From the Division of Medicine, John Henry Mills Echocardiography Lab- oratory, Cardiovascular Research Institute, University of California, San Francisco.

Dr. Winslow is a research fellow sponsored by the United States Army.

Reprint requests: Nelson B. Schiller, MD, Moffitt Hospital, Room 342A, Echocardiography Laboratory, University of California, 505 Parnassus Ave., San Francisco, CA 94143.

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Ruptured chordae tendineae resulting in a flail tricuspid valve leaflet is an uncommon cause of tricuspid insufficiency. Flail tricuspid valve has been described in the set- ting of nonpenetrating or penetrating chest trauma, infec- tive endocarditis, myxomatous degeneration, and compli- cating endomyocardial biopsy.lm3 Diagnostic signs of a flail tricuspid valve caused by ruptured chordae have been previously described by surface M-mode and two-dimensional echocardiography. Transesophageal echocardiography (TEE) has recently been found to be superior to transthoracic imaging in the diagnosis of flail mitral valve leaflets resulting from ruptured chordae. However, we could find no previous reports describing the use of TEE in the diagnosis of flail tricuspid valve. We report two cases of flail tricuspid valve leaflets causing severe tricuspid insufficiency diagnosed by TEE.

Case No. 1. A 50-year-old man with severe chronic obstructive lung disease presented with progressive dysp- nea. Examination revealed marked respiratory distress. A 316 holosystolic murmur consistent with tricuspid insufficiency with a diastolic rumble was noted on auscultation. Jugular venous pressure was estimated to be 20 mm Hg, with a prominent V wave. Hepatomegaly and 3+ peripheral edema of the lower extremities were present. His respiratory status worsened after admission and he required me- chanical ventilation. A bedside two-dimensional echocar- diogram showed severe tricuspid insufficiency and marked right heart enlargement. A TEE was performed to exclude an atria1 septal defect as the cause of his profound right- sided heart failure. TEE demonstrated a flail anterior tricuspid valve leaflet (Fig. 1). A thin mobile density consistent with ruptured chordae tendineae could be seen prolapsing into the right atrium during systole. An eccentric jet of severe tricuspid insufficiency was directed posteriorly. The patient was treated medically but subsequently died from his severe lung disease.

Case No. 2. A 56-year-old man with a history of systemic lupus erythematosus presented with generalized malaise and fatigue. Physical examination revealed a murmur consistent with tricuspid insufficiency and prominent V waves in his jugular venous pulsations. A transthoracic echocar- diogram showed severe tricuspid insufficiency. Marked right atrial and right ventricular enlargement was present, with paradoxic ventricular septal motion (Fig. 2, A). His inferior vena cava was plethoric and failed to respond to respiration. A TEE was performed to further evaluate the etiology of his enlarged right heart. TEE showed a flail anterior leaflet of the tricuspid valve with ruptured chordae tendineae prolapsing into the right atrium during systole (Fig. 2, B). Both the valve and the chordae tendineae were thickened. An eccentric jet of severe tricuspid insufficiency was present and was directed posteriorly (Fig. 2, C). Transesophageal continuous wave Doppler examination showed a dense jet of tricuspid insufficiency with a V wave cutoff sign (Fig, 2, D). The patient was treated medically and is being observed for signs of worsening right-sided heart failure.

We present two cases with echocardiographic findings consistent with ruptured tricuspid valve chordae tendineae. Although they lack anatomic correlation, our findings