cardiac after myocardial infarction · to have sustained a myocardial infarction. this was...

Postgrad. med. J. (October 1968 )44, 775-784.

Cardiac aneurysm after myocardial infarction

BERNARD M. GRODENM.B., Ch.B., M.R.C.P.(Glasg.), M.R.C.P.(Edin.)

WILSON B. JAMESM.B., Ch.B., F.F.R.

IAN MCDICKENM.B., Ch.B.

The Departments of Medicine, Radiology and Pathology, Southern General Hospital, Glasgow, S. W.1

SummaryTen cases of post-infarction cardiac aneurysm

have been described in detail. Many of the patientshad survived for several years after the infarctionwhich was held to be responsible for the forma-tion of the aneurysm. It is suggested that in mostcases the diagnosis can be made on the basis of aPA chest radiograph combined with carefulcardiac fluoroscopy. If surgery is contemplatedbecause of cardiac failure which does not res-pond to medical treatment or because of embolicphenomena not controlled by anticoagulant ther-apy, left heart angiography and coronary arterio-graphy are indicated.

IntroductionThe term aneurysm was used by early writers

to describe generalized cardiac enlargement. Theearliest report of an aneurysm of the ventricle wasmade by John Hunter (1757). The incidence ofaneurysm in autopsy reports of patients after amyocardial infarction has varied from 3 % (Dub-now, Burchell & Titus, 1965) to 38% (Parkinson,Bedford & Thomson, 1938). The diagnosis is rarelymade in life although Master et al. (1940) foundabnormalities of pulsation of the cardiac contourafter myocardial infarction in 73 % and Kurtzman& Lofstrom (1963) in 78% of patients. Not all ofthese patients had aneurysms but recently Gorlin,Klein & Sullivan (1967) demonstrated twenty-fourcases of aneurysm by left heart angiography, in aseries of 100 patients with coronary arterydisease, and two of the present authors (Groden& James, 1968) have found radiological featuressuggestive of aneurysm in 20% of patients whohad survived a myocardial infarction more than3 months previously.We describe here ten cases of ventricular

aneurysm following myocardial infarction seen inrecent years at this hospital.

Case reports

Case 1: P.McC., died age 69For I week before admission to hospital in

December 1965, this patient had been sufferingfrom anginal chest pain on exertion, and about24 hr prior to admission he began to experienceprotracted chest pain which was accompanied bysweating and breathlessness.On admission his pulse was 48/min, regular.

BP 130/80 mmHg. Heart sounds were of poorquality and there were crepitations at both bases.ECG showed the changes of a recent transmuralantero-septal infarction and sinus bradycardia.The serum glutamic oxalacetic transaminase(SGOT) level rose to 120 units (Dade).At the time of discharge 5 weeks later his ECG

continued to show R-ST elevation in the precordialleads. He returned to normal activity and wasfollowed up as an outpatient. Three months later,cardiac screening showed a marked prominenceof the left heart border in the right anterioroblique projection (Fig. 1) which was thought tobe an aneurysm. ECG still showed Q waves andR-ST elevation. One year after the original inci-dent he sustained a further infarction and wasre-admitted to hospital. His ECG at this timerevealed posterior ischaemia in addition to theabove changes. A temporary phase of A.V. dis-sociation occurred with frequent ventricularextra-systoles and small R waves appeared in V2.V3 and V4.He died suddenly on 26 December 1966.Necropsy: The heart was enlarged (530 g) with

both left and right ventricular hypertrophy, thewalls being 24 and 9 mm in thickness, respectively.Above the apex of the heart, there was a largeaneurysmal dilatation overlying which was a fib-rinous pericarditis with adhesions obliterating thepericardial space (Fig. 2). Section through the leftventricle showed the aneurysm filled with well

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776 Bernard M. Groden, Wilson B. James and Ian McDicken

FIG. 1. Case 1. P.McC. Prominence of left heart borderin RAO projection.

