atrial infarction the heart -...

Atrial Infarction of the HeartBy CHI KONG Liu, M.D., GILBERT GREENSPAN, M.D.,

AND RONALD T. P1ccIRILLO, M.D.

CLINICAL REPORTS of atrial infarctiondiagnosed during life are few. This

may be due to two major factors. First, theclinical features of isolated atrial infarctionare not known, for it is usually associatedwith ventricular infarction, which dominatesthe clinical picture. Secondly, the diagnosisof atrial infarction can be made only fromthe electrocardiogram by small, transientelevations' and reciprocal depressions of theP-Ta segment usually associated with changesin configuration of the P wave.

Langendorf,2 in 1937, reported one case ofatrial infarction found at autopsy that inretrospect could have been recognized antemortem from electrocardiographic changes.Subsequently, the electrocardiographic mani-festations of atrial infarction in the standardleads were described3-6 in cases in whichnecropsy evidence had prompted a retrospec-tive reinterpretation of the electrocardiogram.

Hellerstein,7 in 1948, reported the first casewith the correct ante mortem diagnosis ofatrial infarction confirmed by necropsy, andother cases were subsequently reported.8-10The number of cases described, however, isfar below the anticipated percentage of 3 to17 reported by others.3 11,12The purpose of this paper is to present the

changes in the 12-lead electrocardiogram fromsix cases of atrial infarction associated withventricular infarction, which were diagnosedclinically and confirmed by autopsy.

Case ReportsCase 1A 54-year-old diabetic, hypertensive woman en-

tered the hospital because of mental confusionand convulsive seizures. Four days later rapidatrial fibrillation developed that stopped shortly

From the Departments of Medicine, Los AngelesCounty Harbor General Hospital, Torrance, California,and the University of California at Los Angeles,California.

after intravenous lanatoside C. The P waves wereof the negative-positive type in lead I, predomi-nately negative in V,, and largely positive in V3(fig. la). Changing contour of the P wave in leadI suggested a wandering pacemaker. The P-Tasegment was depressed in leads III, aVF, V1, andV2, and was elevated in leads I, aVL, V5, and V6.Complete left bundle-branch block was present.A diagnosis of atrial infaretion was made. Thecharacteristic P-Ta changes in aVL and V5 almostcompletely disappeared during the next 3 days(fig. ib). The patient died 3 weeks later in coma.The serum glutamic oxaloacetic transaminase levelswere 62 and 36 units.Necropsy revealed a 1-cm.2 hemorrhagic area

on the endoeardial surface of the anterolateral wallof the right atrium, at the atrioventricular junc-tion. Small hemorrhagic areas, 2 mm. in diameter,were seen on the endocardial surface of the leftatrium. The left circumflex coronary artery nearits origin was completely occluded.

In the atrial myocardium (fig. 2) were severalareas of hemorrhagic necrosis surrounded by amild neutrophilic and lymphocytic infiltration.There was moderate patchy fibrosis. The left ven-tricular myocardium showed necrosis.Case 2A 54-year-old white man entered the hospital

complaining of chest pain with shortness of breathfor 2 weeks. The electrocardiogram revealed in-complete left bundle-branch block (fig. 3), occa-sional premature atrial contractions, and a briefrun of atrial tachycardia at 160 per minute. TheP-Ta segment was depressed in leads II, III,aVF, all the precordial leads, and elevated in aVL.The P waves were of the positive-negative varietyin V,. The serum glutamic oxaloacetic transaminaselevels were 58 and 56 units. Since there was noevidence of acute ventricular myoeardial infare-tion, a diagnosis of isolated atrial infarction wasmade. The patient was digitalized for mild con-gestive heart failure. He died suddenly 2 dayslater.Autopsy revealed severe generalized coronary

arteriosclerosis with a recent thrombus occludingthe left anterior descending coronary artery andan old occluding thrombus of the right coronaryartery. An extensive infarction was seen in theventricular septum from the anterior to the pos-terior wall of the left ventricle. The hemorrhagicarea of the left ventricle extended into the left

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Figure 1Left, case 1. Electrocardiogram 30 minutes afterlanatoside C shows abnormal P and P-Ta wavesand complete left bundle-branch block. Right,Case 1. Notched P waves are seen in lead I. P-Tasegments in aVL and V5 have almost returned tonormal.

posterior atrial wall and appendage. Grossly theright atrium appeared normal.

