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MITRAL VALVOTOMY DURING PREGNANCYEighteen Cases

By A. W. FAWCETT, M.B., F.R.C.S.Consultant Thoracic Surgeon, Royal Infirmary, Sheffield

and B. S. DHILLON, M.B., F.R.C.S.Ed., F.R.C.S.(Eng.).Senior Surgical Registrar

Mitral stenosis is especially common in womenof child bearing age. Of our first 350 mitralvalvotomies, 64 per cent. were women below theage of 45 and i8 of these women were pregnant.There are several reports in the literature

of the value of mitral valvotomy duringpregnancy.6, 7, 8.11, 12, 13, 20, 21, 25

Organic heart disease, especially mitral stenosis,is one of the leading causes of maternal morbidityand mortality. Rheumatic heart disease accountsfor 90 per cent. of pregnant cardiac patients and in75 per cent. of these there is involvement of themitral valve,4 usually with mitral stenosis.The object of this communication is to present

clinical details, criteria for selection of these cases,discussion about the optimum time for surgery,operative findings, immediate post-operative com-plications and correlation of operative findingswith the post-operative progress.Material

Eighteen patients are included in this series.

AgeTheir ages range between zo and 45 years.

TABLE I20 to 25 25 to 30 30 to 40 40 to 45years years years years

4 6 7 I

Previous PregnanciesThere was one primipara and 17 multipara

patients in this series. The number of previouspregnancies in multipara are shown in Table 2.

.,

TABLE 2Multipara

One Two Three Four

9 3 3 2

Duration of Present PregnancyThe length of gestation at the time of mitral

valvotomy is indicated in weeks in Table 3.TABLE 3

14 to 15 I6 to I7 18 to I9 20 to 21 24 to 25 28 to 29weeks weeks weeks weeks weeks weeks

2 7 2 3 2 2

Duration of Follow-upThe duration of follow-up after mitral val-

votomy or cardiotomy is shown in Table 4.TABLE 4

Over Over Over Over4 years 3 years 2 years i year

2 8 4 4

Clinical AssessmentDyspnoea on exertion is a common complaint

especially in the latter half of the pregnancy, butdyspnoea before the fourth month of pregnancyneeds careful evaluation and is an ominous signin a pregnant patient with mitral stenosis.The limitation of activity due to dyspnoea and

fatigue has been graded into four classes, I, II,III, IV (New York Heart Association Classifica-tion). We have graded our patients accordingly.Dyspnoea during the present pregnancy was

assessed and compared with the dyspnoea duringthe previous pregnancy in 17 multipara patients.The dyspnoea which is worse and progressiveduring the present pregnancy is an unfavourablesign.

I. Two patients who were placed in Class Iduring the previous pregnancy had deterioratedto Class III during the present pregnancy.

2. Ten patients who were placed in Class IIduring the previous pregnancy had deterioratedto Class III.

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3. Four patients were placed in Class II duringthe present pregnancy and their classification wasthe same during the previous pregnancy. Thesefour patients developed recurrent attacks of acutepulmonary oedema.

4. One patient was placed in Class II duringthe present pregnancy but she had a history ofcongestive cardiac failure during the previouspregnancy.

5. One primipara patient was placed in Class I.She developed an attack of acute pulmonaryoedema.The grading of dyspnoea is notoriously difficult.

A patient in Class II may rapidly deteriorate toClass III in a month's time.There were: 12 patients in Class III; 5

patients in Class II; one patient in Class I.Paroxysmal Nocturnal Dyspnoea. There were

15 patients who complained of frequent attacks ofparoxysmal nocturnal dyspnoea. Eleven patientswere in Class III and four patients in Class II.Pseudo - paroxysmal - nocturnal dyspnoea canclosely resemble attacks of true paroxysmal noc-turnal dyspnoea. One of our patients had thissymptom, though the nature of this was notrealized until after the operation. At operationthe valve was almost normal except for slightcalcification around the medial commissure.

Haemoptysis. The cardiac and respiratoryembarrassment of normal pregnancy never givesrise to haemoptysis. Haemoptysis in mitralstenosis is a sign of pulmonary hypertension.Eleven patients complained of frequent attacks ofhaemoptysis and two patients had one attack ofmassive haemoptysis each.