FIG. 2. Case 1. P.McC. Showing aneurysm above theapex of the heart.

organized, firmly adherent thrombus (Fig. 3).The wall of the aneurysm consisted of fibroustissue. The I.V. septum showed old and recentinfarctions and histological examination of sectionsfrom the I.V. septum confirmed this. Sectionsfrom the wall of the aneurysm showed it toconsist of dense acellular scar tissue with under-lying organized thrombus. There was no musclein this tissue.Comment. The aneurysm was almost certainly

the result of the infarction in November 1965.Death was due to arrhythmia following the secondinfarction.

Case 2: A.E., died age 70This patient was admitted to hospital in Novem-

ber 1965 for investigation of cardiac failure. Pulserate 96/min, BP 165/85 mmHg. The apex beatwas forceful, a third heart sound was present atthe apex, and crepitations were heard at the bases.ECG showed marked left axis deviation and Qwaves in leads V1 to V3. R-ST segments wereelevated in leads Vl to V4. Chest X-ray showedcardiac enlargement with an area of calcificationat the apex (Fig. 4). She improved with bed rest,digoxin and diuretics and was discharged home.The patient was re-admitted 1 year later with a

totally irregular pulse rate of 130/min. The apexwas 15 cm from the mid-line in the sixth left inter-

... .w.....

FIG. 3. Case 1. P.McC. Section of heart through aneur-ysm, which is filled with adherent thrombus.


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FIG. 4. Case 2. A.E. Chest radiograph (PA) showingcalcified aneurysm at the apex of the heart.

FIG. 5. Case 2. A.E. Showing aneurysm at apex ofheart.

space. The heart sounds were muffled and therewas a systolic murmur at the apex. Crepitationswere heard at both bases. ECG, apart from atrialfibrillation, was very similar to the one recordedpreviously. Chest X-ray showed cardiac enlarge-ment and pulmonary congestion and the area of

calcification was again noted. On this occasion adiagnosis of cardiac aneurysm was made. She didnot respond to treatment and died on 17 January1967 of bronchopneumonia and congestive cardiacfailure.

Necropsy. The heart was considerably enlarged(540 g). Near the apex, in the anterior wall of theleft ventricle, there was a large calcified aneurysm(Fig. 5). On opening the heart the left ventriclewas found to be markedly hypertrophied (30 mmin thickness). The aneurysmal opening was 3 cmin diameter and the wall of the aneurysm was thin,fibrotic and calcified. There was no thrombus inthe sac. There were no valve defects present. Thecoronary arteries were narrowed by atheroma butno occlusion by thrombus could be demonstrated.Histological examination of sections from the leftventricle showed extensive ischaemic changes inall areas examined. No recent infarction was seen.Sections of the wall of the aneurysm showedfibrosis, hyalinization of the connective tissue andcalcium deposition in the pericardium. In the sub-endocardial region there was a relatively thickcontinuous band of viable cardiac muscle.Comment. In retrospect the ECG abnormalities

detected in November 1965 were not the result ofrecent infarction but resulted from an infarctionat some undetermined time in the past.

Case 3: E.L., died age 53This patient who had a previous history of hypo-

thyroidism suddenly developed severe retrosternalchest pain on 5 December 1966 and was thoughtto have sustained a myocardial infarction. Thiswas confirmed by an ECG which showed thechanges of an early transmural antero-septalinfarction and a rise of SGOT. Left heart failuredeveloped and she died on 22 January 1967. ECGthroughout had shown R-ST elevation and Qwaves and there was little evidence of sequentialchange although she had been observed for about6 weeks in hospital.

Necropsy. The heart was slightly enlarged(400g), with a large bulge on the anterior wallof the left ventricle. The orifice of this aneurysmwas 8 cm in diameter (Fig. 6). At the site of theaneurysm the wall was extremely thin and fibrotic.The valves were normal. The coronary arterieswere extensively atheromatous and the descendingbranch of the left coronary artery was occluded.Pericardial adhesions were present over theaneurysm and obliterated the pericardial space.(No sections were examined histologically.)Comment. The appearance of the heart at

autopsy suggested that the aneurysm was exertingan haemodynamic effect, and may have beenpartly responsible for heart failure.

