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* Pressures in parentheses are mean pressures .RA = right atrium ; R V = right ventricle ; PA = pulmonary artery ; PC = pulmonary capillaries ; LV = left

ventricle ; LA = left atrium; BA = brachial artery .

At operation severe mitral stenosis with a valvularopening of less than 05 cm 2 was found but no re-gurgitation . A 2+ tricuspid insufficiency was present .

CASE 3 . A 30 year old woman experienced dyspneaon exertion for the previous three years. On ex-amination the apex beat was palpable in the fifthinterspace at the midaxillary line. A left parasternalsystolic heave was present . The first heart sound wasloud at the apex ; it was followed by a grade 4/6holosystolic murmur which faded in intenisty towardthe axilla and the lung base . An opening snap and adiastolic rumble were heard . A grade 3/6 systolicmurmur present at the xiphoid area increased during

Fie . 1 . Case 1 . Plmnocardiograms recorded at the tricuspidarea ( .4) and at the apex (B) show a systolic murmur (SM)and a diastolic rumble (DR) at the apex . Over the tri-cuspid area a systolic murmur and a short diastolicrumble are present . The electrocardiogram is shownbelow .

TABLE ICathetcrization Data (Seven Patients)

inspiration ; P 2 was loud . The neck veins weredistended, and the liver was enlarged two finger-breadths below the right costal margin . Blood pres-sure was 125/85 mm. Fig .The phonocardiogram (Fig . 3) confirmed the

above findings . The electrocardiogram (Fig. 3,bottom) demonstrated atrial fibrillation . right atrial,right ventricular and possible left ventricular hyper-trophy . Chest roentgenograms showed enlargementof the right atrium, right ventricle and left atriumand prominence of the pulmonary artery . Cardiaccatheterization was not performed .

FIG . 2, Gate 2 . Phwmcordiograrn at the tricuspid area (A)shows a systolic murmur (SM) and a short diastolicrumble (DR) . At the apex (B) a systolic murmur, adiastolic rumble (DR) and an opening snap (OS) arerecorded . The electrocardiogram is shown below.

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Case AgePressures

Hg)Onto .LV LA BAR RV PA PC*

1 30 13/3 110/10 110/40 . . . 110/15 36/22 125/802 22 5/2 75/4 60/30 25/12(20) 110/6114 46 18/5 60/12 60/30 30/18(26) 100/8 100/705 35 15/7 75/10 75/29 36/18(28) 128/12 130/60

35 (,12) 65/8 60/35 31/19(25) 110/7021 18/2 118/12 106/30 (27) 114/4 124/8438 6/2 40/6 32/15 80/55

Tricuspid Insufficiency Masquerading as Mitral Insufficiency

FtG . 3 . Ga.re 3. Phonocardiogram at the tricuspid area (A)demonstrates a systolic murmur (SM) . Over the apexis a systolic murmur (SM), an opening snap (OS) and adiastolic rumble (DR) . The electrocardiogram i shownat the bettmu .

At operation severe mitral stenosis with a valvularopening of 0 .5 cm 2 was found but no regurgitation .A 2y- tricuspid insufficiency was present.

CASE 4 . A 46 year old man had noticed increasingdyspnea on exertion, orthopnea and fatigue for severalyears . On examination he appeared dyspneic andorthopneic ; the apical impulse was in the fifth in-terspace at the midaxillary line . A prominent sys-tolic heave was present at the lower left parasternalborder . The first heart sound, loud at the apex, wasfollowed by a grade 4j6 holosystolic murmur thatfaded toward the axilla and the lung base ; an openingsnap and a diastolic rumble were heard . At thexiphoid area a grade 4/6 systolic murmur withoutinspiratory accentuation was present ; P, was loud .Blood pressure was 140/90 mm . Hg. The neck veinswere distended, and the liver was palpable threefingerbreadths below the right costal margin .The phonocardiogram (Fig. 4) confirmed the

clinical findings . The electrocardiogram (Fig . 4,bottom) showed atrial fibrillation, right atrial andright ventricular hypertrophy ; minor S-T and Twave changes were present in leads V, V, . Chestroentgenograms demonstrated an enlarged heartwith dilatation of the right atrium, left atrium, rightventricle and the pulmonary artery ; enlargement ofthe left ventricle was also suspected . Data fromcardiac catheterization are shown in Table i .

