developingcardiac rupture initial sign acute...

British Heart Journal, 1976, 38, 1073-1079.

Developing cardiac rupture as initial sign ofacute myocardial infarction

J-P. van Mantgeml and A. E. BeckerFrom the Department of Pathology, University of Amsterdam, Wilhelmina Gasthuis, Amsterdam, The Nether-lands

Pathological data are given of 4 patients in whom the development of cardiac rupture was the initial signof myocardial infarction. The term 'concealed cardiac rupture' is proposedfor this condition. In each instancethe clinical diagnosis was 'onset of infarction', whereas the necropsy suggested that the acute onset ofsymptomswas caused by the start of rupture.

The arguments for classifying the cases as 'concealed rupture' are (1) the lack of correlation betweenhistological and clinical dating of the infarct, (2) the observation that the tear may take considerable timebefore actual epicardial breakthrough occurs, and (3) the fact that a high percentage of infarcts may passclinically unnoticed.

Cardiac tamponade is at present an important causeof death in patients with acute myocardial in-farction. At the coronary care unit of the depart-ment of cardiology an incidence of 27 per centwas found among patients who died of acuteinfarction (Lie, Roels-van Ijsseldijk, and VanCapelle, 1975). To the clinician the occurrence ofcardiac rupture is often sudden and unexpected,since definite warning signs are not present.However, morphologists have previously suggestedthat the heart specimen often shows featuresindicative of a delayed rupture (Lautsch andLanks, 1967). It has also been stated that occa-sionally a patient may present with symptoms ofacute infarction, which actually represented thestart of the rupture (Lautsch and Lanks, 1967;Van Tassel and Edwards, 1972). In a recentcorrelative study of 50 patients with cardiactamponade this was confirmed (Becker and vanMantgem, 1975). The term 'concealed rupture'was proposed to indicate the circumstance in whichsuch a lack of correlation existed between clinicalsymptomatology and morphological features. It isthe purpose of this report to re-emphasize theoccurrence of this phenomenon.

Received 8 December 1975.

LArmy reserve Medical Officer stationed at the Departmentof Pathology, University ofAmsterdam, Wilhelmina Gasthuis.

Case reportsCase 1A 61-year-old woman was known to have hyper-tension for 7 years. She first complained of pain inthe left arm after a minor traffic accident. Twodays later she developed vague pain in the chest.However, after two more days she suddenly ex-perienced severe chest pain and she collapsed. Onimmediate admission she was sweating. Physicalexamination revealed a systolic blood pressure of70 mmHg and a heart rate of 110 per minute.The central venous pressure judged from thejugular veins was not raised. The electrocardiogramshowed the signs of recent anterolateral myocar-dial infarction. She rapidly developed signs ofcardiogenic shock. She was treated with ligno-caine, but no anticoagulants were given. Sixteenhours after admission she suddenly died.The necropsy showed a large transmural myo-

cardial infarction in the anteroseptal wall of theleft ventricle. It showed a central rupture whichhad led to a tamponade of 400 ml blood. At thesite of rupture there was a distinct erosion of thenecrotic myocardium (Fig. 1A). The actual tearwas slit-like and located at the top of the erosion.Thrombus was covering the site of rupture andpart of the eroded area. There was two-vesseldisease of the coronary arteries, with total recentocclusion of both the anterior descending artery

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FIG. 1 Case 1. The clinical dating of the infarct was 16 hours. (A) The gross aspect ofpart of the anterolateral wall of the left ventricle. The transmural infarct is seen. At the siteof rupture an erosion of the affected myocardium has occurred. The actual epicardial break-through cannot be seen. (B) A representative microscopical section of the infarcted myocardium.There is massive infiltration of dead myocardium by polymorphonuclear leucocytes. This isnot in agreement with an infarct of 16 hours' duration but, instead, suggests that the vaguecomplaints two days before admission represented the onset of infarction. The erosion at thesite of rupture indicates a slowly progressive tear. Therefore, the sudden onset of severe chestpain could have been caused by the onset of the rupture process. (Haematoxylin and eoszn.

x 200.)

and the left circumflex branch.Microscopical sections of the infarct showed a

massive leucocytic infiltration of the necroticmyocardium, indicative of a myocardial infarctionof a much older date than the 24 hours indicated bythe clinical history (Fig. 1B). In retrospect, there-fore, this patient probably experienced an infarctionafter her minor traffic accident, while the acuteepisode in effect represented the onset of rupture.