Microscopically both atria showed perivascularlymphocytic infiltration, hemorrhage, necrosis, andhyalinization of the muscle fibers, typical ofinfarction (fig. 4).Case 3A 62-year-old white woman with severe ulcera-

tive colitis, developed tachycardia with occasionalpremature beats, dyspnea, chest pain, and con-gestive heart failure. The next day the patienthad more cardiac pain, transient multifocal atrialtachycardia of 200 per minute and hypotension.An electrocardiogram (fig. 5) at that time re-vealed a septal and inferior ventricular myocardialinfarction. The P waves in lead II were wide andslurred and 1.25 mm. high in lead II. In V1 andV2 the P waves were diphasic and were followedby a depression of the P-Ta segment of 1.5 to1.8 mm. The P waves were notched in V3 and V4and low and notched in V5 where the P-Ta segmentwas elevated 1.0 to 1.5 mm. The P wave in V6was wider and the P-Ta segment was slightlyelevated. The deviations of the P-Ta segments inV5 and V1 and V2 probably represented reciprocalchanges of an atrial injury current. A definitediagnosis of left atrial infarction was made. Thepatient died 4 hours later in shock.Necropsy showed a 1 by 2 em. area of hemor-

rhage in the left atrium and infarction of theinterventricular septum. The coronary arteriesshowed only slight arteriosclerosis, with no occlu-sion. Microscopically congestion of the vessels andhemorrhages into interstitial tissue were compatiblewith an early stage of atrial infarction.Case 4A 52-year-old white man had repeated episodes

of congestive heart failure for 4 years. An electro-cardiogram (fig. 6) revealed incomplete leftbundle-branch block and evidence of left ventricu-lar enlargement. The P-R interval was 0.22 second.The P waves were notched in I, II, III, andaVF with depression of the P-Ta segment. InaVL the P-Ta segment was elevated 0.5 mm. TheP waves in V1 and V2 exhibited a slight positiveand wide negative wave with a total durationof 0.11 second. A diagnosis of atrial infarctionwas suggested.

Three weeks later chest pain and increasedfailure occurred. The serum glutamic oxaloacetictransaminase levels were 207 and 316 units, and thewhite blood count and temperature were elevated.An electrocardiogram showed changes in the Pwaves and P-Ta segments. The P waves in leadsV1 3 were biphasic and 0.10 second wide; in leadsI, II, and aVF, the terminal portions of the Pwaves were depressed and notched. The P-Ta seg-ments were depressed in leads I, II, III, aVF, andV6 and elevated in aVR. Terminally the P-Ta seg-

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ATRIAL INFARCTION OF HEART

Figure 2Case 1. Section of the atrium shows focal fibrosisand necrosis of the myocardium with polymorpho-nuclear infiltration.

ment became more depressed in lead I, and theterminal part of the P wave was more negative,being depressed 4 mm. in V1.At autopsy the heart weighed 650 Gm. A 2

by 2 cm. clot was adherent to the posteriorsurface of the right atrium. Thrombi were alsopresent on the posterior wall of the left ventricle.The coronary arteries showed extensive arterio-sclerotic changes. Moderate interstitial fibrosis waspresent histologically. An area of acute inflam-matory change with necrosis was seen under themural atrial thrombus.Case 5A 79-year-old white man was admitted to the