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Bernard M. Groden, Wilson B. James and Ian McDicken

FIG. 6. Case 3. E.L. Section of heart showing large thinwalled aneurysm of left ventricle with thrombus.

Case 4: A.C., died age 63This patient was admitted to hospital on 4 April

1967 with severe central chest pain radiating to hisarm, of 2-hr duration. Pulse rate 92/min regular,BP 170/90 mmHg. Acute myocardial infarctionwas diagnosed and confirmed by electrocardio-graphic changes of anterior transmural infarction,and a rise of SGOT and ESR. He was treated withbed rest and anticoagulants. His blood pressurefell after admission but gradually improved. Four-teen days after the infarction his cardiac outputas estimated by the photo-electric earpiece dyedilution technique, using Coomassie blue, was6-8 1/min. The ECG continued to show Q wavesand R-ST elevation and aVR was upright. Award radiograph revealed pulmonary congestion,bilateral pleural transudates, slight cardiac enlarg-ment and a small 'step' on the left heart borderwhich was thought to represent an aneurysm(Fig. 7). Cardiac failure became worse, his bloodpressure fell and despite treatment with diuretics,digoxin and oxygen, the patient died on 17 May1967. Cardiac output 48 hr prior to his death hadfallen to 2-6 1/min.

Necropsy: The heart was enlarged (450 g) duemainly to left ventricular hypertrophy (leftventricular wall thickness was 24 mm). On theantero-lateral aspect of the left ventricle there wasa large aneurysm almost completely filled with

FIG. 7. Case 4. A.C. Chest radiograph showing 'step'on left heart border.

layered thrombus (Fig. 8). The area of theaneurysm almost coincided with that of the infarc-tion. In the region of the I.V. septum, there was asmall area of recent infarction. The posteriorwall of the left ventricle was hypertrophied. Thedescending branch of the left coronary artery wasoccluded by thrombus overlying an area of athero-sclerosis. There was extensive pericarditis withfirm adhesions over the aneurysm. Histological ex-amination showed extensive infarction of theanterior wall of the left ventricle with stretchingand thinning of the tissue forming the wall of theaneurysm. Bundles of viable muscle fibres werefound in the wall of the aneurysm.Comment. In this case too the aneurysm may

have been partly responsible for the onset offailure and death.

Case 5: J.W., died age 51This patient was admitted on 31 March 1967

with chest pain which had been present for severalhours. Pulse rate 84/min, BP 120/80 mmHg. Adiagnosis of acute myocardial infarction was con-firmed by a rise of SGOT and of ESR and thetypical electrocardiographic changes of an exten-sive transmural anterior myocardial infarction.Three days after admission she developed furtherchest pain and pericardial friction was heard.ECGs continued to show the changes of acute

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myocardial infarction and persistent R-ST eleva-tion. A chest X-ray revealed cardiac enlargementwith some atelectasis at both lung bases. She diedon 18 April 1967.Necropsy. The heart size was normal (380 g).

The pericardial sac was filled with ante-mortemblood clot and there were fibrinous adhesionspresent between the heart and the pericardium. Ananeurysm (6 cm in diameter) extended from theapex of the left ventricle to the I.V. septum. Thewall of the aneurysm was composed of fibroustissue which had ruptured at several places andat one point there was communication between theventricles (Fig. 9). Within the aneurysm there wasorganized ante-mortem clot and several thrombiwere present in the right ventricle. An area of morerecent infarction was present in the I.V. septum.The coronary arteries showed marked atheroscler-otic changes and the descending branch of the leftcoronary artery was occluded by recent thrombus.