Acute Pulmonary Oedema. There were fivepatients who developed acute pulmonary oedemaduring their present pregnancy. Four of thesepatients had recurrent attacks of haemoptysisand paroxysmal nocturnal dyspnoea. The fifthpatient was a 22-year-old primipara. Her heartwas not enlarged. She was in sinus rhythm. Shecomplained of slight breathlessness for the pasttwo weeks. She suddenly developed an attackof acute pulmonary oedema, fortunately survivingthe attack.

Cough. This was present in I6 cases. In a fewcases the cough became worse on exertion andafter going to bed.Pulmonary Congestion and Bronchitis. Sixteen

patients had recurrent attacks of bronchitis and'colds.'

Congestive Cardiac Failure. Two patients de-veloped congestive cardiac failure during thepresent pregnancy and one patient had a historyof congestive cardiac failure during the previouspregnancy.

PeripheralEmboli. One patient gave a history oftwo episodes of peripheral embolism.

Operative Findings in i8 PatientsThese patients were referred to us by various

physicians, with a diagnosis of pure or pre-dominant mitral stenosis. Six of these patientswere suspected to have slight aortic regurgitation.At operation: Fifteen patients were found to

have pure or predominant mitral stenosis. Onepatient was found to have mitral stenosis andmitral incompetence; the mitral incompetencewas thought to be equally important as the stenosisin producing the symptoms in this case. In onepatient the predominant lesion was mitral in-competence. There was an almost normal valueexcept for slight calcification around the medialcommissure in one other patient.There is progressive acceleration of circulatory

speed from the third to the ninth month. Thisacceleration of blood flow diminishes during thelast few weeks before term.24 Due to this in-creased velocity of blood flow the auscultatorysigns of mitral stenosis become markedly aug-mented. Thus, a mild mitral stenosis in a non-pregnant patient may produce auscultatory signsof tight mitral stenosis during pregnancy, i.e. loudsnapping first sound, long diastolic murmur withpresystolic accentuation in the mitral area and anopening snap just internal to the apex beat.n

Clinical Findings in 15 Patients with Pure orPredominant Mitral Stenosis

Radial pulse was of small volume in eightpatients and full volume in seven patients. Therewas no relationship between the size of the mitralorifice and character of the pulse, but threepatients who had severe pulmonary hypertensionhad a small volume pulse.Jugular venous pulse-three patients with marked

pulmonary hypertension had giant ' A' waves inthe jugular venous pulse.

Blood pressure and pulse pressure were withinnormal limits in all the patients.Apex beat was tapping in character in eight

patients.Parasternal heave and palpable P2I. There was marked parasternal heave with

palpable P2 in three patients.2. There was moderate parasternal heave in 12

patients.Diastolic thrill was flalpable in all the patients.First Sound in Mitral Area. In seven patients

there was marked accentuation of the first sound.When the patient was placed in the left lateralposition the snap was almost deafening in quality.The mitral orifice (before split) was: 0.5 cm. or

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FAWCETT and DHILLON: Mitral Valvotomy During Pregnancy

less, five cases; I.o cm., one case; 2.0 cm., onecase.In six patients the first sound was accentuated.

The mitral orifice (before split) was: 0.5 cm.,four cases; I.o cm., one case; 2.0 cm., one case.

In two patients the first sound was not ac-centuated. The mitral orifice (before split) wasI cm. in diameter in both cases. The anteriorlateral cusp was mobile, but one case had slightcalcification around the medial commissure.

Opening snap was present in 13 cases. It wasabsent in two cases who did not have accentuatedfirst sound in the mitral area.

Diastolic Murmur in Mitral Area. A longrumbling diastolic murmur with presystolicaccentuation was present in 14 patients in sinusrhythm. The presystolic accentuation was absentin a patient with auricular fibrillation.

Systolic murmur in mitral area was heard ineight patients.

Soft in quality, four patients (no regurgitationwas detected at operation). Mild systolic murmurin two patients (slight regurgitation was present atoperation). Harsh, systolic murmur conductedto axillae in two cases (there was moderate ' blowback' in one case at operation).

Pulmonary Second Sound. This was accentu-ated in all cases. In three cases with marked pul-monary hypertension, the sound was narrowlysplit, with more accentuation of the secondelement.

ConclusionThus, every pregnant patient with pure mitral

stenosis may not necessarily have a loud firstsound nor an opening snap. The constant find-ing was a long rumbling diastolic murmur withpresystolic accentuation. The presystolic accentu-ation was absent in one patient with auricularfibrillation.