At operation mitral stenosis with a valvular openingof 0 .8 cm 2 was found but no regurgitation. A 2+tricuspid insufficiency was present .

CASE, 5 . A 35 year old woman had severe dyspnea,

voi .s :i-: 20, SEPTEMBER 1967

419

FIG . 4 . (.'ase 4 . Phweoeardiograra at Uee trie,upid area i ,reveals a systolic murmur (SM), an opening snap (OS)and a third he :ut sound (3) . At the apes (B) a systolicmurmur (SM), an opening snap (OS) and a diastolicrumble (DR) arc present . The electrorardiogram isshown or the bottom .

orthopnea and paroxysmal nocturnal dyspnea forthe preceding 10 years . There was a history of bac-terial endocarditis three years prior to admission . Atthat time the diagnosis of mitral stenosis, mitral in-sufficiency and tricuspid insufficiency was made .On admission to the hospital, the patient appearedchronically ill and wasted ; she was dyspncic, orthop-ncie and cyanotic . The apical impulse was in thesixth interspace at the anterior axillary line. Thefirst heart sound was loud and was followed by a grade4/6 holosvstolic murmur which was transmittedposteriorly but faded in intensity ; an opening snapand a diastolic rumble were heard . A grade 4,'6systolic murmur and a short diastolic rumble werepresent at the lower left parasternal border ; both.were accentuated during inspiration . R; was loud .Blood pressure was 130,!70 mm . ilg . 'I he neck veinswere distended, and the liver was enlarged fourfingerbreadths below the right costal margin .

The phonocardiogram demonstrated the clinicalfindings . The electrocardiogram showed atrial fibril-lation, right atrial and right ventricular hypertrophy :S-T and T wave changes were shown in leads V,Vs .Chest roentgenograms revealed enlargement of theright atrium, left atrium and right ventricle andprominence of the pulmonary artery . Data fromcardiac catheterization are presented in Table t .

At operation severe mitral stenosis with a valvularopening of 0 .5 CM .2 was found but no regurgitation .A 2+ tricuspid insuffiriency was present .

CASE 6 . A 35 year old man had dyspnea on exer-tion, orthopnea and bouts of bloody sputum for the

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preceding five years. On examination lie appeareddyspneic, orthopneic and cyanotic ; the apex beatwas in the fifth interspace at the anterior axillaryline ; there was a systolic heave at the lower leftparasternal area . The first heart sound, loud at theapex, was followed by a grade 3/6 holosystolic mur-mur that faded in intensity toward the axilla and thelung base ; an opening snap and a diastolic rumblewere heard . A grade 3/6 systolic murmur was pres-ent at the xiphoid region without inspiratory ac-centuation. P 2 was loud. Blood pressure was 115/80mm. Hg . The neck veins were distended, and theliver was enlarged three fingerbreadths below theright costal margin .

The phonocardiogram confirmed the above find-ings. The electrocardiogram showed atrial fibril-lation and right atrial and right ventricular hyper-trophy; minor S T and T wave changes were presentin leads V I-V 6 . On x-ray examination, the rightatrium, left atrium and the right ventricle were en-larged, and the pulmonary artery was prominent .Data from right heart catheterization are shown inTable I .

At operation severe mural stenosis with a valvularopening of0.5 em . 2 was found but no mitral regurgita-tion . A 2+ tricuspid insufficiency was present .

CASE 7 . A 21 year old man had noticed progres-sively increasing dyspnea on exertion during the pastfew years. On examination the apex beat was inthe fifth interspace at the anterior axillary line ; asystolic heave was present at the left lower parasternalborder . The first heart sound at the apex was notaccentuated ; it was followed by a grade 4/6 holo-systolic murmur that faded in intensity toward theaxilla and the lung base . An opening snap and adiastolic rumble were also heard . At the xiphoidarea a grade 3/6 systolic murmur was present with-out inspiratory accentuation . P2 was loud . Bloodpressure was 115/75 mm . Hg. The neck veins weredistended, and the liver was enlarged .