Case 2A 53-year-old man had complained for some weeksof intermittent chest pain, occasionally radiatingtowards the left arm. The pain was always related

to periods of emotional disturbance. Four daysbefore death he woke up in the middle of the nightwith severe chest pain, radiating to the left arm andaccompanied by heavy sweating. He was admittedto hospital 4 hours later and on examinationshowed a blood pressure of 160/110 mmHg, witha heart rate of 100 per minute. His central venous

pressure was not raised, as judged from the neckveins. The electrocardiogram showed recent in-ferior wall infarction. He was treated with lignocaineand he was given anticoagulants. The pain dis-appeared. The next day he developed signs ofacute abdominal distress, for which no conclusiveexplanation was found. Three days later, that is 4

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Cardiac rupture 1075

FIG. 2 Case 2. The clinical dating of the infarctwas 4 days. (A) Microscopical section of the tear inthe posterior wall of the left ventricle, at the junctionwith the ventricular septum (VS). The site ofrupture shows an erosion at the inner aspect of theaffected myocardium covered by thrombus (T).(B) A detailed view of a representative section ofthe infarct. It is characterized by a proliferation offibroblasts and capillaries, indicative of an earlyreparative response. A recent haemorrhage, secondaryto the dissecting tear, is present. These features are

not in agreement with an infarct of 4 days but,instead, fit an infarct of between 1 and 3 weeks old.In retrospect this could correlate with the patient'shistory. (Haematoxylin and cosin. A x 4 7, B x 165.)

days after admission, he suddenly died.The necropsy confirmed the presence of a large

transmural inferior wall infarct, which extendedfrom the apex to the base of the heart and alsoinvolved the posteromedial papillary muscle group.

The heart had ruptured posteriorly, close to theventricular septum (Fig. 2A). There was a tam-ponade of 500 ml blood. The coronary arteries

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FIG. 3 Case 3. The clinical dating of the infarctwas 24 hours. (A) The gross aspect of the rupturesite in a transmural anteroseptal myocardial infarct.The area shows a distinct erosion, covered withthrombus (T). The rupture is located centrallyin the infarct. (B) A microscopical view of thesame area in which the localized loss of myocardiumand subsequent covering by thrombus (T) is againseen. (C) A representative microscopical section ofthe infarct. Thore is massive infiltration by poly-morphonuclear leucocytes, indicative of an infarctolder than 24 hours. (Haematoxylin and eosin.B x2.0,C x130.)

showed two-vessel disease, with total occlusionsdistally in the right coronary artery and proximallyin the anterior descending branch. There were nosigns of previous myocardial infarctions.The microscopy of the myocardium showed signs

of an early reparative response with ingrowth offibroblasts and capillaries (Fig. 2B). The cellular



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infiltrate was mainly composed of macrophages,carrying lipofuchsin and iron pigments, and thesechanges were consistent with an infarct of asomewhat older date than the 4 days judged fromthe clinical history. In fact, the histological datingsuggests myocardial infarction of somewhere be-tween 1 and 3 weeks earlier. Again the distinct dis-crepancy suggested concealed rupture, in a silentinfarct. The sudden onset of symptoms 4 daysbefore death could represent the onset of rupture.There were no signs of acute infarction.

Case 3A 70-year-old man was known to have had hyper-tension for two years. He occasionally complainedof chest pain during the night. One day before deathhe was rushed to hospital, after collapsing at home.The electrocardiogram revealed recent antero-septal myocardial infarction. He rapidly developedsigns of cardiogenic shock. Anticoagulants were notadministered. He died suddenly one day afteradmission.The necropsy confirmed the presence of a

recent transmural anteroseptal myocardial infarctwith rupture and tamponade (Fig. 3A). The amountof blood in the pericardial cavity was 300 ml. Themyocardium at the site of rupture showed extremethinning, with loss of necrotic muscle and adherentthrombosis (Fig. 3A and B). The rupture hadoccurred through a moderately thinned area. Theheart exhibited one-vessel disease, restricted to theanterior descending artery. The vessel showed arecent total occlusion in its proximal segment.The aortic valve was slightly calcified, complicatinga congenitally bicuspid valve. The left ventriclewas very hypertrophic.

Microscopical studies of the myocardium showeda massive infiltration with polymorphonuclearleucocytes, indicative of myocardial infarctionof more than one day's duration (Fig. 3C). Basedupon the microscopical studies the 'age' of theinfarct was estimated as between 3 and 7 days. Themorphological aspects, therefore, suggest that thiswas another example of concealed rupture. Thesudden clinical onset probably represented theonset of rupture in the setting of an unrecognizedinfarction.