Sections from the aneurysm showed the wallto consist of organizing infarction with some areasof viable muscle.Comment. This is an example of rupture of an

aneurysm. It is unusual for this to occur in ananeurysm of long standing. The histologicalappearances in this case were compatible with theclinical impression that the aneurysm dated fromthe infarction at the time of admission.

Case 6: W.R., died age 79This patient was admitted on 19 May 1967 with

.....................~~~~~~~~~~~~~~.

FIG. 8. Case 4. A.C. Showing aneurysm coinciding witharea of infarction.

chest pain of 48 hr duration radiating to the leftarm and through to the back. Pulse rate 85/minregular, with good volume. BP190/110mmHg.The apex beat was heaving and was localized inthe fifth intercostal space outwith the mid-clavicu-lar line. A pericardial friction rub was heard allover the praecordium. Heart sounds were other-wise normal. ECG showed the changes of acutetransmural antero-septal myocardial infarctionand non-penetrating inferior infarction. Thepatient died suddenly 18 days after admission. Atthe time of death the R-ST segment was stillelevated.

Necropsy. The heart was considerably enlarged,weighing 730 g, mainly due to left ventricularhypertrophy. The wall of the left ventricle wasthickened (26 mm), at the apex of the left ventriclethere was a large thin-walled aneurysm. Themyocardium showed extensive infarction of theanterior and lateral surface of the left ventriclewith more recent infarction of the I.V. septum.On its endocardial surface, the aneurysm wascovered with friable thrombus while on the peri-cardial surface there was extensive haemorrhagicpericarditis, with numerous fine adhesions (Fig.10). The wall of the aneurysm was found toconsist of organizing infarct. In the sub-endocardial region viable cardiac muscle persisted.The myocardium of the posterior wall of theventricle was hypertrophied.Comment. This is another example of aneurysm

occurring soon after infarction.

FIG. 9. Case 5. J.W. Showing the heart with rupture ofaneurysm.

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FIG. 10. Case 6. W.R. This shows the heart cut through the aneurysm. There is gross leftventricular hypertrophy.

Case 7: A.H. (born 30 June 1909)This patient was referred to hospital in April

1965 because of breathlessness on exertion ofalmost 2 years duration. He also complained ofattacks of palpitation and stabbing praecordialpain of 5-6 months duration, but no true angina.Physical examination was not helpful. BP 130/75 mmHg. A chest X-ray revealed a marked bulgeon the left heart border suggestive of aneurysm,and fluoroscopy confirmed that it was expansile(Fig. 11). An electrocardiogram showed Q wavesin leads 1, aVL, V1-V5 and R-ST elevation inleads V2 and V3. Further close questioning at thisstage elicited history of an attack of chest painsome years previously which could have been dueto myocardial infarction. A diagnosis of post-infarction cardiac aneurysm was made and thepatient underwent aneurysmectomy on 20 October1965 under heart-lung bypass, at 30°C (Mr T. M.Welsh). The aneurysm was found to occupy theproximal half of the anterior panel of the leftventricle, the remainder of which was distinctlyfibrotic. It was filled with darkly coloured frag-mented clot. A firm fibrous margin in excess of0 5 cm thick was left leaving a large gap 5 cm indiameter, the edges of which were well clear ofvessels. A circle of pericardium was sutured to theinner aspect of the margin and the gap closed

with a piece of dacron. The post-operative coursewas complicated by a short-lasting confusionalstate and occasional chest pain but subsequentlyhe made a good recovery although he is stillbreathless on exertion and his electrocardiogramstill shows Q waves and R-ST elevation.Comment. The aneurysm in this case was pre-

sumably the result of the infarction several yearspreviously. The stabbing pain may have been dueto the pericarditis which is almost invariablypresent in association with aneurysm.