hospital because of chest pain of 2 weeks' dura-tion associated with nausea and vomiting. He hadbasilar rales but no other signs of congestiveheart failure. Leukocytosis was present initially,and the sedimentation rate became elevated. Aninitial electrocardiogram (fig. 7) showed sub-endocardial injury of the posterior surface ofthe left ventricle. The P-Ta segments were de-pressed 1 mm. in leads V1 3 and elevated from1.0 to 1.5 mm. in leads V5 and V6. The P-Tasegments in the limb leads were obscured by achanging T-P baseline. These changes in the P-Tasegments varied in subsequent tracings and adiagnosis of atrial infarction was made. thepatient became cyanotic and hypotensive and diedin 1 week. The serum glutamic oxaloacetic trans-aminase levels varied from 17 to 34 units.At autopsy the heart weighed 300 Gm. The

myocardium of the left and right ventricle wasflabby and contained numerous petechiae and focalhemorrhages as did the posterior third of theinterventricular septum. There were also hemor-


Figure 3Case 2. Electrocardiogram shows incomplete leftbundle-branch block and no evidence of acuteventricular infarction and P-Ta segment devia-tions. An atrial premature beat is seen in V6.

rhages in the posterior wall of both atria extendingdown to the atrioventricular junction. The rightcoronary artery was occluded 3 cm. from its originby a thrombus and the left circumflex was occludedby a fresh thrombus. Histologic sections showedchanges of acute myocardial infarction withnecrosis and a large area of subepicardial atrialhemorrhage.Case 6A 72-year-old white man entered the hospital

because of severe congestive failure and pain inthe arms of 1 week's duration. Moderate congestiveheart failure followed a myocardial infarction 3years earlier. A leukocytosis of 23,000 per mm.3and a serum glutamic oxaloacetic transaminaselevel of 26 units were present on admission. Anelectrocardiogram (fig. 8) revealed sinus tachy-

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Figure 4Case 2. Section of the atrium shows congestionof the small vessels with hemorrhage and necrosisand hyalinization of the muscle fibers.

cardia with a wandering pacemaker, prematureatrial beats, and rare premature ventricular beats.The P wave was positive-negative in V1 3. Therewas also evidence of apical myocardial infarction,age undetermined. Subsequently supraventriculartachycardia and electral alternans appeared (fig.8, lower). A diagnosis of atrial infarction wasmade. Finally ventricular tachycardia appeared andthe patient died.At autopsy the heart weighed 750 Gm.; it

showed bilateral hypertrophy, an old scar at theapex, and a mural thrombus in the right atrium.The proximal portion of the left coronary arterywas slightly narrowed by a calcium plaque. His-tologic sections revealed the old apical infarctionof the ventricle and showed an atrial infarctionunder the mural thrombus with subendocardialnecrosis.

Results and DiscussionThe clinical diagnosis of atrial infarction

was made correctly ante mortem in six casesfrom the electrocardiogram. Both atria wereinvolved in cases 1, 2, and 5, the right atriumalone in cases 4 and 6, and the left atriumin case 3. All cases had associated ventricularinfarction. Changes of the P-Ta segment inthe precordial leads were especially helpfulin cases 1, 3, and 5. The diagnosis of atrialinfarction is easily missed because the changesare less dramatic than those of the ventricularinfarction usually accompanying it. Conse-quently relatively few cases have been re-ported in the literature, despite the reportedincidence of 1 to 17 per cent among ventric-ular myocardial infarctions.3 13 14 The widerange may be due to the varying care and

criteria for its autopsy diagnosis. The atriumunderlying a mural thrombus is probablyrarely sectioned for histologic study, and incases of ventricular infarction with grosslynormal atria, histologic sections of the atriaare seldom made.

