role echocardiography and phonocardiography diagnosis ... · tolerance or the development of...

British Heart Journal, I973, 35, I2I7-I225.

Role of echocardiography and phonocardiography indiagnosis of mitral paraprosthetic regurgitation withStarr-Edwards prostheses

H. C. Miller', D. G. Gibson, and J. D. StephensFrom the Cardiac Department, Brompton Hospital, Fulham Road, London

Twenty-three patients who were symptomatic after mitral valve replacement, and in whom mitral parapros-thetic regurgitation was a possible cause of deterioration, were investigated by cardiac catheterization, phono-cardiography, and echocardiography. Severe paraprosthetic regurgitation was present in ii patients and slightregurgitation in 2 patients. Two patients had aortic regurgitation which was responsible for their symptomsand the remaining 9 patients had either poor left ventricular function, an obstructed mitral prosthesis, or anobstructed tricuspid prosthesis. The various groups could not be identified on clinical, radiological, or electro-cardiographic features, but severe paraprosthetic regurgitation was associated with a reduced A2-OC intervalon phonocardiography and normal septal movement with a large stroke volume on echocardiography. In viewof the difficulties in clinical diagnosis, the value ofphonocardiography and echocardiography has been empha-sized, particularly in ill patients in whom, on the basis of these investigations, cardiac catheterization may beavoided.

The results of mitral valve replacement continue toimprove (Barclay et al., I972; Morrow et al., I967;Najafi et al., I969; Starr, I971). In a small pro-portion of patients, however, the outcome may bedisappointing and though this is usually due toirreversible left ventricular disease, the possibilityof malfunction of the prosthesis or of additional un-corrected valve disease must always be considered(Peterson et al., I967; Rockoff et al., I966). Un-fortunately, clinical diagnosis in this situation isunreliable, so that a number of attempts have beenmade to use non-invasive techniques in order toimprove diagnostic accuracy (Willerson et al., I972;Wise, Webb-Peploe, and Oakley, 197I). We havestudied a group of patients who deteriorated aftermitral valve replacement with a Starr-Edwardsprosthesis, correlating the clinical, phono-, andechocardiographic features with the results of in-vestigation by cardiac catheterization and angio-graphy in order to define their role in the diagnosisof mitral paraprosthetic leak.

SubjectsTwenty-four patients were studied. All had mitral valvereplacement with a Starr-Edwards prosthesis, and allReceived 25 June 1973."Present address: Department of Medicine, Duke UniversityMedical Center, Durham, North Carolina, U.S.A.

were investigated on account of deteriorating exercisetolerance or the development of clinical evidence ofheart failure, with mitral paraprosthetic regurgitationas an important diagnostic possibility. They were di-vided into 4 groups on the basis of the final diagnosismade after cardiac catheterization (23 patients) or re-operation. Pertinent clinical details are given in Table i.Group i consisted of 9 patients in whom there was no

evidence of paraprosthetic leak demonstrable by leftventriculography. Symptoms were eventually ascribedto an obstructed mitral prosthesis in i, to an obstructedtricuspid prosthesis in a second, and to left ventriculardisease in the remainder, one of whom had in addition asmall fistula between the left ventricle and coronary sinus.Group 2 consisted of 2 patients in whom symptoms

were ascribed to left ventricular disease, but who had, inaddition, small leaks associated with the prosthesis.Operation was not advised in either and they continue onmedical treatment.Group 3 consisted of ii patients with severe mitral

paraprosthetic leak, which was felt to be the cause ofsymptoms and who were therefore referred for operation.Group 4 contained 2 patients in whom symptoms were

due primarily to aortic regurgitation, not corrected atthe time of the first operation. Both were considerablyimproved after aortic valve replacement.

