Similar component scores were obtained by TEE and TTE for valve mobility (1.7 f 0.8 vs 1.8 f 0.8, p = not significant), and valve thickness (I .8 f 0.7 us 2.0 f 0.6, p = not significant). Howeuer, valvular calcification was scored lower using TEE (1.3 f 0.7 us 1.6 f 0.8, p = 0.03). Similarly, subvalvular disease (Figure 2) was scored lower by TEE (1.2 f 0.5 US I .8 f 0.8, p 20 years of age underwent simultaneous replacement of dysfunctioning native tricuspid and mitral valves at the Surgery Branch of the National Heart, Lung, and Blood Institute between September 1963 and December 1989. Of the I 13patients, the mitral valve was stenotic before valve replacement in 96 (85%) and purely regurgitant in 17 (I 5%). This report focuses exclusively on the latter 17

patients. Certain pertinent clinical and morphologic findings in them are listed in Table I and illustrated in Figures 1 to 5. Methods of diagnosis of both mitral and tricuspid regurgitation in the patients have been described elsewhere.‘J The 17patients (8 (47%) women and 9 (53%) men, aged 27 to 73 years [mean 541) underwent double valve replacement from 1975 to 1983. None of the 17 patients had clinical evidence of aortic valve dysfunction. Sixteen patients (94%) had pulmonary hypertension, including8 (47%) with peak pulmonary arterial systolic pressure 270 mm Hg. All

FIGURE 1. Case 4 (Table I). Opened mitral valve (upper) and tricuspid valve (lowerj. A portion of posterior mitral leatlet (arrow) is prolapsed. Tricuspid leatlets also show mild hooding.

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THE AMERICAN

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68

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15, 1991

had clinical evidence of severe tricuspid valve regurgitation and none had a pressure gradient between right atrium and right ventricle during ventricular diastole. Likewise, none had a pressure gradient between pulmonary arterial wedge position or left atrium and left ventricle during ventricular diastole.

The various etiologies of the mitral regurgitation are listed in Table I. Five patients had isolated mitral valve prolapse, 3,4 2 had mitral valve prolapse associated with hypertrophic cardiomyopathy5 and 2 had mitral valve _prolapse _ associated with secundum type atriaf septal defect. Infective endocarditis that

FIGURE 2. Case 9 (Table I). Opened mitral valve (upped ad trlcuspld valve (lower) aesociated with atrial eeptel defect. CEnically, a portion of posterior mitral leaflet had prolaps by left ventriculer angfogram.

FIGURE 3. Case 12 (Table I). Gpened mitral valve (upper) and tricuspid valve (lower). Mitral teaflefs are fhiikened in a fashion typical of hypertrophic cerdiomyopathy. Tricuspid valve leeflets are normal.

FIGURE 4. Ceee 13 (Table I). Intact mitrel valve (/eft) showing ~m&aI A--a-s:-Mn [rrrr”“, I-----> --* “l”l I--I”55 ” -f chordae tendineae in anterolateral vatve (lower right) in pattent with hypertrophtt cardiomyopathy

a ditated am&s, opened mitral hatf of anterior mitral leaflet. associated with severe mitral

valve (upper right) showing an inand ~~-- aaened -r --~~ normel tricuqid and tricuq ii valve regurgftation. BRIEF

REPORTS

ilo9

patients, 5 died within 2 months of the double valve replacement and 4 others died from 34 to 95 months afterwards, I was known to be alive 7 years and 3 were known to be alive 10 years after valve replacement, and 3 were lost to follow-up within 2 months of the valve replacement operation.

TABLE II Functional

and Anatomic Status of the Tricuspid Valve in Patients Having Simultaneous Replacement of Both Mitral and Tricuspid Valves with Pure Mitral Regurgitation

Study Hauck et al (1988) Roberts & Eways (1991)

No. of Pts. with Pure MR

No. of Pts. with PureTR

Anatomic Status of No. of Tricuspid Valve Pts. with TS Normal Abnormal

28

28

0

16 (57%)

12” (43%)

17

17

0

15 (88%)

2t (12%)

‘All 12 patients had “post-inflammatory” (rheumatic) heart disease of both the mitral and tricuspid valve leaflets. tBoth patients had hypereosinophdic syndrome with thrombi involving both mitral and tricuspid valve cusps. MR = mitral regurgitation; TR = tricuspid regurgitation; TS = tricuspid stenosis.

healed6 was the cause of mitral regurgitation in 4 patients, 1 of whom also had hypertrophic cardiomyopathy. Two patients had involvement of both the tricuspid and mitral valves by the hypereosinophilic syndrome.7 In I patient, the causeof mitral regurgitation was rheumatic heart disease.8The etiology of the mitral regurgitation was unclear in 1 patient who had a heavily calcified papillary muscle but angiographitally normal coronary arteries. Except for the 2 patients with hypereosinophilic syndrome,. the operatively excised tricuspid valve leaflets and chordae tendineae were anatomically normal. The tricuspid valve anuli were described as being dilated at operation in all 17 patients. Of the 17

Pure tricuspid valve regurgitation associated with pure mitral regurgitation in the absence of hypereosinophilic syndrome is usually associated with an anatomically normal tricuspid valve. Therefore, the tricuspid regurgitation in this setting appears to result from tricuspid anular dilation, which appears to be a consequence of right ventricular dilatation. The peak right ventricular systolic pressure averaged 66 mm Hg in the 17 patients and was consisted of adults (aged >21 years) with PS undergoing valvuloplasty at 7 hospitals3 from May 1986 to September 1989. Baseline clinical information and hemodynamic results were recorded on a standardized form and forwarded to a central data analysis center (University of From the Cardiovascular Section, 9 Founders Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104. Manuscript received March 8, 1991; revised manuscript received and accepted June 25,199 1.

and gave informed consent as required by each center’s institutional review board. Results are expressed as mean values f standard error of the mean. Hemodynamic data were compared before and after valvuloplasty using the paired t test, and p values