Atrial infaretions produced experimentallyin dogs and cats have been studied byAbramsonl5 and several other investigators,16-19 but the diagnostic electrocardiographiccriteria have not been agreed upon. Elevationsand depressions of the P-Ta segment havebeen of prime importance in the diagnosisof this condition. Analysis of the electro-cardiograms of the patients presented showsthat the P-Ta segment, when plotted vec-torially, is directed toward the area of atrialinfarction. This may be analogous to thedirection of the current of injury (S-Tsegment) in ventricular infarction.20 There-fore this segment might be called P-STa-Tarather than the P-Ta segment. Because thereis little atrial gradient,2' a direct comparisonbetween ventricular repolarization and atrialrepolarization may not be possible. For wantof a better term, we use the P-Ta segmentwith the above understanding. The P-Ta seg-ment usually extends through the QRS andS-T sections of the electrocardiogram, so thatits complete examination is impossible unlesscomplete heart block is present.

In our only case of isolated right atrialinfarction (case 4, fig. 6) the P-Ta segmentvector was directed to the right atrium andposteriorly. The P-Ta segment was depressedin leads I, II, III, aVF, V1, V2, and occasion-ally V3. It became isoelectric in lead V6.It was elevated in leads aVR and aVL. Inisolated left atrial infarction (case 3, fig.5) the P-Ta segment was depressed in leadsII, III, aVF, V1, V2, and elevated in I, aVR,aVL, V5, and V6. In bilateral infarction thedirection of the P-Ta segment vector maydepend on which atrium is infarcted themore. In cases 1 (fig. 1) and 5 (fig. 7)(bilateral atrial infarction) the P-Ta segmentvectors pointed to the left atrium and thuscannot be distinguished from isolated leftatrial infarction.

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Figure 5Case 3. Electrocardiogram shows P and P-Tadeviations and anteroseptal and diaphragmaticmyocardial infarction.

In case 6 (fig. 7) there was no definiteP-Ta segment vector that could be plotted.In this case, only supraventricular arrhyth-mias were present, which with the clinicalpicture of ventricular myocardial infarctionled to the ante mortem diagnosis of atrialinfarction as well. In this case the rightatrium alone was involved where the sino-atrial node is located. It would be of interestto collect enough cases of left and right atrialinfarction to determine whether these ar-

rhythmias were more common in right atrialinfarction.

Atrial arrhythmias are very common in

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Figure 6Case 4. Electrocardiogram shows depressed seg-mnents in leads I, II, III, and aVF, positive-negative P waves in V1, and V2, notched P wavein V3 and V4, and some intraventricular block.

our cases of atrial infarction as well as thosereported in the literature. The importanceof a small infarction of the right atriumnear the sinoatrial node has been stressed byYoung and Koenig6 and could account fordeath by arrhythmia, despite its small size.The beginning of the P waves may be

fused with the T and U waves, especiallyin sinus tachycardia. The Q of the P has

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rigure 7Case 5. There is a depression of the P-Ta seg-ment in V, to 173, and elevation in 175 and V6.

been described"' as in ventricular infarction,its vector may point away from the infarctedarea. In case 3 in V4 a negativity before the

rigure 8Case 6. Sinus tachycardia with wandering pace-maker and electrical alternans in a subsequent(lower) strip. Also present is an old apicalmyocardial infarction.

P might represent the atrial Q wave. It isat times difficult to determine where the Pwave ends and the P-Ta segment begins,particularly in the right precordial chestleads and in tachycardia with short P-Rinterval. Often the end of the P wave mergeswith the P-Ta segment so that a clear sepa-ration is not possible. Some cases of atrialinfarction reported in the literature4' 11, 9


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present P-Ta segment. elevations in leads II,III, and aVF. These cases probably corres-pond to more inferior-posterior locations ofthe atrial infarction. Notching, widening,peaking, slurring, and positive-negative ornegative-positive biphasic P waves are moredifficult to evaluate in localization of atrialinfarction.The changes in the P-Ta segment in atrial

infarction may last for only a few hours ora few days. In case 1, elevation of the P-Tasegment almost returned to the isoelectricline in 1 day. Complete electrocardiogramsare advisable while the patients are havingatrial premature beats, wandering pacemaker,or other forms of atrial arrhythmias. If atrialinfarction is suspected, an electrocardiogramshould also be taken immediately after sinusrhythm has resumed following supraventricu-lar tachycardia or paroxysmal atrial fibrilla-tion.