Cardiac catheterization and angiographyThis was performed using standard techniques. Leftventriculography was performed in the right anterior

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TABLE I Clinical features

Case Age Onset of Previous operation Factors Tricuspid Systolic Haemolysis RemarksNo. and deteriora- on mitral valve predisposing to regurgn murmur

sex tion after mitral para-operation prosthetic

regurgitationGroup II 65F 8 mth2 44F I5 ,,

3 5iF 9 ,,4 siF 3 ,,5 4iF 71 yr

6 54F IS mth

7 6oF I I ,

8 46M 44 yr

9 58F 2 mth

Group 2I0 56F 39 mth

II 64M 5 yr

GrouP 3I2 56F 20 mth

I3 40F 6 is

I4 58F 3 ,,

I5 47F I 33

i6 48M 5I ,

17 59F 13,i,

NilClosed mitral

valvotomy (2)NilNilNil

Nil

Closed mitralvalvotomy

Closed mitralvalvotomy (2)

Closed mitralvalvotomy

Closed mitralvalvotomy (3)

Nil

Closed mitralvalvotomy;homograftmitral valvereplacement

Homograftmitral valvereplacement


Homograft mitralvalve replace-ment

Mitral para-prostheticregurgitation(reattd)


Ruptured chordae Present Soft apical NilNone - None +

Floppy valve Present Soft apical NRNone Present Soft apical NilNone - None Nil

None Present Soft apical NR+ leftsternal edge

Calcification + Present Soft left NRsternal edge

Calcification+ + Present Soft left NRsternal edge

Calcification + + Present Soft apical NR

None Present Soft apical Nil+ left sternaledge, aorticsystolicmurmur

Calcification+ + Present Soft apical Nil

Calcification + Present Soft apical+ + +left sternaledge; aorticsystolicmurmur

Calcification + Present Soft left +sternal edge

Calc

Nil

Calc

Calc

cification+ + Present Soft apical +

Present Soft apical+ Nilleft sternaledge

cification+ + Present Soft apical+ + +left sternaledge

cification + Intermittent Nilapical

LV failureObstructed mitral

prosthesisLV failureLV failureAlso tricuspid

valve replace-ment, partiallyobstructed

LV failure

LV failure

LV failure

LV failure: alsoLV to coronarysinus fistula

Slight mitralparaprostheticregurgn +LV failure

Slight mitralparaprostheticregurgn+LV failure

Mitral parapros-thetic regurgita-tion, alsoaortic valvereplacement

Mitral para-prostheticregurgitation

Mitral para-prostheticregurgitation,also aortic valvereplacement



Mitral para-prostheticregurgitationon angiogram;not seen atre-op.; furthermitral valvereplacement;patient well



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Role of echocardiography and phonocardiography in diagnosis of mitral paraprosthetic regurgitation 1219

Case Age Onset of Previous operation Factors Tricuspid Systolic Haemolysis RemarksNo. and deteriora- on mitral valve predisposing to regurgn murmur

sex tion after mitral para-operation prosthetic

regurgitation

i8 56M 2 wk Mitral valve Ruptured chordae Present Soft apical+ NR Mitral para-repair; homo- left sternal prostheticgraft mitral edge regurgitationvalvereplacement

I9 35F 8 mth Closed mitral Calcification+ Present Left sternal + + Mitral para-valvotomy; edge in- prosthetichomograft creasing regurgitation +mitral valve inspiration intravalvarreplacement leak

20 47F 2 ,, Nil Calcification+ Present Soft left Nil Mitral para-sternal edge prosthetic

regurgitation2I 36F 29 ,, Nil Nil Present Soft left NR Mitral para-

sternal edge prosthetic+ apex regurgitation

22 49M 5 wk Nil Floppy valve - None NR Sinus rhythm,aortic valvereplacement;not catheter-ized; mitralparaprostheticregurgitation

Group 423 34M i6 mth Nil Calcification+ + Present None Nil Aortic

regurgitation +LV failure;sinus rhythm;ventricularfibrillation atcatheterization

24 57F 4 yr Nil Calcification+ Present Aortic systolic NR Aorticmurmur regurgitation

NR not recorded.+ = mild/moderate.+ + = severe.

oblique position, and particular care was taken to ensurethat the catheter did not interfere with the function oftheprosthesis. In two cases, of whom one had a parapros-thetic leak, the left atrium was entered from the leftventricle. Mitral regurgitation was classified as mild,moderate, or severe, puffs of 'smoke-ring' incompetencebeing considered a normal finding (Rockoff et al., I966).Left ventricular function was considered to be impairedif ejection fraction was reduced, if the left ventricularend-diastolic pressure was greater than I2 mmHg withrespect to the mid-thorax, or if dyskinetic areas werepresent. Cardiac output was measured by the Fickmethod, oxygen uptake being measured by expired airanalysis in 8 patients, and an assumed basal value beingused in the remainder (Robertson and Reid, 1952).