Predominant mitral incompetence, one case.(Mitral orifice was 2.5 cm. in diameter.) Mitralstenosis with severe mitral incompetence, onecase. The mitral incompetence was thought tobe as important as stenosis in producing hersymptoms. Mitral orifice (before split) was2 cm. in diameter. Both patients had a loudfirst sound, a long rumbling diastolic murmur withpresystolic accentuation and a localized harshsystolic murmur in the mitral area.The patient with an almost normal valve had a

loud first sound, long rumbling diastolic murmurwith presystolic accentuation and a localized harshsystolic murmur in the mitral area. She hadcongestive cardiac failure during the previouspregnancy, which might have been a congestedcirculatory state2l (Eichna et al., 1954).

Criteria for Advising SurgeryThese cases were referred to us by seven

different physicians and the criteria they usedfor advising surgery are listed below.

Acute Pulmonary Oedema (5 cases). Thedevelopment of attacks of pulmonary oedema is aserious complication. Morgan Jones (1951) con-siders acute pulmonary oedema to be one of theleading causes of death during pregnancy. Asituation of utmost gravity arises if the attacks ofpulmonary oedema are not controlled by adequatemedical measures.l4

(i) One patient was a young primipara. Shehad complained of dyspnoea for two weeks beforeshe suddenly developed an acute attack of pul-monary oedema. She fortunately survived thisattack.

(ii) Four patients had recurrent attacks of acutepulmonary oedema which were not controlled byadequate me(lical measures.

Class III Disability. The I2 patients in thisgroup were all multipara and their disability hadbecome worse during the present pregnancy.

Congestive Cardiac Failure. Two patients de-veloped congestive cardiac failure during thepresent pregnancy and one patient had had con-gestive cardiac failure during the previous preg-nancy. A patient who failed during the previouspregnancy will certainly do so during the presentpregnancy.

Auricular Fibrillation. When auricular fibrilla-tion supervenes it usually occurs during the laststage of rheumatic heart disease. The maternalmortality in pregnant patients with auricularfibrillation is 3I.5 per cent. The one patient inthis group also had class III disability.Optimum Time for Mitral ValvotomyPregnancy imposes an additional load on the

heart.2 3 4 24 There is gradual increase in thecardiac output from the i2th to the 36th week ofgestation. By that time the cardiac output isabout 50 per cent. above normal. The bloodvolume also increases and by the 36th week it isabout 50 per cent. above the non-pregnant state.After the 36th week of gestation there is gradualdecrease in the cardiac output and the bloodvolume. Thus it would be hardly necessary tooperate after the 36th week when 'lightening ofthe burden has occurred.' This rule of thumbcannot be applied to every case. O'Connell andMulachy (I955) have reported successful mitralvalvotomy at full term for threatened pulmonaryoedema.There is general agreement that mitral val-

votomy should be carried out early in pregnancyto give the heart its best chance before the maxi-mum load of pregnancy is reached.

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The length of gestation, in our cases, at thetime of mitral valvotomy is shown in Table 3.OperationThe following points were noted at operation:i. The diameter of the mitral orifice before the

valve was split.2. Valvular calcification.3. Mobility of the antero-medial cusp of the

mitral valve.4. Regurgitation. The degree of the mitral

incompetence was estimated from the stream ofregurgitant flow of blood felt by the tip of the indexfinger. It was slight, moderate or severe, accord-ing to the amount of blow back.

5. The diameter of the mitral orifice aftercompletion of the split.The diameter of the mitral orifice before the

valve was split: 0.5 cm. or less, nine cases; I cm.or less, four cases; 2 cm. or less, three cases;over 2.5 cm., one case; over 3 cm., one case.Diameter of mitral orifice after mitral

valvotomy:3 cms. 2.5 cms. i cm. Less thanor over or over or over I cm.

12 3 Nil

One patient had an almost normal valve; onepatient had predominant mitral incompetence.We grouped these patients into ' unfavourable '

and 'favourable' groups from the findings atoperation.

Unfavourable Group. There were three casesin the unfavourable group.

I. Predominant mitral incompetence with heavycalcification of the valve. The valve orifice wasover 2.5 cm. There was marked calcification andthe calcium was heaped'up in friable lumps aroundthe commissures. It was not considered safe toattempt valvotomy.

