Acta Medica Scandinavica. Vol. CXV, fasc. VI, 1943.

From the Medical Clinic, University of Lund , Sw’eden. Chief: Prof. Sven Ingvar.

. Case of Coronary Thrombosis - a Contribution

to the Discussion of the <Silent. Electro- cardiogram.

BY

K N U T LIEDHOLM.

(Submitted for ~~ublical iori July 12, 1943).

, + l h e surest way to diagnose a cardiac infarction is hy cleclro- cardiographic examination, which does not only indicatc the cventual prescnce of an infarction but also its localization - tlic knowledge of which is of no small importance for the just valuation of thc symptoms in an individual case.

In not n fcw clinically typical cases (also verif icd after necropsy) we find however none of the characteristic electrocardiographic changes usually presenl in cases of infarction. The elcctrocardiogranis, obtained in such cases, liavc therefore sometimes becn cnllcd d e n t ) ) . In some cases this has been explaincd as being due to a simultaneous infarction of t h e anterior and the posterior ventricular wall, during which the electrocardiographic changes, caused by these two types of infarction and pointing in opposite directions, would cancel each otlirr, thus makjng the electrocardiogram seeniingly normal. In other cases i t has been conjcctured t h a t the infarction might be localized to a ((silent)) zone. The existence of such ((silent)) zones has been verified in dogs, hut as yet not with certainty in nian.

In the Lund Medical Clinic we liavc had the opportunity of obscrving onc! case which easily might have been registered ah a tdento infarction, if not especially favourable circunis Lances had heen a t hand. As i t is, this case points to other possible explann-

r - - A CASE OF CORONARY THROMBOSIS ETC. .X?3

tions than tliosc mentioned above of why tlie electrocardiographic examination sometimes fails.

Case report: J . 2404/36. A. J., medical attendant a t the St. Lars' Hospital, 4 8 ycars old. Her~di tar i ly nothing of interest, perhaps with tlie exception of his father's death of a renal disease. The patient w i s married and hzd a healthy child. He had not had rheumatic fever, chorea minor or lues. He had ;11Ways been in good health until 6 years before h i s admit.tance to I he hospital, when he got epidemic parotitis with orchitis.

The last three years he had been troubled periodically xvith attacks of' p i n in t h r rhest specki illy after exertion. He had also begun to suffer fiom hre:ithlessncss during work. As thcsr symptoms began to be more pronounced about a year ago, the patient sought a doctor. His blood pressure w a s 21O/120 mm Hg, and the heart enlarged to t,he left with a soft systolic niurniur over the apex and accentuated A,. The patient's blood pressure varied during thr? following year between 180/100 nnd 240/150 mIn Ifg and as his subjective state was not markedly iin- proved by t h c s priwrihtd regimvn, he was admitted l o the Lund Medical Clinic. h'othing in thc anamnchsis pointid to tlic presence of a ciinimlly nianifcst, cardik-c infarction.

State of the putierit on adiirission to the &led. Clin., Lund, Oct. General state good. Flesh and muscles in good condition. No cyanosis.

Heart: left cardiac border 1.5 cm outside the rriammillary line. Right Systolici murmur over the apex. Xz

h-0 dyspnoea in wst . No oecltma.

cardiac hordw ill the s t t m a l h i ( , .

slightly acccritnat ed. Lungs and :;bdonicn norniul. Hioorl pressurv 1\)5/125. ~ ~ ~ ~ s s I ~ I ~~i i !ni i rccictiori negat.iVc.. Stdimentation

IIaemoglobin 90 per cent. IIIy Ilwocytc count 4.4 million, leucocyte

Venoiis pre5sure 2.5 cm I 1 2 0 . Vital c:ip:'ciiy 3 100 cm3. I ioc~ntgr i io lo~i~~;~l exaniinal ion: The maximum transverse diameter was

16.5 ern, of ~ l i i c h 12 t o the left of the midsternal line. Corresponding n'idth of the chest Zi.5 cm. Thc roentgcmdogic:~l examination revealed distinct, rn1argthmc)nt of the a r tc~ia l ~ e n t r i c ~ l r . No enlargement of the ;3111 i t . 1 ~ ~ . Pulmonsry fields normal.

Electrocardiogram: P Q interval 0.10 sec. PIII ncgative. Distinct QII and QIII. Deprrssion of t h r S-T segment in Leads I and 11. Nega- tive T waves in all leads. Diagnosis: Auricular rhythm. Coronary in- sufficienry and hypertrophy and dilatation of the left vrntiiclc (fig. 1).