EchocardiographyEchocardiograms were recorded with a simultaneous

electrocardiogram using an Ekoline 20 ultrasonoscope.The position of the transducer was adjusted until asatisfactory record was obtained showing the inter-ventricular septum and the endocardial surface of theposterior wall of the left ventricle. In all cases, the twoechoes from the ball of the prosthesis, and those fromthe valve ring and the apex of the cage were identifiedfirst and the position of the septal echo was confirmed tobe anterior to these (Fig. I). In several patients, furtheridentification of the septal echo was obtained by record-ing a tricuspid valve echo immediately anterior to it.Septal movement was considered to be normal if thedominant movement during systole was in a posteriordirection with respect to the transducer, and reversed ifin an anterior direction. End-diastolic volume and strokevolumes were only calculated if septal movement wasnormal, since the measurement of these volumes in thepresence of reversed septal movement has not yet beenvalidated in this laboratory (Gibson, 1973).



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a

Septum

_- EGECG

-*v Erndocordium

- -, * ^ ~ --Posterior left:ventriculor woll

&i.; # ^ > _ .~O

FIG. i a) An echocardiogram from a patient with Starr-Edwards mitral valve replacementdemonstrating reversed septal movement. b) With the transducer in the same position and withthe same gain settings, echoes from the prosthesis are demonstrated at a deeper plane.

PhonocardiographySystolic time intervals were measured from high fre-quency phonocardiograms, which were recorded with asimultaneous electrocardiogram and indirect carotidpulse, using a Cambridge photographic recorder, oper-ating at a paper speed of Ioo mm/sec. At least IO suc-

cessive beats were analysed for each patient, and themean value taken. The following time intervals weremeasured:(i) Left ventricular ejection time (LVET) taken as the

interval between the onset of the rapid upstroke ofthe carotid pulse and the incisura.

(2) Pre-ejection period (PEP). This was taken as electro-mechanical systole (QA2) less LVET.

(3) QS,, taken as the interval between the onset of the qwave and the high frequency closing click of themitral prosthesis.

(4) A20C interval, between the aortic closing soundand the mitral opening sound. LVET and PEPwere corrected for heart rate according to the re-

gression equations of Weissler and Garrard (1971),and differences between observed and predictedvalues expressed as ALVET or APEP.

HaemolysisThis was considered to be present if there was a raisedreticulocyte count in the absence of recent blood loss, orevidence of red cell fragmentation on the blood film. Itwas classified as mild or severe depending on whetherthe haemoglobin level was greater or less than 12 g/iOOml provided that there was no other cause for anaemia.

ResultsPredisposing factors (Table I)Seven patients with severe regurgitation (Group 3)had previously had a mounted homograft valvebefore the current prosthesis, and i further patienthad had a paraprosthetic leak repaired. No patientin groups I or 2 had previously had an open opera-tion on the mitral valve. The incidence of calci-fication, ruptured chordae, or 'floppy cusps' at theprevious operation was similar in all groups andnone had had subacute bacterial endocarditis. Only2 patients with severe paraprosthetic regurgitationwere found to have none of these predisposingfactors.

Clinical presentation (Table I)There was no significant difference between thegroups in the time between operation and onset ofdeterioration, or in the mode of deterioration. Mostdeteriorated gradually after initial improvement, buttwo (Group 3) deteriorated suddenly and onedeteriorated in the postoperative period. All hadreduced exercise tolerance or clinical evidence ofheart failure. The venous pressure was raised in allbut i, and evidence of right or left ventricular en-largement was present in a proportion of all groups.All but 3 had a systolic murmur whose origin wasnot clear before investigation. In retrospect, of the3 patients who had no systolic murmur, i had a

- ECG

Cage ofprosthesis-Boll ofprosthesis

ri-b-

.. . .. ..