The phonocardiogram confirmed these findings .The electrocardiogram showed right atrial and rightventricular hypertrophy. On x-ray examination,the right atrium, left atrium and the right ventriclewere enlarged ; the pulmonary artery was prominent .Data from cardiac : catheterization are presented inTable I.

At operation severe mitral stenosis with a valvularopening of 0.5 CM .2 was found but no regurgitation ;a 2+ tricuspid insufficiency was present .

CASE: 8 . A 38 year old woman had experiencedexertional dyspnea for the preceding 10 years . Onexamination she appeared severely dyspneic andorthopneic . The apical impulse was in the fifthinterspace at the anterior axillary line ; a lower leftparasternal systolic heave was present . The firstheart sound, loud at the apex, was followed by a grade4/6 systolic murmur that faded in intensity toward

the axilla and the lung base ; an opening snapand a diastolic rumble also were heard . At thexiphoid area a grade 2/6 systolic murmur with in-spiratory accentuation was present. P2 was loud .Blood pressure was l 10/70 mm . Hg. 'l'he neck veinswere distended, and the liver was enlarged .The phonocardiogram confirmed the findings.

The electrocardiogram showed atrial fibrillationand right atrial and right ventricular hypertrophy .On x-ray examination the right atrium and rightventricle were enlarged and the pulmonary arterywas prominent. Data from the cardiac catheteriza-tion are shown in Table I .The patient refused an operation. She was re-

admitted four months later because of fever, increaseddyspnea and bloody sputum . In spite of intensivetreatment, she died .

Autopsy proved tight mitral stenosis with an open-ing of the valve of 0 .4 cm - 2 The tricuspid valve wasconsiderably incompetent . Bacterial endocarditiswas found, as well as multiple pulmonary infarctions,and a fresh embolus occluding the left pulmonaryartery .

DISCUSSION

The impact of cardiac surgery has led to in-creasing interest in the auscultatory diagnosisof valvular heart diseases . Cardiac auscultationhas been proved usually reliable in diagnosing"pure" mitral stenosis but sometimes unreliablein evaluating those patients with a systolicmurmur at the apex. Data from intracardiacand external phonocardiography, and betterunderstanding of the dynamic significance of theacoustic phenomena, led to a revision of the"classic" areas of auscultation of the heart . 2

A loud systolic murmur at the apex withtransmission to the axilla and the lung base wastraditionally believed to be the most importantsingle clinical criterion for the diagnosis ofmitral insufficiency . While this is still valid ina categorical sense, it does not always guaranteethe presence nor indicate the severity of such alesion . Sometimes, despite a loud systolicmurmur at the apex, mitral stenosis withoutinsufficiency may be found, and less frequently,significant mitral insufficiency has been demon-strated without a systolic murmur .''^

Tricuspid insufficiency often exists in associa-tion with rheumatic mitral stenosis, and con-gestive heart failure may exaggerate its clinicalmanifestations . Patients with tight mitralstenosis, in whom the disease has advanced tothe Stage of severe heart failure, frequentlypresent signs of associated functional tricuspidinsufficiency ; an organic lesion of the valve isless common than a functional ones Doubt

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has been expressed that the diagnosis of tri-cuspid valve disease can be made on the basisof the auscultatorv phencinena, and opinionsrange from one extreme to anot}rcr .s_s Ingeneral, the diagnosis of tricuspid insufficiencycan be made in patients with known rheumaticheart disease who present a systolic ruurnntr atthe xiphoid area and systolic pulsation of theperipheral veins and liver : however, this lesionmay escape clinical diagnosis and about onethird of Such patients do not have sufficientsymptoms for diagnosis . 7

The murmur of tricuspid insufficiency is usuallytypical in character and location and increasesin intensity during inspiration through an in-crease in venous return ; however, in a numberof patients this inspiratory increase does notoccur, and paradoxically, its intensity can de-crease .8 , s In such cases the flow across thetricuspid valve is already maximal, and theright ventricle cannot increase cardiac outputsignificantly ; a large, dilated right atrimu isan additional factors Five of our patients didnot have an inspiratory accentuation of thetricuspid systolic murmur .