2. Severe mitral incompetence with mitralstenosis. The mitral orifice was enlarged from2 cm. to over 3 cm.

3. The commissures could neither be adequatelyfractured with a finger nor cut with knife. Themitral orifice was 0.3 cm. in diameter and wasenlarged to 0.75 cm.

Favourable Group (14 cases).I. Eleven cases: the diameter of the mitral

orifice was over 3 cm. and no incompetence wasdetected after the completion of valvotomy. Thevalve cusps were mobile.

2. Three cases: the diameter of the mitralorifice after splitting the valve was over 2.5 cm.,though there was a trace of incompetence at theend of the operation. The valve cusps weremobile.

Normal Valve. One patient had an almostnormal mitral valve. The diameter of mitralorifice was over 3 cm., the valve cusps weremobile. There was slight calcification along themedial commissure. She had a minimal lesionof the mitral valve and a history of congestivecardiac failure during the previous pregnancy.It is probable she had a circulatory congestivestate (Eichna et al., I954) during the previouspregnancy and it had very little to do with theminimal lesion of the mitral valve.

Follow-upUnfavourable GroupThe patient who had predominant mitral in-

competence had to be readmitted one month afterthe valvotomy and she aborted at 24 weeks. Afterthis she steadily improved. The second patient inwhom mitral incompetence was considered to be asimportant as mitral stenosis in producing hersymptoms, did not by any means have a smoothantenatal period. She had to be maintained on astrict medical regime to keep her free of pulmonarycongestion and had to be hospitalized early beforethe delivery. She underwent a normal labour atfull period but in the immediate post-partumperiod she developed congestive cardiac failureand responded well to the usual medical treatment.The third patient who had a mitral orifice less than0.5 cm. which could not be enlarged beyond0.75 cm. had a rather stormy antenatal period.She had to be hospitalized one month aftervalvotomy with congestive cardiac failure. Shewent into labour at full term and only very strictmedical regime kept her just free of trouble. Thesetwo patients in the unfavourable group wouldcertainly seem to support those who maintain thatmost women would do well without valvotomy ifmedical supervision was adequate, but such aregime entails considerable worry to the patientand the attending physician.Favourable Group (14 cases)

All the patients in this group had a smoothantenatal period. One patient aborted at fourweeks after the valvotomy. The remaining13 patients went through their pregnancies withoutgiving undue anxiety and there was no maternal orfoetal mortality. Two of these patients have gonethrough further pregnancy each without anycomplication.

Eleven patients (mitral orifice after split over3 cm. and mobile cusps) have maintained'excellent' progress and three patients (mitralorifice after split over 2.5 cm. slight calcificationand trace of incompetence) have also maintained' good' progress.

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February I958 FAWCETT and DHILLON: Mitral Valvotomy During Pregnancy 8

Mitral stenosis and PredominantPure mitral stenosis mitral incompetence incompetence Almost normal

Without calcification I11 2 slight incompe-tence

*I marked incompe-tence

With calcification *2 slight calcification ti heavy calcification *I slight calcification

*Valve cusps mobile. tValve cusps rigid.

The Risk of Mitral ValvotomyMortality

All patients survived the operation. Mitralvalvotomy can be safely carried out during preg-nancy without undue harm to the mother or thefoetus.

MorbidityCerebral Embolism. One patient had a left

cerebral embolism at the time of operation anddeveloped right hemiplegia with aphasia. Shegradually recovered from this and the remainderof her pregnancy has been uneventful. She hasundergone a subsequent pregnancy without anycomplications.

Tracheo-bronchial Secretions and Collapse ofLung. Three patients had marked difficulty inbringing up their sputum and one patient de-veloped collapse of the left lower lobe. Theirdistress was relieved by bronchoscopic aspirationof the bronchial tree.

Arhythmia. One patient who was in sinusrhythm before the operation developed auricularfibrillation in the immediate post-operative period.She spontaneously reverted to normal rhythmabout eight weeks later.