The patient, was kept a t rest in bcd. The first Week was uneventful, and a second elrrtrocardiogrcm w a s laki-n (Oct. 16, 12 a . In.). On com- parison with the electrocardiogram t a kcn at admission no changes could be found (fig. 2).

In connection with a laborioiis defarcxtion 1 1/2 hour after this

rate I6 mni/6O min.

count 8,100.

-- >-

A CASE OF C O R O N A R Y THROMBOSIS ETC. 557 examination the patient turned sick, vomited and transpired profusely. No cardiac pains. Mufflt’d heart sounds. Pulse rate 40/min. Blood pres- sure 90155-80150.

An elcctrocardiogram Was t:iken half an hour after thc patient frll i l l . This showed distinct changcs pointing to a dorso-basal cardiac in- farction. High takeoff trf the S-T segmrnt in Lead 111. 7’111 now ~ o s i - live (fig. :<).

After the initial severe collupse, the patient recovered Within some hours. At 8 p. m. the blood pressure was 160/90 and the temperature had risrn to 35.8’. The temperature reached a maximum (39.2’) in the afternoon of Oct. 18. Imcocyte count (Ocl. 15) 10,600. Oct. 21 sedirniin- tation rate ti3 mm/60 min.

A third -elrctrocardiogram Was taken alrcady a t 5 p. 111. the same day the attack set in, revealing less distinct changes. The high take-off of the 8-T segment in Lead 111 nou’less markcd. TI] once more negative (fig. 4).

Another electrocardiogram (fig. 5), taken the following day at, 1 p. m. is similar to those taken before the onsct of the attack, (fig. 1 and 2). All signs of ;I recent coronary occlusion h a w disappeared.

The temperatiire sank by and by and from Nov. 5 i t was norniai. On Nov. 25 (he sedimentation rate Was 3G mm/(in niin. On Dcc. 2 the pat,ient as disniissed from the hospital. being then subjcctivcly free from complaints. Blootl pressure a t that time 170/105. Roentgenological oxamination of the heart showed no changes whrn compared with the statc a t admission. The electrocardiogram was similar to that taken a t admission.

One morning about s e w n wecbks after the patient left the hospital, h t i was found doad in his bed.

Clinical diagnosis: Essc~ntial hyperttmion 4- Coronary sclerosis -t cardiac myodegcnvr:rtion -+- cardi;ic irifarrtion (dorso-basal infarction).

Post-mortem emmination: iDr AIf Sjovall). . . 11eiir.t hypertrophicd both l o the, right arid th(x l ~ f t , esp(xc’ially the latter, dilated? flaccid. Kormal pericardiurn. No t~mholus in the pulrrionary artery. iYo valvular changes. In all coronary arteries numerous, diffuse, calcified atheromatous plaques narrowing the lunien. The ram. circumflexus of the left coronary art,ery can simply not bc clipped. 11. has bccn corivcrlcd to a hsrdstring, crackling when cut. Corresponding to this branch there is a t the base of the heart, to the back arid somewhat kit ~ r d l y , an rnormous heart, infarction. which is peripherally already fibrously white and cent~al ly gelalinously gray-rcd. The infarction does not quite r t w h the apex and leaves the anterior wn!ri- cular wall and the septum free. Modcralo ;rrt,eriosclerosis of tht. :loria. In other organs no nott~worlhy findings.

Thr patient recovered steadily.

In this case, with a large infarction of the posterior wall, a typical case record and a post-mortem verification, all the electro- cardiographic changes, typical of coronary occlusion, have thus appeared strongly pronounced and then disappeared in the coursc

558 K N U T L I E D H O L M .

of '21 hours or pr l iaps during a still shorter lapse of time. If 110

second elcctrocardiograiri had heeri taken until the day after the coronary occlusion, t h t w changes would no t have brrn observed. I t n ould have seemed as if the patient's electrocardiogram hat1 iindtqonc, no changes during his slay a t the hospital, and we liad had to rcgistcr tht1 case as a ((silent)) infarction.

In some textbooks on electrocardiography, as for cxairlplc Sclicrf and lIolzcr and Polzcr, i t is indeed pointed ou t that thts monophasic cleforriia tion of the clectrocardiogram in cases of cardiac infarction is often excccdingly lransient and may disappear williin sonzc hours. In such cases, howcvcr, the development of lhc typical coronary T wave can be ol)scrved if a series of electro- carcliograms is taken, and the diagnosis thus even hrre elect ro- cardiograpliically vcrificcl. This was irnpossiblc in tlir present case w l i c w Ihc cliangcs quickly disappcared, leaving the clcctrocardio- gram mainly Lhc same as bcforc the attack - that is with a neg a 1' w e TlII .wave but no typical coronary T wavc. 'l'hc electrocardiogram underwent no changes during the re~iiuintlcr of thc ohservation tinrc.