Case 8: I.S. (born 19 September 1898)This patient was admitted to hospital in 1961

with chest pain. A clinical diagnosis of myocardialinfarction was confirmed by electrocardiographicchanges of an inferior transmural infarction (Qwaves, in 2, 3 and aVF and R-ST elevation inthese leads) and rise of SGOT and ESR. BP 145/90 mmHg. She continued to have chest pain afteradmission and was treated in bed for 6 weeks andgiven anticoagulants. She was discharged after 9weeks in hospital. At the time of discharge R-STelevation was still present in leads 2, 3 and aVF.When she was seen in 1965 an area of expansilepulsation was noted in the third and fourth leftintercostal spaces and an ECG still showed R-STelevation in the inferior leads. A PA chest radio-

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FIG. 11. Case 7. A.H. PA chest radiograph showing large aneurysm, left heart border.

graph revealed a bulge on the left heart borderand cardiac screening showed paradoxical pulsa-tion (Fig. 12). Subsequently she has developedcongestive failure which has been controlled withdigoxin and diuretics. A recent electro-cardiogramshowed R-ST elevation in 2, 3 and aVF, potentialheart block and delayed intraventricular conduc-tion.Comment. This is the only patient in the present

series in whom clinical examination would suggestthe diagnosis of cardiac aneurysm.

Case 9: D.McD. (born 15 November 1907)This patient was admitted to hospital on 13 July

1966. It was believed that he suffered from rheu-matic heart disease, since he had been known tobe in atrial fibrillation for about 12 years. He wasin mild congestive failure. Pulse 100/min totallyirregular, BP 140/85 mmHg. Apex beat 11 cmfrom the mid-line and heaving in character. Therewere systolic and diastolic murmurs at the apex.The ECG confirmed atrial fibrillation with occa-sional ventricular extrasystoles. Q waves and R-STelevation were present in V1 and V2, and T waveswere inverted in V5 and V6. There was right axisdeviation and aVR was biphasic. It was consid-ered that these ECG changes were suggestive of

old anterior myocardial infarction with aneurysmformation. Cardiac screening showed cardiac en-largement, with prominence of the left ventricle.There was an aneurysmal bulge of the anteriorsurface of the heart best seen in the right anterioroblique projection, similar to that shown in Fig. 1(Case 1). Treatment with digoxin and diureticsproduced substantial improvement and he wasallowed home.Comment. The clinical and radiological features

of this case are more suggestive of post-infarctioncardiac aneurysm than of mitral valve disease,although both conditions could be present. Themurmurs can be explained by the passage of bloodto and fro through the neck of the aneurysm.

Case 10: W.T. (born 12 March 1904)This patient was referred to the Chest Clinic

of the hospital in May 1967 because of breathless-ness on exertion. He gave a history of a myocardialinfarction 15 years previously and physical exam-ination revealed a mild degree of congestive cardiacfailure. Pulse rate 90/min with extrasystoles, BP130/80 mmHg. ECG showed LBBB and sinusrhythm. Chest X-ray revealed a large plaque otcalcium along the left heart border which wasthought to be calcification in the wall of a cardiac

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FIG. 12. Case 8. I.S. Showing bulge on left heart border.

aneurysm (Fig. 13). Cardiac fluoroscopy confirmedthe presence of a bulge which exhibited diminishedpulsation.Comment. The aneurysm is almost certainly theresult of an infarction 15 years before.

Details of these ten patients are shown in Table 1.

FIG. 13. Case 10. W.T. Showing plaque of calciumalong left heart border.