..L -,.-7--l ;X



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severe mitral paraprosthetic leak, i had an ob-structed mitral prosthesis, and i had an obstructedtricuspid prosthesis. Only 2 of the patients even-

tually shown to have a severe paraprosthetic leakwere felt to have clear-cut clinical evidence ofmitral regurgitation, and, in general, the loudness ofthe systolic murmur bore an inverse relation to theseverity of the leak. The electrocardiogram showedno characteristic features, and chest x-ray was alsounhelpful. It was not possible to separate patientswith and without paraprosthetic leak on the basisof changes in the cardiac silhouette or pulmonaryvascular pattern.

Haemodynamic changesOne severely ill patient was not catheterized, andin 5 patients satisfactory wedge pressures were notobtained due to the presence of pulmonary hyper-tension. Three patients had major complications.One patient in Group 4 developed ventricularfibrillation when the catheter entered the left ven-tricle. Of 2 patients with an additional aortic Starr-Edwards prosthesis in Group 3, in whom the leftventricle was entered by the retrograde approach, i

had an episode of asystole during angiography andthe second had a brief episode of profound hypo-tension after withdrawal of the catheter, requiringexternal cardiac massage. All 3 quickly recovered totheir previous state. Mean values of haemodynamicvariables are shown in Table 2. It was not possibleto distinguish patients with severe paraprostheticleak on the basis of pulmonary artery pressure,cardiac index, left ventricular end-diastolic pressure,or mean mitral diastolic gradient across the prosth-esis. The 'v' wave on the pulmonary artery wedgetrace was significantly higher in the patients withregurgitation, but there was considerable overlapbetween the 2 groups.

TABLE 2 Haemodynamic parameters

Echocardiography (Table 3)All patients in Groups i and 2 showed reversedseptal movement, with a dominant anterior deflec-tion in systole. In Groups 3 and 4, septal move-ment was normal in all but 2, I of whom was foundat operation to have only a small paraprostheticleak, the main abnormality being a para-ball leakdue to a torn cloth-covered valve (Case i9). Thereason for persistence of reversed septal movementin the remaining patient (Case 20) was not clear.After successful surgery in 8 patients in groups 3and 4, septal movement returned to the typicalreversed pattern in all but i patient, who showed aclear-cut change from a normal pattern to one con-sidered to be intermediate but not truly reversed(Fig. 2). In all patients in whom septal movementwas normal, calculated stroke volume was con-siderably greater than that derived at cardiac cath-eterization, consistent with the presence of signi-ficant valvular regurgitation (Fig. 3).

Systolic time intervals (Table 3)Comparisons were restricted to Groups i and 3.There was no statistically significant difference be-tween values of ALVET, APEP, or QS, betweenthese two groups. However, A20C was significantlyreduced in those with mitral regurgitation, with onlyslight overlap between the groups. One patient(Case 9) in Group i had a value below normal(8o msec), and i patient in Group 3 had a valuewithin the normal range (Case 20); in this one septalmovement was also reversed on the echocardiogram.There did not appear to be any relation between theseverity of the regurgitation and the degree ofshortening of the A20C interval.

Haemolysis (Table I)The presence of haemolysis was not assessed in 8patients. Severe haemolysis was confined to 3

PA systolic LVEDP C. Index Mitral mean 'V'wavediastolic gradient LA or PAW

Group I 561i± I5-2 I6-8 ± 4-8 1I7+±0-7 7-6±7-0 9-0± 4-I(9) (9) (9) (9) (8)

P NS NS NS NS < O-OIGroup 2 47 II 2-6 6 I4

(2) (2) (2) (I) (I)Group 3 70±17-8 I5-4±50 i-8+±o6 9-7±7'I I7-8+7-0

(9) (I0) (9) (7) (7)Group 4 74 12 2-5 NR 20

(2) (I1) (I) (I1)

The mean values + SD are shown with the number of observations in parentheses. Statisticalcomparison between Groups I and 3 gives values for P as shown.