A5 t o the importance of the time clement, Ilochrcin in his monog~npii )>Der Myocarclinfarkb only mcntioris the aclvis- ability of taking electrocardiograms every other or third day tluririg the first three weeks in suspected cascs of infarction in ortlcr t o vcrify tlie diagnosis. He says furtlier, referring l o the so-called silent infarctions: ((Wo lrotz genauer clektrokardiografi- schcr l<outrolle kcine charaktcristisclien Vcriindcrungen auftretcn, muss ciincb 1,okalisa tion des Infarktcs in einer sog. ccstuinmcn Zone)) (Morawitz untf Il'oclirein) dcs Myokards angcrioimncn werden. Es ist wuiii~sclieinlic~l, (lass cliesc ((sturnmen Z o n c n ~ mit drr Lokalisation dcr Iattwlcn Infarkle iibcwinstirnrnen. Siclicre Aufschliissc bc- ziiglich clicsrr Fragc fehlen noch zur Zrit.,) Such silent zones havcl I~ccn asccrlnincd in dogs ])if Chavcz a n d Menclcz bu 1 as yet not in inan; Coellio rnorcovrr cloubls their existence. Hochrein men- tions :is another possible explanation: ((Bci multiplcn Infarkten ist ii:it<irlich iainc gcgeiisei tigc Bceinflussung dcr elektrischcn Er- sclicinurlgen inogliclie, that is a seiwiingly normal elcctrocarrliograiti niiglit Iw taken from a heart where tlic elcctrocnrdiograpliic changes. due to simultaneous i~ifarctions of the anterior a n d pas- twior vcntricular \valls, cancel each other. T_Thlcnbruck tricls to

A CASE OF COHONAHY THHOMBOSIS E T C 559

chsplain t he silent zonc in a similar way i n his monograpliy ((Die Iilinik der Coronarerkrflnkungcne, h u t docs not attach any import- a r m l o the element of tirnc. l l c discusses on tlic other hand several C:ISC rqwrts , wlicre it has not Iwen possible to tliagnosc an infarction until scvcral days af tcr tlic illness has sct in.

On account of the casc licre tlcwxibcd, we want to stress the importance of early and of tcn r c p a t c d electrocardiographic examinations, as the el~.ctrocardiographic changes due to infarction rnay disappear already within 24 hours aftcr the attack has sr t in - a t least in such cases where the clectrocardiogratn shows pathological changes, pointing to a coronary insufficiency already before the onset of the coronary occlusion.

Summary.

lkscr ip tion of a cast of coronary thrombosis, verified a t nc’cropsy, (clorso-basal infarction), whcre an electrocardiographic examination had bccn niatle 1 $4 hour before the infarction set in arid thcn scvcral times during the next 21 hours. At the he- ginning of the infarction a typical, monophasic electrocardiogram was obtained, hut already 24 hours later the electrocardiogram WRS quilc similar to that t:iken Iwforc thc coronary occlusion, and did not undergo any furthvr changes (luring the patient’s stay a t thc hospital.

In this conncsction the so-called ((silent)) electrocardiogram in cases of cardiac infarction is discussed, and the importance of early antl rc1pcaLctl clcc trocartliographic examinations underlincd.

Literature.

P(.lic~J’. U.: I,rhrhuch t l v r Eltil;troc.;irdiografi, Wirn 1937. Julius Springer -. HoIzc.13, W. :in(] IC. I ’ O h ’ P : A\i,xtIicahr I~lrc,trocardiog.rafi. Berlin 1 0 4 1 . TVdtcIr. dc Gruytcbi,. ~~ I loc~hrc~i i i , M.: I k r Myokardinfarkt. IJrcstlrn :i11(1 IApzig 1941. Throdor Strinkopff. ~ Morawitz; P. arid M. Ilochrriri: Zur 1)iagnosP und Behandlung drr Koronarsklerose. Munch. med. Wschr8. 3928, 75, l i . -- Cha-vrz, I . tirid 1,. Mrndry;r: IC tliagnostico de localizjcioii dcl infarlo miocardica. Arch. I;rt.-cirnclr. Cardial y Hcrnatol. 1035, 5, 157. Quotcd from Hochrein. - Coelho, E.: Dic Pathologic. tlrs Coroniwkwis- laufs. Lissabori 1935. Livraria Bcrtrand. Quotcd from Ulilrnhruck. - Uhlenbrirc-k, P.: 1)ic’ Kliriik d t ~ i ~ (:c)ronaI.i.rkr:iiikungrn. Brrlin 1940. J u l i i i s Springer.