Case 4A 54-year-old man suddenly developed chest painaccompanied by nausea and sweating 5 days beforedeath. The pain disappeared spontaneously oneday later. Three days later, that is one day beforedeath, he suddenly collapsed while shaving. Onimmediate admission he had signs of cardiogenic

shock. The electrocardiogram showed acute postero-infero- and lateral wall infarction. He was givenanticoagulants. One day after admission he de-veloped signs of mitral regurgitation, and fourhours later he suddenly perished.The necropsy confirmed the diagnosis of a large

transmural posteroinferior wall infarct extendinginto the lateral wall of the left ventricle (Fig. 4A).A rupture in the posterior free wall had occurred,resulting in a tamponade of 400 ml blood. Inaddition to the free wall rupture, a partial ruptureof the posteromedial papillary muscle group waspresent (Fig. 4A). The latter could account forthe sudden onset of signs of mitral regurgitation.Examination of the coronary arteries showed one-vessel disease, with a recent complete occlusiondistally in the dominant right coronary artery.There were no signs of previous myocardialinfarction. Microscopical studies of the infarctrevealed a massive leucocytic infiltration of approxi-mately 3 to 7 days. It was concluded, therefore, thatthe sudden onset of chest pain 1 day before deathprobably represented the onset of rupture. Itcould well be that the period of chest pain experi-enced 5 days before death and which spontaneouslysubsided was the moment of onset of infarction.

Discussion

It has been suggested by Lautsch and Lanks (1967),from a morphological study of heart rupture cases,that features often existed indicating a delayedrupture. These authors concluded, from theircorrelation between morphological studies andclinical histories, that in some instances the onsetof symptoms could have been caused by the onsetof rupture. Van Tassel and Edwards (1972), in arecent study of 28 hearts from patients with afree wall rupture, also found evidence to supportthis concept. Recently the term 'concealed rupture'has been proposed for this phenomenon (Beckerand van Mantgem, 1975).The term is intended for cases where the actual

onset of rupture is clinically 'concealed' andinterpreted as the onset of infarction. The term isproposed to contrast the common situation in whichthe dramatic episode of rupture, though unpredic-ted, is well recognized within the setting of anacute infarction. The observations described herehave in common that in each of the 4 instancesevidence existed for 'concealed rupture'. Thisconclusion is based upon a series of considerations.

Firstly, histological examination of the infarctedmyocardium shows a pronounced difference in theage of myocardial necrosis. It is, of course, appre-ciated that an exact time-table of the reparative



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FIG. 4 Case 4. The clinical dating of the infarct was approximately I day. (A) Gross aspectof opened left ventricle. The cut surface shows a haemorrhage secondary to the rupture. There wasa posteroinferior wall infarct extending into the lateral wall. A partial rupture of the postero-medial papillary muscle group has occurred (arrow). The actual breakthrough is posteriorlyand cannot be recognized in this view. (B) Distinct demarcation of dead myocardium by a zoneof polymorphonuclear leucocytes. A recent haemorrhage related to the rupture is present in theouter part of the left ventricular wall. (C) A detailed view of a representative microscopicalsection. The infarct shows massive infiltration with polymorphonuclear leucocytes, indicativeof an injury older than 1 day. This lends support to the view that the sudden onset of chest pawinonedaG before death could represent the onset of rupture. (Haematoxylin and eosin. B xa46,Cx95.)



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responses upon infarction cannot be given. How-ever, it is widely agreed that the invasion of themyocardium by polymorphonuclear leucocytesneeds time to evolve. The classical studies ofMallory, White, and Salcedo-Salgar (1939) haveshown that the earliest invasion with leucocytescan be expected approximately 24 hours after theonset of infarction. Personal experiences are inagreement with this statement. Therefore, thefindings in Cases 1, 3, and 4 are considered to beof significance. In each of these instances themicroscopical studies showed massive infiltrationwith leucocytes, which were also present in thedeeper parts of the affected myocardium. Since thepeak of leucocytic infiltration is generally thoughtto occur somewhere between 3 and 7 days after theonset of infarction, the myocardial necrosis in the3 patients is considered to be of an older 'age' thanthe clinical history suggests. The same holds truefor Case 2 in whom the infarction was clinicallyconsidered to be 4 days old, whereas the histologyshowed early fibroblastic and capillary prolifera-tion. The cellular reaction, i.e. macrophagescarrying lipofuchsin and iron pigments, was also inkeeping with a reparative response of approximately1 to 3 weeks.The second argument is based upon the gross

aspect of the actual rupture site. In each of thefour instances the site of rupture showed a distincterosion of the necrotic myocardium. It has beenshown that this type of rupture coincides withmyocardial infarction of a somewhat longer stand-ing (Becker and van Mantgem, 1975).

