Electrocardiographic study during a paroxysm of angina pectoris

Electrocardiographic study during a paroxysm of angina pectoris

ELECTROC’ARDIO~:RAPII1CI STUDY DliRlNG ()P’ As(:lsA PECTORIS’” A (:. I 11aw IQ general anoxemia and hy transient coroirwry constriction altered the ...

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ELECTROC’ARDIO~:RAPII1CI STUDY DliRlNG ()P’ As(:lsA PECTORIS’”

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WI\I ;Inimal experimental work, as yet niipl~\~lished, we have concluded that electrocar(lio~l~~l~~liic eliaqw clinrwtrristic of thoscb rnconntered in an&a prctoris can he proclueecl I))- anoxemia. \Vt> 11aw IQ general anoxemia and hy transient coroirwry constriction altered the terminal deflections and aff’ected the normal paths of intracardiac conduction. When adecluate oxypnat,iori was restored, the curves returnetl to normal. Onr results agree with those of Koulitz and Grubr~-.~ 1Zecently we have hat1 the opportmiity to take tracings of a patient, rluring an angina1 attack. The ahrations in tlrc terminal deflections were identical with those we prodneed cxprrimrntall~ iii animals and they were transitory. Within two minutes after tlita an~iual seizure the record was essentially ~~oi~i11a1. is feeling tllese alterations wtw due to anoxrmia.” It

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patient suffered a miCnlunl of fifty severe seizures, ad he cannot be persuaded that ally one was cliflerent from the others. The increased deepening appearing in t,lie Q-waves of Lrads II i11ic1 1 IL is a notable ffAa,tnre iii the light of recent morli.:~

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feel that records t,aken a few niinutt3 a complete reversion to those iii Fig. I. We

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been described ii1 the literature, fall into three groups: those which shorn primary deviations in t tie terminal deflections only,;‘~ 6. ‘. ‘. “, “’ those which show t,he bizarre tleviatiom of intracardiac contluctiou block in one of the bundle brallches,“~ I2 or in the bundle it.self,l:’ and lastly those which stro\recl no tlt~viatiwis at all. All three of these groups also appear with coronary thrombosis. In factT we have concluded t,hat there is only one constant tlifYcrentia1 point and that is the length of time the changes persist. In coronary thrombosis they last, for clays but, t,encl to rctnrn towartl normal in weeks or months ; iii angina pectoris the rct,imi takes only ii few nii1lutes. Our case? for example, had recovcretl in less than two minutes. d second classificat,ion of l)ublished cases can be made into two groups : those which were recorded during spontaneous seizures, and those in whom seizures were artificially produced by unusual exercise. Fe feel that there may be good reason for studying the two groups separately. An entirely different niechanism may be operating in each to produw the attack-pnssibl\ ii coroiiarg T~asospasni in the first group producing localizetl areas of ischeniia, while in the second group a total relative nigoca.rdial ischemia is prodlIce(l by the exercise requirements as they exceed the capacity of the disease-liniit,ed coronary circulation. At any rate? casts which showctl the most marked tleviations in the S-T intervals and in the T-waves? as well as the cases of conduction abnormalities, were all in the spontaneous group. The other group was by far the larger because of the large single series of thirty cases reported by Wood and Wolfertli.!’ \\‘hat deviations occurred in the artificially precipitated seizures not only mere less acute in appearance but it, happened t,hat the cwsw which showed no deviations whatever all fell into this group. We are reporting our case bwanse it atlcls anvthrr record to th(b very small group of spcmtniirous ;tt,tacks ; becaustt it has no predecesSol’ in the literature lllilt I\‘(’ tl;rT(, lj(vii able to locwtc sliowiilg tllc

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THE AMERICSN HEART JO I-RNAI,

1. The electrocarcliographic cliangcs in this pat,ient during all attack of angina pectoris were characteristic of those often seen in acute myocardial infarction. After ho minutes the curve had ret,urned essentially t,o normal. The changes, we hclieve, were due to anoxemia of the cardiac muscle not inrolrinp t,Iie conduction paths. 2. We have been unable to find a sirnil;lr case in the lit,erature. 3. The changes are typical of tllow we have obtained in animal cxperinlrntx with cardiac aiioxcmia ; sinlilwr in conformatioii and as transitory. REFERICX<‘ES 1. Kountz, C\:. B., aud Grubrr, C. M.: ~I’hr Ele~trocardiograpllic (Xaugvs in Anosaemia, Proc. Xoc. Espcr. Biol. &. I\lcd. 27: 170, 19%. 2. Keefer, C. S., and Rerrnik, IT’. II.: Angina Pwtoris: A Syndrome Caused by Auosemia of the Myocardium, Arch. lut. Yled. 41: 760, 19%. 3. Fcnichel, Sathan &I., and Iiugell, Victor II.: The Large Q-wave of the ElcctroA Clorrelation With Pathological Observations, Au. IIEART J. cardiogram. 7: 23Fj; 1931. 4. Wilson, Frank N., Maclcod, A. G., and Barker, Paul R. : ‘(T” Deflection of the Elcetrocardiogrnph, Tr. A. Am. Physicians 46: 29, 1931. 5. Clrrc, A.: hnomalies Elcctroc:lri(iogrnphir(ue nu (yours de 1 ‘Obliteration (loxnariennc, La. Presse Med. 35: 4!)!1, lV7. ~~lectro~:~rdiogr~ll)lli(, Clmngcs During Attacks 6. Feil, Harold, and Siegel, M. L.: of ,4npina Pectoris, Am. .J. M. Sv. 175: Z-55, l!U?. ~Eleetrocardiographir, Changes During 7. Parkinso;, John, nml Brdford, I). I:.: Brief Attacks of nugina Prctoris, Lnncet 1: 15, 1931. Vnleur Scmiologiquc drs Alterations du Complex Ventriculdire 8. Levy, J. R.: klectrirluc dans les Syndromes Anginrns, Arch. d. Xal du Coeur 22: 523, 1929. 9. W’ood, F. C., 3nd Wolferth, Charles CT.: Angina Pectoris. The Clinical and an(l Their Comparison With Electrocnrdiograpllic Phenomena of the Attack the Effects of Experimental ‘l’emporary Occlusion, Arch. Int. Med. 47: 339, 1x1. 10. Hall, Donald: Electrocardiogrnnls of Two T’atients TInring Attacks of Angina Pectoris, Lnncet 1: 1254, 193% in l~l~,ctroc:rrcliogram During Par11. Bousfield, Guy: Angina Peetoris ; (Yhnngcs osvsm. Lancet 2: 457. 1918. dam Sigrlification Prognostiqnr (11, 1 ‘~lr~~troc:lrdiojirmmnr 13. Arillaga, M. F. C.: Bull. ct mr:m. Rw. m&l. (1. 116~. dc Par. 32: les Inwffisancc C’ardinaues,