DiscussionSchlichter, Hellerstein & Katz (1954) and Dub-

now et al. (1965) state that the presence of ananeurysm has serious prognostic significance. Thishas not been borne out by the studies of Douglas,Sferrazza & Marici (1962) and of Abrams et al.(1963). In the present series six of the patientsdescribed survived for more than 1 year afterinfarction with aneurysm formation, and three ofthese for more than 5 years. Four patients are stillalive. In seven patients the diagnosis was made inlife. Physical signs suggestive of aneurysm werepresent in only one patient (case 8) and diagnosisin the others was made on the basis of radiologicaland/or electrocardiographic findings. Fouraneurysms were discovered in the early stages afterthe infarction, and in another patient the diagnosiswas suggested by absence of sequential change onthe electrocardiogram after 3 months, andconfirmed by cardiac fluoroscopy. The other caseswere diagnosed at varying intervals up to 15 yearsafter the original incident. One aneurysm rupturedin the early stages (Case 5) and three patientsdied in congestive cardiac failure to which theaneurysm probably contributed in two. In onepatient, further infarction was the cause of deathand in this patient it seems unlikely that theaneurysm was exerting a functional effect since itwas filled with thick thrombus. One patient hasundergone surgery for the repair of his aneurysmand three patients are receiving medical treatmentonly.

Inadequate bed rest in the early stages after theinfarction is said to predispose to aneurysm forma-tion (Moyer & Hiller, 1951 ; Schlichter et al., 1954).Three of the cases reported were not rested at thetime of the myocardial infarction but all of theother patients had adequate periods of bed rest.A recent clinical study has suggested that schemesof earlier mobilization after infarction do not re-sult in an increased incidence of aneurysm forma-tion (Groden, Allison & Shaw, 1967).Hypertension has been implicated in aneurysm

formation because of the high pressures to whichthe healing infarct is exposed. It has not been afactor in any of our patients nor did Dubnowet al. (1965) feel that it was an important factor.An expansile aneurysm can absorb a consider-

able amount of cardiac output and behave func-tionally in the same way as mitral incompetencewhile a rigid, fibrosed or calcified aneurysm is un-likely to exert a significant functional effect. InCase 4 the cardiac output fell from 6-8 to 2-6 1/mwhile the aneurysm enlarged, but factors involvingmyocardial contractility must also be consideredas responsible for this. Surgery was not feasiblesince there was no precise information concerning

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TABLE 1

Ten cases of post-infarction cardiac aneurysm: clinical radiological, electrocardiographic and pathological features

PathologyAge at death Duration of

or when survival after Clinical ViableCase last seen infarction condition Radiology ECG LV hyper- muscle

(years) trophy in scar

I (P.McC.) 69 13 months Died Aneurysm at Persisting +fluoroscopy Q wave and

R-ST elevation2 (A.E.) 70 >1 year Died Calcification on Persisting Q waves + +

PA radiograph R-ST elevationAtrial fibrillation

3 (E.L.) 53 7 weeks Died Not done Q waves - Histology notR-ST elevation available

4 (A.C.) 64 5 weeks Died Bulge on PA Q waves + +radiograph R-ST elevation

aVR upright5 (J.W.) 51 3 weeks Died PA film-cardiac Q waves -

enlargement only R-ST elevation6(W.R.) 79 18days Died Notdone Qwaves + +

R-ST elevation7 (A.H.) 56 ?2 years Alive after Bulge on PA film Q-waves Histology not

aneurysmectomy Expansile pulsation R-ST elevation availableat fluoroscopy

8 (I.S.) 69 6 years Alive Bulge on PA film Q wavesTreated C.C.F. Paradoxical R-ST elevation

pulsation at (Leads 2, 3, aVF)fluoroscopy

9 (D.McD.) 65 ?12 years Alive PA film-LV + Q wavesFibrillation Bulge at Atrial fibrillation

fluoroscopy aVR biphasic10 (W.T.) 63 15 years Alive PA film-calcn LBBB

Dyspnoea on of myocardiumexertion Bulge atNo failure fluoroscopy

the extent of the recent infarction and whethersuture would be possible after the aneurysm hadbeen excised. The patient who was submitted forsurgery has done reasonably well.From a review of the literature and from our

own observations we feel that the indications forsurgery are as follows:

(1) Expansile cardiac aneurysm with persistentcardiac failure not responding to medicaltreatment.

(2) Repeated systemic emboli not controlled byanticoagulant treatment.