Post-pericardiectomy Syndrome. One patienthas complained of persistent praecordial painsince the operation.Discussion

There is still a considerable difference of opinionconcerning the value of mitral valvotomy duringpregnancy. Burwell and Metcalfe I(954) con-sider valvotomy more hazardous during pregnancy.Laake (I954) reached the conclusion that thenumber of patients with heart disease who haveserious trouble during their pregnancies is small.Eichna et al. (I954) have described circulatorycongestion simulating congestive cardiac failure innon-cardiac pregnant patients. The majority ofpregnant patients with mitral stenosis can be keptfree of trouble with adequate medical measures,but the first 24 to 72. hours after delivery isanother danger period when cardiac decompensa-tion can develop with great rapidity;

Several reports of valvotomy performed during

pregnancy have appeared (Brock, 1952; Cooleyand Chapman, 1952; Logan and Turner, 1952;Watt et al., 1954; O'Connell and Mulachy, 1955;Glover et al., 1955; Bailey and Bolton, 1956;Marshall and Pantridge, I957). From the ac-cumulated experience of these authors combinedwith our own experience, we are convinced thatmitral valvotomy has an important place in thetreatment of mitral stenosis during pregancy. Asituation of the utmost gravity arises if pulmonarycongestion and pulmonary oedemax4 are notcontrolled by adequate medical measures. Mitralvalvotomy in such patients definitely diminishesthe mortality. It appears to us that there is verysmall risk attached to mitral valvotomy duringpregnancy and by relieving the obstruction we arecarrying out a logical and sensible treatment,besides, direct palpation of the valve gives usreliable information which can be useful if we haveto advise sterilization at a later date.

SummaryExploration of the mitral valve was carried out

in x8 pregnant patients with mitral stenosis.From the operative findings, three patients wereplaced in the 'unfavourable group,' and 14patients in the' favourable group,' and one patienthad an almost normal valve.

It is concluded that operative risk is no greaterduring pregnancy than in the non-pregnant state.Mitral valvotomy is the only logical method oftreating the obstruction at the mitral orifice and iftechnically successful it considerably reduces therisk to the mother and the foetus.

AddendumCase II in the unfavourable group has since

died.It is a pleasure to thank Miss M. Pandergaust

and Miss Eunice Baker for careful case recordsand their help in completing this paper.

REFERENCESx. GORDON, C. A., ROSENTHAL, A. H., and O'LEARY, J. L.

(1952), Amer. .. Surg., 83, 72.2. HAMILTON, B. E. (x947), Amer. Heart J., 33, 663.3. MORGAN JONES, A. (I95), 'Heart Disease in Pregnancy '

London, Harvey and Blythe.References continued on page Ioo.

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100 POSTGRADUATE MEDICAL JOURNAL February 1958

Sealy (1953) points out in some detail the indi-cations for surgical treatment of coarctation. Hestates that it has its uses, particularly as a pro-phylactic measure to prevent rupture, cardiacfailure, endocarditis or cerebral catastrophes.He discusses the use of grafts and anastomoses,emphasising that over the age of 30 it is rather ahazardous procedure.

Finally, there is a report by Gross (I95I) of 19cases of coarctation treated by homologous grafts.In this series 80 per cent. of the patients had theblood pressure restored to normal, a fact whichso far has been observed in the present case.

SummaryA case report of a patient suffering from

subarachnoid haemorrhage and coarctation of theaorta, treated successfully by aortic homograft,is presented.The apparent rarity of such a remarkable

sequence of events is indicated.Some attempt has been made to show the

importance of discovering the exact cause ofhypertension in the younger patient at the earliestage whenever possible (the gap of io years, betweenI943 and 1953 in this case being noted), and themodes of presentation of these cases are described,

particularly in relation to cerebro-vascularcatastrophes.

Early diagnosis and recognition of the conditionis stressed, and this is shown vitally to affect theprognosis.The value of an artery bank being available for

the use of thoracic surgeons dealing with thesecases is emphasised.Acknowledgments

I wish to thank Dr. H. Alstead for his kindpermission to publish this case, and Mr. J. K. B.Waddington for the use of his account of theoperation. I am grateful to Dr. E. N. Chamber-lain for his helpful, constructive criticism in thepreparation of this paper.