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1222 Miller, Gibson, and Stephens

TABLE 3 Systolic time intervals and echocardiographic data

ALVET APEP PEPILVET QSI A2-OC Septal movementReversed Normal

Group I 66-I±40o5 62-4+20-8 0-58±0-i6 8I-6±9-9 III-2±24-3(7) (7) (7) (7) (8)

(9) NS NS NS NS P< o-oi 9 0Group 2(2) 2 0

Group 3 72-9±34-7 40-4±28-5 0-46±0-15 67-6±I7-7 79-I+I 83 2 9

(I I) (8) (8) (8) (8) (8)Group 4(2) 0 2

The mean values ± SD are shown with the number of observations in parentheses. Values for P refer to com-parison between Groups I and 3. Values for Groups 2 and 4 have been omitted as only one patient in each grouphad systolic time intervals measured.

7 ,..

(a) (b)FIG . 2 a) An echocardiogram of Case IS after the onset of mitral paraprosthetic regurgita-tion. Septal movement is normal, and stroke volwne increased at 130 ml. b) After correction ofregurgitation by further mitral valve replacement, septal movement has changed to an inter-mediate pattern, being neither normal nor typically reversed.



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140

100

StrokeVolume(cm3)

Catheter EchoFIG. 3 Comparison of stroke volume measured byechocardiography and at cardiac catheterization in 9patients (8 Group 3, I Group 4). The echocardio-graphic value reflects total left ventricular output, andcatheter value netforwardflow, the difference in valuesindicating the regurgitant fraction. Bars represent SD.

patients in Group 3 out of the 8 in whom it was

assessed, and was not seen in the other groups.Slight haemolysis, seen as occasional red cell frag-mentation on a blood film, was seen in i patient inGroup i and 2 in Group 3.

DiscussionThis study shows that reduced exercise tolerance or

clinical evidence of heart failure after mitral valvereplacement may be due to a number of causes,singly or in combination. These include mitralprosthesis obstruction, paraprosthetic leak, othervalvular lesions including tricuspid stenosis andaortic regurgitation, as well as impaired left ven-

tricular function. Since all but the last of these are

potentially correctable by surgery, accurate diag-nosis in such patients is of considerable importancein their management. We were therefore dis-appointed to find that the usual clinical criteria forthe diagnosis of these conditions were almost uni-formly unhelpful.

It has been well documented that important mitralparaprosthetic regurgitation may be silent, and thispicture was shown by one case in the present seriesin whom no murmur was heard at any time (Morrow

et al., I964; Rockoff et al., I966; Sanders, I969).The reason for this is not clear. It has been attri-buted to the murmur being in an unusual site, suchas posteriorly over the right scapula (Sawkar, I969),and, though this emphasizes the need for carefulphysical examination, it was not present in our case.A more common problem, however, was that of asoft systolic murmur whose amplitude was reducedwith medical treatment, and which was present inpatients with or without mitral regurgitation. Thisappeared to be due to tricuspid regurgitation,though a soft systolic murmur may also result froma normally functioning mitral prosthesis caused bythe presence of the cage in the left ventricular out-flow tract. In the present series, as well as in pre-vious ones (Willerson et al., I972), a loud systolicmurmur was more frequently due to a small leakwhich presumably causes more turbulence than alarge one. It is clear, therefore, that the presence orabsence of a systolic murmur is irrelevant in assess-ing the competence or otherwise of a mitral Starr-Edwards valve.Absence of the opening click of mitral prosthesis

has been considered valuable evidence of mitralparaprosthetic leak (Aravanis, Toutouzas, andStavrou, 1972), but failure to demonstrate this signin all i i patients in the present series makes usquestion its reliability. We were, however, able toconfirm the finding of Willerson et al. (I972) that adecrease in the A20C interval is a useful physicalsign of mitral paraprosthetic leak. Only i patient(Case 20) with significant mitral regurgitation hada value in the normal range. She also had an echo-cardiographic anomaly showing reversed septalmovement which we were unable to explain. Re-duction in A20C interval has also been reportedwith obstruction of a mitral prosthesis by Wise et al.(197I) who suggested that the increased mitralgradient caused a more rapid excursion of the ball.One patient in the present series with mitral obstruc-tion had a 25 mm diastolic gradient across theprosthesis and a normal A20C interval. However,there was no difference in mitral gradient betweenthose patients with mitral paraprosthetic regurgita-tion and those with normally functioning prosthesesin spite of the differences in A20C interval. We con-clude, therefore, that a reduction in A20C intervalis a valuable sign of mitral paraprosthetic leak butnot necessarily of obstruction. Unlike Willersonet al., we found ALVET not to be significantlydifferent between patients with and without mitralregurgitation. This may reflect our comparisonwith patients with heart failure rather than asympto-matic controls as used by them. The presence of sig-nificant haemolysis also failed to provide evidencefor paraprosthetic regurgitation, being present in



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1224 Miller, Gibson, and Stephens

only 3 patients out of 8 in whom it was sought. Thisfinding is in line with previous reports by Kastoret al. (I968) and Sanders (I969).