Apparently, the 'erosion' needs time, thoughexamples are present where the phenomenon oferosion had occurred in about 24 hours. It is anindication, however, that the tear leading to tam-ponade is not necessarily a sudden event. Instead,the 'erosion' in our opinion indicates that a con-siderable time lapse may exist between the onset ofthe tear and the actual epicardial breakthrough.This endorses the opinion previously expressed bymorphologists (Lautsch and Lanks, 1967; VanTassel and Edwards, 1972; Becker and van Mant-gem, 1975) and is in keeping with a number ofclinical reports, some of which indicate the possi-bility of early recognition and surgical intervention(Lillehei et al., 1969; Buckley et al., 1971; Mundth,1972; Lofstrom et al., 1972; O'Rourke, 1973;Cobbs, Hatcher, and Robinson, 1973; Calicket al., 1974).A third argument is based upon the clinical

history of the patients. In retrospect, each of thepatients experienced symptoms which could wellbe attributed to the onset of infarction. For various

reasons, however, these symptoms were notinterpreted as such. It seems likely that each ofthese patients experienced an infarct, with onlyminimal or non-specific signs, for some time beforeadmission. Indeed, the high frequency of undiag-nosed or clinically 'silent' infarction among alarge necropsy series has previously been empha-sized (Melichar, Jedlicka, and Havlik, 1963).What then caused the sudden onset of symptoms?

The possibility of recurrent infarction should beconsidered. However, the postmortem studies didnot support this supposition. In each instance thetear went through the infarct, which itself showedthe lack of correlation with the clinical history asdiscussed previously. The aspect of the tear,moreover, endorses the view that the process ofrupturing took some considerable time. This, then,leads to the concept that the moment of suddenpain, interpreted as the onset of an infarction,represented the onset of rupture.

We are grateful to our clinical colleagues and in particular toDr. K. I. Lie, Department of Cardiology, WilhelminaGasthuis, Amsterdam, for his help in evaluating the clinicalrecords.

References

Becker, A. E., and van Mantgem, J-P. (1975). Cardiactamponade. A study of 50 hearts. European Journal ofCardiology, 3, 349.

Buckley, M. J., Mundth, E. D., Daggett, W. M., DeSanctis,R. W., Sanders, C. A., and Austen, W. G. (1971). Surgicaltherapy for early' complications of myocardial infarction.Surgery, 70, 814.

Calick, A., Kerth, W., Barbour, D., and Cohn, K. (1974).Successful surgical therapy of ruptured myocardium.Chest, 66, 188.

Cobbs, B. W., Jr., Hatcher, C. R., Jr., and Robinson, P. H.(1973). Cardiac rupture. Three operations with two long-term survivals. Journal of the American Medical Associa-tion, 223, 532.

Lautsch, E. V., and Lanks, K. W. (1967). Pathogenesis ofcardiac rupture. Archives of Pathology, 84, 264.

Lie, K. I., Roels-van Ijsseldijk, Y. C., and Van Capelle,F. J. L. (1975). Factoren die de prognose van het acutehartinfarct beinvloeden. Nederlandsch Tijdschrift voorGeneeskunde, 119, 466.

Lillehei, C. W., Lande, A. J., Rassman, W. R., Tanaka, S.,and Block, J. H. (1969). Surgical management of myo-cardial infarction. Some promising concepts utilizingrevascularization, mechanical circulatory assistance, oper-ative treatmnent of severe complications, and cardiacreplacement. Circulation, 39-40 (Suppl. IV), 315.

Lofstrom, B., Mogensen, L., Nyquist, O., Orinius, E.,Sjogren, A., and Werner, B. (1972). Studies of myocardialrupture with cardiac tamponade in acute myocardialinfarction. III. Attempts at emergency surgical treatment.Chest, 61, 10.

Mallory, G. K., White, P. D., and Salcedo-Salgar, J. (1939).The speed of healing of myocardial infarction. A study ofthe pathologic anatomy in seventy-two cases. AmericanHeart journal, 18, 647.

Melichar, F., Jedlicka, V., and Havlik, L. (1963). A studyof undiagnosed myocardial infarctions. Acta MedicaScandinavica, 174, 761.



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Mundth, E. D. (1972). Rupture of the heart complicating cases including nine examples of left ventricular falsemyocardial infarction. Circulation, 46, 427. aneurysm. Chest, 61, 104

O'Rourke, M. F. (1973). Subacute heart rupture followingmyocardial infarction. Clinical features of a correctable Requests for reprints to Dr. A. E. Becker, Depart-condition. Lancet, 2, 124.enofPtooyWfhliaGsus,EreVan Tassel, R. A., and Edwards, J. E. (1972). Rupture of ment of Pathology, Wilhelmi Gasthuis, Eersteheart complicating myocardial infarction. Analysis of 40 Helmersstraat 104, Amsterdam, The Netherlands.



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