ELECTROCARDIOGRAPHICSTUDIES DURING ATTACKSOF ANGINA PECTORIS AND OF OTHER

PAROXYSMALPAIN

By MORTIMERL. SIEGEL AND HAROLDFEIL

(From the Medical Service and the Cardiac Clinic of Mt. Sinai Hospital, Cleveland)

(Received for publication July 13, 1931)

The mechanism of the pain in angina pectoris has been the subjectof speculation and investigation since the original report of this clinicalcondition by Heberden (9). Among the many theories there are twowhich today receive most support: (1) Coronary origin-(a) myo-cardial ischemia due either to sclerosis of the coronary arteries andconsequent loss of elasticity or to coronary artery spasm; (b) distensionof the sclerosed coronary arteries with stimulation of the periarterialsympathetic nerve fibers; and (2) Aortic origin-due to distension of thediseased supra-sigmoid portion of the aorta with tension on the nerveendings in the adventitia (Wenckebach; Allbutt). Recent electro-cardiographic observations made during transient attacks of anginahave revealed inversion of the T wave or S-T segment of the curve,usually in leads I and II. There is immediate return of the curve tonormal after subsidence of the pain. These electrocardiographicstudies have been reported by several observers: Clerc (3), Arrilaga (1),Bousfield (2), Feil and Siegel (4), Levy (5), Parkinson and Bedford (6)and Wood and Wolferth (7). The clinical observations have beensubstantiated by the experimental work of Wood and Wolferth (7)who produced "temporary and rapidly reversible electrocardiographicchanges analogous to those seen in angina pectoris tracings." Thesechanges were: greater inversion of previously negative T waves insome experiments and the production of a high take-off in the S-Tcomplex in others. These investigators obtained abnormalities in theT wave more readily in abnormal hearts. Clamping of the circumflexand posterior descending coronary arteries caused greater changes thanobstruction of the ramus descendens or branches of the right coronaryartery. Feil, Katz, Moore, and Scott (8) in a recent experimental

795

ANGINA PECTORIS

study obtained similar curves from ligature of the ramus descendens ofthe left coronary artery. These changes were most pronounced afterfurther ischemia of the heart muscle was produced by obstruction ofthe inferior vena cava. These clinical and experimental data arestrong evidence that myocardial ischemia is responsible for the changesin the T wave and S-T segment of the curves. Likewise, they indicatethat the pain is probably due to or associated with myocardial ischemia.

In this report are given the electrocardiographic findings in elevenadditional cases with transient anginal attacks. Clinically, these casesmay be divided into four groups: (1) Patients with coronary sclerosisand who were not known to have had coronary artery thrombosis; (2)Patients who had in addition, an attack of coronary thrombosis previ-ously; (3) Patients whose angina was associated with aortic regurgita-tion; and (4) Patients who had angina and who subsequently developedcoronary artery occlusion.

The results of these observations during anginal attacks are sum-marized in Table I.

TABLE I

Electrocardiographic changes

Case Diagnosis t TI TII TIIl Depression of S-T Segment

1 C.S. Leads 2 and 32 C.S., R.C.T. Leads 2 and 33 C.S.; O.C.T. Leads 1 and 24 C.S.; O.C.T Lead 15 C.S.; O.C.T. Leads 1 and 26 C.S. neg. neg.7 A. I. neg. neg.8 C.S. neg. Leads 1 and 29 C.S.; O.C.T.1) C.S.11 C.S.

t C.S. Coronary sclerosis. R.C.T. Recent coronary thrombosis. 0.C.T. Old coronary thrombosis. A.I. Aortic insufficiency, rheumatic.