We would be reluctant to recommend opera-tion on a heart in which there is fresh infarctionbefore organization of the necrotic tissue has takenplace. It would appear that at least 6 weeks andpossibly 3 months would have to elapse before thishas occurred (Mallory, White & Salcedo-Salgar,1939). Since organization takes place from the

periphery of the aneurysm, surgery might be con-sidered even in the early stages after the infarct,in cases with a poor immediate prognosis.Although the physical findings associated with

aneurysm are well known and have been fullydescribed previously (Parkinson et al., 1938) thediagnosis is seldom made in life (Holmes & Mac-Fadyen, 1964). In this series of ten cases only onepatient demonstrated clinical features which sug-gested a diagnosis of aneurysm. It was possible tomake a diagnosis of cardiac aneurysm from thepostero-anterior and lateral radiographs of six ofthe ten cases. In another case cardiac enlargementwas noted radiologically and with the lack of se-quential change on the ECG, cardiac aneurysm wassuspected. We have found careful cardiac fluoro-scopy using an image intensifier television systemto be useful in detection of even small cardiacaneurysms (Groden & James, 1968). Althoughrecent reports have indicated the value of angio-

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784 Bernard M. Groden, Wilson B. James and Ian McDicken

graphy (Holmes & MacFadyen, 1964; Bjork, 1966Steinberg, 1966; Gorlin et al., 1967), it was notnecessary in any of the patients described here.In many of the reports in which angiography hasbeen used the diagnosis was apparent from conven-tional radiological examination. If surgery werecontemplated on the basis of the indications dis-cussed above we would proceed to ventriculo-graphy and coronary arteriography would becarried out at the same time in order to assess thestate of vascularity of the myocardium.

Persistent Q waves and R-ST elevation morethan 6 months after infarction are said to behighly suggestive of aneurysm formation (Rosen-berg & Messinger, 1949; Ford & Levine, 1951;Moyer & Hiller, 1951 ; Douglas et al., 1962). Thisphenomenon was present in all but one of the caseswho had long-standing aneurysms. Sequentialchanges were noted to be absent in the electro-cardiogram of those patients who died in the earlystages after the infarction. The reason for persis-tent R-ST elevation is not clear but several hypo-theses have been put forward. Ford & Levine(1951) suggest either: (1) that there is a layer ofischaemic subendocardial muscle in these heartsand that an intraventricular ECG would displayR-ST elevation which is recorded on the anteriorsurface through the 'aneurysmal window', or (2)that R-ST elevation results from the pericarditiswhich commonly exists in these cases. Moyer& Hiller (1951) suggest that hypertrophy of thesurrounding muscle is responsible. Table 1 givesan indication of the frequency of these findings inour cases. An upright QRS in aVR in the presenceof LV hypertrophy has also been reported to besuggestive of aneurysm (Goldberger & Schwartz,1948; Ford & Levine, 1951). This was present inone of our patients (Case 4) and aVR was bi-phasic in another (Case 9).

AcknowledgmentsWe would like to express our gratitude to the Physicians

of the Southern General Hospital for permission to reportdetails of patients under their care, and to Mr T. Welsh forproviding us with the operation notes on Case 7. We wouldalso like to acknowledge the assistance and helpful advice ofDr Gavin Shaw in the preparation of the manuscript andof Dr A. Dick of the Department of Pathology.

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DOUGLAS, A.M., SFERRAZZA, J. & MARICI, F. (1962) Naturalhistory of aneurysm of ventricle. N. Y. St. J. Med. 62, 209.

DUBNOW, M.H., BURCHELL, H.B. & TITUS, J.L. (1965) Postinfarction ventricular aneurysm. Amer. Heart J. 70, 753.

FORD, R.V. & LEVINE, H.D. (1951) The electrocardiographicclue to ventricular aneurysm. Ann. intern. Med. 34, 998.

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cardiac after myocardial infarction · to have sustained a myocardial infarction. this was...

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