BIBLIOGRAPHYABBOTT, M. E. (I928), Amer. HeartJ., 3, 392, 574.BLACKFORD, L. M. (1928), Arch. intern. Med., 41, 702.BROCK, R. C. (953), Proc. roy. Soc. Med., 46, II5.CRAFOORD, C. (1948), Brit. Heart J., 0o, 71.CRAFOORD, C., and NYLIN, G. (I949), J. thorac. Surg., 14, 347.DORAMAN, F. de S., and BECK, D. (I954), Arch. Middx Hosp.,

4, 144.GROSS, R. E. (I95I), Ann. Surg., 134, 753.GROSS, R. E., et al. (1949), J. Amer. med. Ass., 139, 285.KIRKLIN, J. W., et al. (I952), Circulation, 6, 411.LICHTENBERG, H. H., and GALLAGHER, H. F. (I933),Amer. J. Dis. Child, 45, 1253.RIEFENSTEIN, G. H., and LEVINE, S. A. (1947), Amer. HeartJ,.

33, 146.SEALY, W. C. (I953), Surg. Gynec. Obstet., 97, 30I.WOLTMAN, H. W., and SHELDEN, W. D. (I927), Arch. Neurol.

Psychiat. (Chicago), 17, 303.

RUTHIN CASTLE, NORTH WALESA Clinic for the diagnosis and treatment of Internal Diseases (except Mental or Infectious Diseases). The

Clinic is provided with a staff of doctors, technicians and nurses.The surroundings are beautiful. The climate is mild. There is central heating throughout. The annual

rainfall is 30.5 inches, that is less than the average for England.The Fees are inclusive and vary according to the room occupied.

For particulars apply to THE SECRETARY, Ruthin Castle, North Wales.Telegrams: Castle, Ruthin Telephone: Ruthin 66

References continuedfrom page 8--A. W. Fawcett, M.B., F.R.C.S., and B. S. Dhillon, M.B.. F.R.C.S.Ed.,

4. MACRAE, D. J. (1948), J. Obstet. Gynaec. Brit. Emp., L.V. 184.5. BUINIM, J. J., and TAUBE, H. (i951), Med. Clin. N. Amer.,

35, 667.6. COQLEY, D. A., and CHAMPAN, D. W. (1952), J. Amer.

Wed. Ass., 150, II3.7. LOGAN, A., and TURNER, R. W. D. (1952), Lancet, i, 1286.8. BROCK, R. C. (1952), Proc. roy. Soc. Med., 45, 538.9. BURNWELL, C. S., and METCALFE, J. (1954), Mod. Cone.

cardiovas. Dis., 23, 250.Io. BURNWELL, C. S., and RAMSEY, L. H. (1953), Trans. Ass.

Amer. Phys., 66, 308.ix. PARKINSON, T. (I953), Proc. roy. Soc. Med., 46, 48.I2. WATT, G. L., BIGELOW, W. G., and GREENWOOD,

W. F. (1954), Amer. J. Obstet. Gynaec., 67, 275.13. GLOVER, R. P., McDOWELL, D. E., and O'NEILL, T. J. E.

(i955), J. Amer. med. Ass., 158, 895.14. HOLMES SELLORS, T., EVAN BEDFORD, D., and

SOMERVILLE (1953), Brit. med. J., ii, o059.*IS. MARQUIS, R. M., GILCHRIST, A. R. (1954), Edin. med.

6.,D xi, 3I .*x6. DOUGLAS, D. M., and HILL, I. G. (I954), Ibid., Ixi, 133.

F.R.C.S.(Eng.).*I7. BAKER, C., BROCK, R. C., CAMPBELL, M., and

WOOD, P. (1952), Brit. med. J., i, 1043.*I8. WOOD, P. (1954), Ibid., Ios, III3.*I9. GLOVER, R. P., DAVILA, J. C., O'NEILL, T. J. E., andJANTON, O. H. (I955), Circulation, I, 14.

20. BAILEY, C. P., and BOLTON, H. E. (I956), N.Y. St.J. Med.,56, 825.21. O'CONNELL, T. C. J., and MULACHY, R. (1955), Brit.

med. J., i, 1191.22. EICHNA, L. W., FARBER, S. J., BERGER, A. R., RADER,B., SMITH, W. W., and ALBERT, R. E. (x954), Trans.

Ass. Amer. Phys., 67, 72.23. LAAKE, H. (I954), Acta med. Scandinav., 148, I47 (Fax. a).24. BADER, R. A., BADER, M. E., ROSE, D. J., and

BRAUNWALD, E. (x955), . clin. Invest., 34, 1524.25. MARSHALL, R. J., and PANTRIDGE, J. F. (i957), Brit.med. J., 1, 1097.

* These articles have not been quoted in the text. Each one ofthese artcles is a classical contribution to this branch of medicine.

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