CASE REPORTSCase 1. L. F., female, aged 56. Diagnosis: Coronary sclerosis with

gradual obliterative arteritis and myocardial fibrosis. She had attacks ofsubsternal pain with radiation to the left shoulder and dowvn the left arm.These attacks had been recurring for two years, usually after emotional up-

796

MORTIMERL. SIEGEL AND HAROLDFEIL

set and were not precipitated by exercise. The blood pressure was usually150/90 but during the attack rose to 170/100. The heart rate usually 80,rose to 120 and the cardiac mechanism remained normal. Physical examina-tion revealed a heart normal in size and heart sounds that were feeble.The first heart sound at the apex was especially faint and gallop rhythm waspresent much of the time. During the latter part of the patient's illnessthere were attacks of pulmonary edema and the terminal illness was dom-inated by congestive failure. Postmortem examination revealed advancedarteriosclerosis of both coronary arteries with almost complete obliterationof the lumen of the ramus descendens. There was advanced sclerosis of themuscle of the anterior and lateral part of the left ventricle. An electrocar-diogram taken on November 13, 1928 (Fig. 1, a) during an attack revealednormal mechanism, rate 136; the S-T segment in lead I rose after the com-pletion of R and T was elevated 2 mm. The S-T segment in lead II wassomewhat depressed and T was upright. Lead III shows depression of theS-T portion of the curve. An electrocardiogram taken after the attack sub-sided (Fig. 1, b) showed T 1 to be almost isoelectric; S-T 2 was slightlydepressed; T 2 and T 3 were both upright. The rate was 100.

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Case 2. C. H., male, aged 62. Diagnosis: Coronary sclerosis with anginapectoris, recent coronary thrombosis. For several months he had attacksof substernal pain on eff ort, relieved by nitrites. A severe attack of sub-sternal pain occurred three weeks before the electrocardiographic study wasmade. This attack was probably due to coronary thrombosis. The patienthad had ele-7ation of the systolic and diastolic blood pressure for approxim-

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ately eighteen years (180/110). An electrocardiogram (Fig. 2, a) taken onDecember 29, 1929 revealed inversion of T 1; depression of S-T 2 and T 2was upright; T 3 was upright. Immediately after this record was taken thepatient complained of severe pain (Fig. 2, b) which showed a greater depres-sion of S-T 2. There was less depression of the S-T segment in lead III.The patient inhaled amyl nitrite and was relieved of pain. Figure 2, c,shows a striking change: T 1 is more deeply depressed; S-T 2 is isoelectric;S-T 3 is slightly elevated and T 3 is larger.

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Case 3. J. W., male, aged 61. Diagnosis: Coronary sclerosis with anginapectoris, old coronary thrombosis. Chief complaint: substernal pain on

effort, with radiation to neck, left shoulder and arm. Symptoms dated froma sudden and severe attack of substernal pain August 1927 (1 year beforeobservation). Generalized arteriosclerosis. Blood pressure 150/100.Moderate enlargement of left ventricle. An electrocardiogram taken on

May 31, 1928 during an attack of angina (Fig. 3, a) revealed a depression ofthe S-T segment in leads I and IIL A very deep Q is seen in lead III andS-T 3 has a high take-off and is curved with its convexity upwards. A recordtaken a few minutes later after subsidence of the pain (Fig. 3, b) shows lessdepression of S-T in leads I and II.

52

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Case 4. 11. M., male, aged 48. Diagnosis: Coronary sclerosis, anginapectoris, recent coronary thrombosis. Coronary thrombosis July 1929.Attacks of typical angina with effort and emotion. Moderate cardiac en-largement. Blood pressure 160/120. An electrocardiogram was taken onemonth after occlusion during an attack of angina. Figure 4, a, shows con-siderable depression of the S-T segment in lead I; slight inversion of T 2and a moderately high take-off of S-T 3 with in-version of T 3. Immediatelyafter subsidence of the pain the electrocardiogram (Fig. 4, b) shows less in-v-ersion of S-T 1; greater inversion of T 2 and an altered QRScomplex inlead III.