'I lie systolic murmur of tricuspid insufficiencyis best heard at the xiphoid area and the lowerleft parastcrnal border . However, in thepresence of severe right ventricular enlargementand rotation of the heart, this area may extendto the point of maximaI impulse (i .e ., the cardiacapes, which in such cases is formed by the rightventricles) . Consequently, loud murmurs gemcrated at the tricuspid vane may be heard inmaximal intensity at the apex or beyond thisarea where murmurs of mitral insufficiency areordinarily expected . In such cases the Hurt-turn- of tricuspid insufficiency can be confusedwith the one of mitral insufficiency, and thesystolic murmur at the apex may be erroneouslyattributed to significant mitral insufficiency ." - "All of our patients had the systolic murmur oftricuspid insufficiency at the apex . At thesame time, althoughh the apex beat was palpableat the anterior or midaxillary line as a resultof the marked clockwise rotation of the heart,it was not prominent : on the other hand, aprominent systolic heave was present at thelower left parastcrnal border in all cases .Initially these patients were suspected of havingmitral insufficiency in addition to mitral stenosisand tricuspid insufficiency. On re-evaluation oftheir condition, the systolic murmur proved tohe that of tricuspid insufficiency transmitted tothe apex .

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Tricuspid Insufficiency Masquerading as Mitral Insufficiency 421

The acaustir and phonorardiograph,c findings ofmitral stenosis, although present at the apex,were more distinctly heard over the anterior,middle and posterior axillary lines, where atthe satire tine the systolic rnurmur faded in in-tensity or vanished . When the loud systolic[nurumtr at the apex is that of uiitral insuffi-ciency, one should expect to hear it posteriorlytowards the axilla and the lung base . hence,when tight mitral stenosis is suspected and thereare signs of tricuspid insufficiency with thesystolic mmirmur transmitted to the apex, onehas to listen more posteriorly, where the findingsof "pure" mitral stcnosis arc distinctly present ;the murtmits and sounds produced at the mitralvalve are clearly heard at this area . In suchcases the "apex" is occupied not by the leftventricle but by an enlarged and markedlyrotated right ventricle that is responsible forthe systolic murmur . Confusion between thesystolic murmurs of mitral and tricuspid insuf-ficiency can he lessened in such cases b) givingmore careful attention to the precise locationand transmission of these murmurs : when tiresystolic murmur is loudest at the apex or medialto this point and fades or vanishes towards theaxilla and the lung base, then it is more apt tohe due to tricuspid than to ndtral insuflicienc}- .

The phonocardiogram in 5 patients showed asystolic murmur at the apex that appearedlouder than at the tricuspid area ; a diastolicrumble was present in all cases . An openingsnap was recorded in 7, with the interval tothe second sound ranging from 0 .06 to 0 .09seconds . At the tricuspid area in 4, a diastolicrumble and an opening snap were recorded,transmitted probably from the initial area .Sometimes in the presence of considerabletricuspid insufficiency such phenomena canresult from relative tricuspid stenosis .

The electrocardiogram revealed right atrialand right ventricular hypertrophy in all cases ;the pattern was characterized by a small QRScomplex in 5 and an increased intrinsicoid de-flection in 7 . These findings arc in agreementwith previous data.,i+.w

Flemodynamic studies were performed in 7patients ; the pressures in the pulmonary ar-tery and right ventricle were increased in allbut 1 . The mean pulmonary wedge pressurewas obtained in i and ranged from 20 to 28mm. Hg . Tricuspid insufficiency was evidentfrom the right atrial pressure tracing in only4 cases ; this finding supports previous datathat the atrial pressure tracings in the presence

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of tricuspid insufficiency may not show theexpected characteristic alterations, 5,16

Chest roentgenograms showed enlargement of theright atrium, left atrium and right ventricle ;the pulmonary artery was distended . Leftventricular enlargement was believed to bepresent in 3 patients ; but when severe rightventricular dilatation coexists, the roentgeno-logic features are not always helpful in estimatingthe size of the left ventricle . Cineangiocardi-ography with injection of the contrast mediuminto the left ventricle was performed in 1 case,and no mitral insufficiency was found .

At operation all patients were found to havetight mitral stenosis . The opening of the mitralorifice was estimated to he 0 .5 clef .` or less in7 and 0.8 em'- in 1 ; no mitral regurgitationwas noted . Moderate tricuspid insuficiencywas present in all cases . In Case 8 autopsy re-vealed tight mitral stenosis also and an in-competent tricuspid valve .