In view of these uncertainties in clinical assess-ment, cardiac catheterization was performed in allbut i patient. Though abnormalities in intracardiacpressures give information about the physiologicalconsequences of an abnormality, they may notallow the nature of the underlying abnormalityto be diagnosed. This was emphasized in the patientin Group 4 who developed ventricular fibrillationwhen the catheter entered the left ventricle so thatangiography was not performed, and an incorrectdiagnosis of a paraprosthetic leak was made on thebasis of a tall 'v' wave on the pulmonary arterywedge trace. We consider, therefore, that leftventriculography is the definitive investigation forthe diagnosis of mitral paraprosthetic leak, thoughit should be recognized that false positive resultsmay occur due to interference with valve functionby the presence of the catheter across the cage(Barold, Javier, and Linhart, I968). In addition, itcarries a significant morbidity, particularly inseverely ill patients, and especially in those inwhom an aortic prosthesis is crossed retrogradely.Additional non-invasive tests would therefore be ofvalue in screening patients for more definitive in-vestigation.We found that observation of septal movement

was of value in the diagnosis of mitral parapros-thetic regurgitation. Septal movement was reversedin all patients in Groups i and 2, while it showed anormal pattern of movement in 9 out of the i ipatients in Group 3 in whom there was a significantparaprosthetic leak. Normal septal movement wasnot specific for mitral paraprosthetic regurgitationsince it also occurred in the presence of aortic re-gurgitation even if this is clinically undetected(Group IV). The mechanism is not certain. Itappears to be unrelated to right ventricular overloador tricuspid regurgitation whose incidence wassimilar in Groups i and 3, and which, in other con-ditions, is usually associated with reversed, ratherthan normal, septal movement. It is not due to thecage of the prosthesis, since it may also occur with aBjork-Shiley prosthesis (unpublished observation)which has no cage. It is possible that it reflectsabnormalities of diastolic filling, since a normallyfunctioning mitral Starr-Edwards valve is obstruc-tive (Kezdi, Head, and Buck, I964). In early dias-tole, therefore, filling of the right ventricle might beexpected to occur more rapidly than that of the left,causing posterior movement of the septum. Thiswould explain its reversion to normal with condi-tions causing significant ventricular filling by someroute other than through the prosthesis itself

either by a paraprosthetic dehiscence, or from theaortic root. Normal septal movement would notoccur, therefore, with a small paraprosthetic leak(Group 2), or a leak dominantly through the ringrather than around it (Case I9).A second echocardiographic feature of mitral

paraprosthetic regurgitation was the presence of avery large stroke volume measured by echocardio-graphy in comparison with that derived from cardiaccatheterization. This was also present with aorticregurgitation. Though estimation of stroke volumemay be affected by abnormalities of ventricularshape or by the presence of dyskinesia (Gibson,I973), in the present series it was found that thedisparity between stroke volume measured echo-cardiographically and at cardiac catheterizationbore a relation to the severity of mitral parapros-thetic regurgitation or aortic regurgitation as assessedby angiography or at reoperation.

In conclusion, we feel that dysfunction of themitral prosthesis should be considered in anypatient who fails to show sustained improvementafter mitral valve replacement. Unfortunately,physical examination, chest x-ray, electrocardio-gram, and assessment of haemolysis are all unhelp-ful in establishing the diagnosis. A reduced A20Cinterval, and normal septal movement with an in-appropriately large stroke volume on echocardio-graphy, are all extremely suggestive of a mitralparaprosthetic leak, and indicate that definitivediagnosis should be made by left ventriculography.This may carry a significant risk, however, and onthe basis of these results, we are now prepared torecommend operation in a severely ill patient on thebasis of echocardiographic findings alone.