In our series, the left atrium was involvedby infarction in all cases except cases 4 and6. This is not in agreement with the reportedincidence of the literature of more right-sided than left-sided lesions. Theoretically,one would expect to have a greater incidenceof left atrial infarction because of the greaterincidence of left ventricular infarction.

All six cases had sinus tachycardia duringtheir illness. Atrial arrhythmias occurred inall but case 5. Among the atrial arrhythmiascases 2, 3, and 6 had atrial premature beatsand runs of atrial tachycardia, case 1 hadsupraventricular tachycardia and paroxysmalatrial fibrillation, and cases 1, 3, 4, and 6 hada wandering pacemaker. Atrial flutter wasnot observed in our series. We consider thatany form of atrial arrhythmia occurring inpatients with ventricular myocardial infarc-tion is highly suggestive of an accompanyingatrial infarction as in case 3.The diagnosis of atrial infarction is not only

of academic interest but also of some clinicalimportance. In case 2, a diagnosis of acuteventricular myocardial infarction could notbe made from the electrocardiographic changesbut atrial infarction could.We strongly believe that all patients with


electrocardiographic evidence of atrial myo-cardial infarction should be treated as ifthey had ventricular myocardial infarctionbecause there may be ventricular involvementthat does not show in the electrocardiogram.The serum glutamic oxaloacetic transami-

nase levels were not helpful in the evaluationof isolated atrial infarction; in our caseselevations were always associated with ven-tricular infarction.

Since mural thrombi are so common inatrial infarction (2 of 6 cases) anticoagulanttherapy seems indicated to decrease the proba-bility of the formation of a mural atrialthrombus. Migration of atrial thrombi may bethe cause of fatal cerebral or massive pul-monary infarction.

SummarySix cases of atrial infarction associated

with ventricular infarction are presented. Allcases were diagnosed during life and wereconfirmed by autopsy.A clinical diagnosis of atrial infarction

should be suspected in patients with ven-tricular myocardial infarction having anyform of atrial arrhythmia. Frequent electro-cardiograms should be obtained, especially ifsinus rhythm has just been re-establishedafter episodes of supraventricular tachycardiaor atrial fibrillation.The major electrocardiographic criteria for

the diagnosis of atrial infarction are as fol-lows: elevation of the P-Ta segment of over0.5 mm. in V5; and V6 with reciprocal depres-sion of the same segment in V, and V2;elevation of the P-Ta segment of over 0.5mm. in lead I and its depression in leads IIor III; depression of the P-Ta segment ofmore than 1.5 mm. in precordial leads and1.2 mm. in leads I, II, and III in the presenceof any form of atrial arrhythmia.The minor electrocardiographic criteria in

making the diagnosis of atrial infarction areas follows: abnormal P waves: M-shaped,W-shaped, irregular or notched; depressionof the P-Ta segment of small amplitudewithout elevation of this segment in otherleads cannot be regarded by itself as positiveevidence of atrial infarction.A diagnosis of atrial infarction can some-

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38LU, GREENSPAN, PICCIRILLO

times be made when the presence of ventricu-lar myocardial infarction cannot be definitelyestablished by electrocardiogram.The treatment of atrial infarction is similar

to that of ventricular infarction. Attentionshould be directed to the control of atrialarrhythmias and to the prevention of muralthrombi.

AcknowledgmentThe authors wish to thank Frederick Kellogg,

M.D., and Melvin R. Kaplan, M.D., for their assist-ance in the preparation of this manuscript. Theauthors are indebted to Dr. Benjamin Konwaler,the Department of Pathology and its staff for theautopsy reports of these cases.