SUMMARY

Eight patients with tight mitral stenosis andassociated tricuspid insufficiency are presented .Initially, significant mitral insufficiency wassuspected because of a loud apical systolicmurmur, which after careful re-evaluation wasproved to be of tricuspid origin transmitted tothe apex .

Mitral commissurotoaty was performed in 7cases, and tight mitral stenosis without mitralinsufficiency was found ; tricuspid insufficiencyof considerable degree was noted in all .

These cases prove that the murmur of tri-cuspid insufficiency can be heard at the apexor beyond, where the systolic rnururur of mitralinsufficiency is usually expected, and thus anerroneous diagnosis of mitral insufficiency canbe made .

Taking into consideration that a mitral core-missurotomy is not indicated in the presence ofmitral insufficiency, one should search care-fully for those cases with tight mitral stcnosisand associated tricuspid insufficiency mas-querading as mitral insufficiency .

ACKNOWLEDGMENES

We express our thanks to Drs . D . Lekos, Head of theDepartment of Cardiac Cathcterization, and D. Lazar-ides, Director of the Department of CardiovascularSurgery, University of Athens Medical School .

REFERENCES1 . Ansv reS, C. Direct-writing pllonocardiography in

clinical diagnosis. Am. J . Cardiol ., 14: 101, 1964.2 . LUISADA, A. A . and SHArs, D . M. Controversial

and changing aspects of auscultation . Am . J .Cardiol ., 13 : 243, 1964 .

3 . ABELMAN, W. H ., ELLIS, L. B . and HARKEN, D . E .The diagnosis of mitral regurgitation . Am. J .Med., 15: 5, 1953 .

4. ARAVANIS, C. Silent initral insufficiency . Am .Heart J., 70 : 620, 1965 .

5 . SEPULVEDA, G. and LUKAS, D. S. The diagnosis oftricuspid insufficiency . Circulation, 11 : 552, 1955 .

6 . New York Heart Association Criteria Committee .Nomenclature. and Criteria for Diagnosis of Dis-cases of the Heart and Blood Vessels, ed . 5, p . 42.New York. 1953. New York Heart Association .

7 . MU LLER, O. and SHILLINGFORD, .1 . Tricuspidincompetence . Brit . Heart J ., 16 : 195, 1954 .

8 . COE.LHO, E. Physiopathologic study of the tricuspidvalve . Am. J . Cardiol ., 3 : 517, 1959 .

9 . RIVERO-CARVALLO, J. M . and GARZA DE LosSANTOS, A . Differentiation of mitral and tri-cuspid murmurs and sounds. Am. J. Card¢ol ., 4 :367, 1959 .

10 . HARVEY, W ., CORRADO, M. and PERLOFF, J . Sonicnewer and poorly recognized auscultatory find-ings of the heart. Circulation, 16 : 415, 1957 .

11 . URICCano, L, GOLDBERG, II . and I sKOFF, W. 'Tri-cuspid regurgitation masquerading as mitral re-gurgitation in patients with pure mitral stcnosis.Circulation, 16: 945, 1957 .

12 . ELLIS, L . H., ABELALANN, W . H . and HARKEN, D. E .Selection of patients for mitral and aortic valvuln-plasty . Circulation, 15 : 924, 1957 .

13 . SHILDER, D . P . and HARVEY, W. P . Confusion oftricuspid incompetence with mitral insufficiency .A pitfall in the selection of patients for mitralsurgery . Am. Heart J., 54 : 352, 1957 .

14 . PELLON, R. and SODI-PALLARES, D . Significadoclinico del retardo dc In inscription de la defiec-cion intrinseca en precordiales dereehas . Arch .lnrt - cwd,,d . Mexico, 18 : 649, 1948 .

15 . CABRERA, L. and MONROY, J . R. Systolic anddiastolic loading of the heart . u. Electrocardio-graphic data. Am. Heart .7 ., 18 : 669, 1952 .

16 . RUDER, G . A . and DAWIER, I. K. Study of rightatrial pressure pulse in patients with functionaltricuspid regurgitation and normal sinus rhythm .Carculatioa, 24 : 1026, 1961 .

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