We wish to thank our colleagues for permission to reporton their patients.

ReferencesAravanis, C., Toutouzas, P., and Stavrou, S. (I972). Dis-

appearance of opening sound of Starr-Edwards mitralvalve due to valvular detachment. British Heart3Journal, 34,1314.

Barclay, R. S., Reid, J. M., Stevenson, J. G., Welsh, T. M.,and McSwan, N. (I972). Long term follow-up of mitralvalve replacement with Starr-Edwards prosthesis. BritishHeart_Journal, 34, I29.

Barold, S. S., Javier, R. P., and Linhart, J. W. (I968). Facti-tious mitral insufficiency. A pitfall in the hemodynamicassessment of prosthetic mitral valves by retrogradecatheterization of the left side of the heart. New EnglandJournal of Medicine, 279, 8io.

Gibson, D. G. (1973). Estimation of left ventricular size byechocardiography. British Heart journal, 35, I28.

Kastor, J. A., Akbarian, M., Buckley, M. J., Dinsmore, R. E.,Sanders, C. A., Scannell, J. G., and Austen, W. G. (I968).Paravalvular leaks and hemolytic anemia following inser-tion of Starr-Edwards aortic and mitral valves. Journal ofThoracic and Cardiovascular Surgery, 56, 279.



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Kezdi, P., Head, L. R., and Buck, B. A. (I964). Mitral ball-valve prosthesis. Dynamic and clinical evaluation. Circu-lation, 30, 55.

Morrow, A. G., Harrison, D. C., Ross, J., Jr., Braunwald,N. S., and Clark, W. D. (I964). The surgical managementof mitral valve disease: a symposium on diagnosticmethods,operative techniques, and results. Annals of InternalMedicine, 6o, 1073.

Morrow, A. G., Oldham, H. N., Elkins, R. C., and Braunwald,E. (I967). Prosthetic replacement of the mitral valve.Preoperative and postoperative clinical and hemodyn-amic assessments in Ioo patients. Circulation, 35, 962.

Najafi, H., Dye, W. S., Javid, H., Hunter, J. A., Ostermiller,W. E., and Julian, 0. C. (I969). Mitral valve replace-ment. Review of seven years' experience. AmericanJournalof Cardiology, 24, 386.

Peterson, C. R., Herr, R., Crisera, R. V., Starr, A., Bristow,J. D., and Griswold, H. E. (I967). The failure of hemo-dynamic improvement after valve replacement surgery.Etiology, diagnosis, and treatment. Annals of InternalMedicine, 66, I.

Robertson, J. D., and Reid, D. D. (1952). Standards for thebasal metabolism of normal people in Britain. Lancet, I,940.

Rockoff, S. D., Ross, J., Jr., Oldham, N. N., Jr., Mason, D. T.,Morrow, A. G., and Braunwald, E. (I966). Ventriculo-atrial regurgitation following prosthetic replacement ofthe mitral valve. Angiocardiographic and hemodynamicfindings. American Journal of Cardiology, 17, 8I7.

Sanders, C. A. (I969). Editorial: prosthetic problems. NewEngland Journal of Medicine, 28I, 501.

Sawkar, L. (1969). Unusual location of the mitral-prosthesismurmur. New England Journal of Medicine, 28i, 1075.

Starr, A. (I97I). Mitral valve replacement with ball valveprosthesis. British HeartJournal, 33, Suppl., 47.

Weissler, A. M., and Garrard, C. L. (197I). Systolic timeintervals in cardiac disease. Modern Concepts of Cardio-vascular Disease, 40, I.

Willerson, J. T., Kastor, J. A., Dinsmore, R. E., Mundth, E.,Buckley, M. J., Austen, W. G., and Sanders, C. A.(1972). Non-invasive assessment of prosthetic mitralparavalvular and intravalvular regurgitation. British HeartJ'ournal, 34, 56i.

Wise, J. R., Webb-Peploe, M., and Oakley, C. M. (I97I).Detection of prosthetic mitral valve obstruction by phono-cardiography. American Journal of Cardiology, 28, 107.

Requests for reprints to Dr. D. G. Gibson, CardiacDepartment, Brompton Hospital, London SW3 6HP.



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