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Case 5. 'I. F., male, aged 58. Diagnosis: Coronary sclerosis: anginapectoris; old coronary thrombosis. Had attack of coronary thrombosisApril 28, 1927. i\loderate cardiac enlargement to the left. Blood pressure200/110. MIoderate generalized arteriosclerosis. An electrocardiogramtaken on August 30, 1930 (Fig. 5, a) during a severe anginal attack revealed adeeply depressed S-T segment in leads I and II and in lead III T is iso-electric. A record taken after relief by inhalation of amyl nitrite shows veryslivht depression of S-T in leads I and II and in lead III T becomes depressed.

Case 6. M. B., female, aged 53. Diagnosis: Coronary sclerosis; anginapectoris. Typical angina of effort in substernal region with radiation to theleft shoulder and arm. Duration six years. Heart not enlarged. Bloodpressure 180/100. An electrocardiogram was taken on October 16, 1930

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during an attack of severe angina. Figure 6, a, shows the striking inversionof T 1 and T 2. A record taken immediately after relief by the inhalationof amyl nitrite shows a lessening of this depression of T 1 and 2 (Fig. 6, b).

Case 7. E. F., female, aged 24. Diagnosis: Free aortic insufficiency(rheumatic) with nocturnal attacks of angina pectoris. Chorea at the ageof 13 (heart affected then) with recurrent attacks of rheumatic fever duringsucceeding years. For 7 or 8 years patient had had nocturnal attacks ofpain in the substernal region, radiating to the left shoulder and down the_ _ _ r _ _ _v_l ,A.A | -- ---!-

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left arm. There have been no signs of congestive failure. The bloodWassermann was negative. An electrocardiogram taken during an attack(Fig. 7, a) shows slight inversion of the S-T segment in lead I and a deepdepression of this portion of the curve in leads II and III, the S-T portioncoming off below the iso-electric level. A record taken after the inhalationof amyl nitrite (with relief from symptoms) shows a deeper inversion of T 1but a less deep inversion of T 2 and 3. In addition the S-T portion of thecurve started at a higher level in lead II and near the iso-electric level inlead II I.

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Case 8. A. C., female, aged 49. Diagnosis: Coronary sclerosis with an-gina pectoris. Pain in lower xiphoid region for two years with radiation toleft shoulder and arm, related to effort and emotion. Blood pressure 142/82.Wassermann negative. An electrocardiogram taken as a control (Fig. 8, b)shows left axis deviation and T 1 and 2 are upright. T 3 is iso-electric.1 cc. of 1-1000 solution of adrenalin hydrochloride was injected subcutane-ously. This was followed by a typical attack of pain and a record taken 18minutes after the injection (Fig. 8, a) shows a depression of the S-T segmentin leads I and II with a low "take off." In lead III the S-T segment iscurved with the convexity directed upwards and T is inverted.

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the T wave.Case 10. M. K., male, aged 58. Attacks of substernal pain of three

years' duration caused by exertion. Blood pressure 164/90. Patient laterdeveloped coronary thrombosis and died. Electrocardiograms during at-tacks of angina showed no change.

Case 11. M. K., male, aged 43. Diagnosis: Coronary sclerosis withangina of effort. Sense of substernal oppression related to exertion and emo-

802

MORTIMERL. SIEGEL A-ND HAROLDFEIL 803

tion. Radiation of pain to both arms. Duration one year. Blood WNasser-mann negative. Electrocardiogram taken after subcutaneous injection of1 cc. of adrenalin hydrochloride 1-1000 solution showed very slight changesin the T wave. The patient suffered pectoral constriction.

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Electrocardiographic observtations made dutring paroxysmal painnot dute to angina pectoris

1. Labor pains. Electrocardiograms were taken during active laborin five patients. In each case tracings of the standard leads were re-corded during an interval when the uterus was relaxed. This -was re-

peated while the patients were having severe uterine contractions whichwere visible and palpable. Records were again taken after the uterinecontractions had subsided. In twxo cases records were obtained whichshowed some deviation from the normal which was present during bothactive contraction and during relaxation. In these t-wo cases recordsw%Nere obtained a fewvx days postpartum for comparison.