References1. ABILDrKOV, J. A.: The atrial complex of the

electrocardiogram. Am. Heart J. 57: 930, 1959.2. LANGENDORF, R.: Elektrokardiogram bei Vorbiof-

Infarkt. Acta med. scandinav. 100: 136, 1939.3. CUSHiNG, E. H., FEIL, H. S., STANTON, E. J.,

AND WARTMAN, W. B.: Infarction of thecardiac auricles, clinical pathological and ex-perimental studies, Brit. Heart J. 4: 17, 1942.

4. Di IELSI, A. J., PINSKY, H. A., AND EYNON, H.K.: Auricular infarction; report of two cases.Ann. ITt. Med. 36: 640, 1952..

5. ROBERTS, J. T.: Congenital single coronary arteryin man; report of nine new cases, one havingthrombosis with right ventricular and auricularinafarction. Am. Heart J. 34: 188, 1947.

6. YOUNG, E. W., AND KOENIG, A.: Auricular infarc-tion. Am. Heart J. 28: 287, 1944.

7. HELLERSTEIN, H. K.: Atrial infarction withdiagnostic electrocardiographic findings. Am.Heart J. 36: 422, 1948.

8. WILSON, J. L., AND KNUDSON, K. P.: Infarction

of the cardiac atria. New England J. Med.251: 559, 1957.

9. SHIELDS, P. L.: Auricular infarction. J. IndianaState M. A. 50: 177, 1957.

10. FREUNDLICH, J., AND SERENO, L. R.: Auricularinfarction. Am. Heart J. 57: 654, 1959.

11. WARTMAN, W. B., AND HELLERSTEIN, H. K.:Incidence of heart disease in 2,000 consecutiveautopsies. Ann. Int. Med. £8: 41, 1948.

12. SLAPAK, L.: -Cber die Mitbeteiligung der Vorhofebeim Myokardinfarkt, Cardiologia 22: 228,1953.

13. BEAM, Wmr. B.: Infaretion of the heart, III.Clinical course and morphologic findings. Ann.Int. Med. 12: 71, 1938.

14. SODERSTROM, N.: Myocardial infarction andmural thrombosis in the atria of the heart.Acta. med. scandinav., suppl. 217: 1, 1948.

15. ABRAMSON, D. I.: A study of electrical activityin the auricles. Am. Heart J. 15: 471, 1938.

16. CORSI, V., SANGIORGI, M., AND CORELLI, D.: Con-tribution to the electroeardiographic localizationof auricular myocardial damage, an experi-mental study. Cardiologia 23: 255, 1953.

17. LADISLAU, L., CARAMELLI, Z., MONFORT, J., ANDGUERRRA, J. C.: Initial electrocardiographicchanges in experimental occlusion of the coro-nary artery in non-anesthetized dogs withclosed thorax. Am. Heart J. 53: 334, 1957.

18. SANDERS, A.: Experimental localized auricularnecrosis; electrocardiographic study. Am. J.M. Sc. 198: 690, 1939.

19. THOMAS, J. N., AND GEOGNEGAN, T.: Sequentialelectrocardiographic changes following auricularinjury. Am. Heart J., 46: 830, 1953.

20. GRANT, R.: Clinical Electrocardiography. NewYork, McGraw-Hill Book Co., 1957.

21. LEPESCHKIN, E.: Modern Electrocardiography.Baltimore, Williams & Wilkins Co., 1951.

Do not squander heartbeats in cardiac disease-live within your income.-SIR WILLIAMOSLER. Aphorisms from His Bedside Teachings and Writings. Edited by WilliamBennett Bean, M.D New York, Henry Schuman, Inc., 1950, p. 96.


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CHI KONG LIU, GILBERT GREENSPAN and RONALD T. PICCIRILLOAtrial Infarction of the Heart

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1961 American Heart Association, Inc. All rights reserved.

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