804 ANGINA PECTORIS

In none of the five cases was any inversion of the T wave or depres-sion of the S-T segment of the curve observed during uterine contrac-tion. In one case the T wave in lead III was depressed both duringuterine contraction and relaxation. A record taken six days post-partum showed less inversion of T 3.

2. Renal and biliary colic. One patient had severe biliary colic andwas found at operation to have pericholecystitis with numerous adhe-sions. Records taken during biliary colic showed no deviation fromthe record taken after relief from pain.

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FIG. 8, a FIG. 8, b

Two cases of renal colic were investigated. One who had severe

colic for several days had marked sinus arrhythmia which disappearedwith relief from pain. However, neither of these two cases presentedany alteration of the S-T segment or T wave during pain.

DISCUSSION

The changes in the T wave and S-T segment which occur frequently(in more than 50 per cent of cases) during attacks of angina pectorisare indicative of myocardial changes which are not related to exercise(Wolferth, personal observations) or to reflex effects from pain as such(labor pain, gallbladder and renal colic). In one patient, with a

MORTIMERL. SIEGEL AND HAROLDFEIL

gastric ulcer and paroxysmal epigastric pain, slight depression of theT wave occurred which varied in successive beats and was perhaps re-lated to changes in the axis of the heart. In eight cases electrocardio-graphic changes were associated with characteristic pain (due to effortor emotion) and subsided with rest and inhalation of amyl nitrite.Myocardial changes may then be said to be associated with transientanginal attacks and this may be due to spasm of the coronary arteriesor to transient variations in the coronary flow (reversal of coronaryflow). The inversion of T or the S-T segment in the electrocardio-gram during brief paroxysms of pain of angina pectoris gives additionalevidence of the nature of the anginal attack and may be helpfuldiagnostically.

CONCLUSIONS

Electrocardiographic observations are reported in eleven additionalcases made during transient attacks of angina pectoris. In eight ofthese patients, there was inversion of the T wave and (or) inversion ofthe S-T segment of the curve. In some instances a negative T becamemore deeply depressed. These changes disappeared after subsidenceof the pain. This evidence supports the conception that transientanginal attacks are due to myocardial ischemia, presumably due toalteration in coronary artery flow. Electrocardiograms taken duringother types of paroxysmal pain (labor pains, renal and gallstone colic)did not show any changes in the T wave or S-T portion of the curves.

BIBLIOGRAPHY

1. Arrilaga, M. F. C., Bull et mem. Soc. med. d. h8p. de Paris, 1924, xlviii,1493. Signification Pronostiqtue De L'Electrocardiogramme DansLes Insuffisances Cardiaques.

2. Bousfield, G., Lancet, 1918, ii, 457. Angina Pectoris: Changes in Electro-cardiogram During Paroxysm.

3. Clerc, A., Presse med., 1927, xxxv, 499. Anomalies Electrocardio-graphiques Au Cours De L'Oblit6ration Coronarienne.

4. Feil, H. and Siegel, M. L., Am. J. Med. Sci., 1928, clxxv, 255. Electro-cardiographic Changes During Attacks of Angina Pectoris.

5. Levy, J. R., Arch. d. mal. du coeur, 1929, xxii, 523. Valeur SemiologiqueDes Alterations Du Complexe Ventriculaire flectrique Dans Les Syn-drome Angineux.

6. Parkinson, John and Bedford, D. Evan, Lancet, 1931, 15. Electrocardio-graphic Changes during Brief Attacks of Angina Pectoris.

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806 ANGINA PECTORIS

7. Wood, F. C. and Wolferth, C. C., Arch. Int. Med., 1931, xlvii. 339.Angina Pectoris: The Clinical and Electrocardiographic Phenomenaof the Attack and their Comparison with the Effects of ExperimentalTemporary Coronary Occlusion.

8. Feil, H. S., Katz, L. N., Moore, R. A., and Scott, R. W., Am. Heart J.,1931, vi, 522. The Electrocardiographic Changes in MyocardialIschemia.

9. Heberden, W., Mod. Trans. Coll. Phys., 1768-70, ii, 58. AnginaPectoris.