Transient S-T elevation detected by 24-hour ECG monitoring during normal daily activity

Transient S-T elevation detected by 24-hour ECG monitoring during normal daily activity

Transient S-T elevation monitoring during Basil Gold&g, E,liana Wolf, Dan Tzivoni, Shlomo Stern, Jerusalem, M.B., M.D. M.D. M.D. Israel detected...

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Transient

S-T elevation

monitoring

during

Basil Gold&g, E,liana Wolf, Dan Tzivoni, Shlomo Stern, Jerusalem,

M.B., M.D. M.D. M.D. Israel

detected

normal

daily

by 24-hour

ECG

activity

Ch.B.

T

he detection of transient S-T elevation and its interpretation poses a difficult problem. That this condition has clinical significance was stressed by Prinzmetal’ in his description of “variant angina pectoris.” Until recently cases with documented S-T elevation were found to have this feature mainly by chance, because their ECG at rest and on exercise are usually normal.2 The finding of transient S-T elevation during exercise in patients after myocardial infarction has been described by using radiotelemetry.3 The continuous around-theclock recording of the ECG by the Holter system4 enables the examinee to carry his normal daily routine during the monitoring and recently sporadic cases with transient S-T elevation have been described using this method.:‘-’ In this study, patients in whom transient S-T elevation was found by continuous ambulatory monitoring are presented, their clinical background is described, and the possible significance of this finding in each case is discussed.

Material

and

methods

The 7 patients described here were among 174 patients who were referred to us with atypical chest pain and/or palpitations for 24-hour ECG monitoring. A conventional 12-lead ECG was performed on all patients, while a single R’Iaster step test and multistage bicycle ergometric examination was performed when indicated. The Halter* tape recording system was used with the model E Electrocardiocorder, which has an improved low frequency response. Three non-polarizable silver-silver chloride electrodes (Mannen-Greatbach) were used. The exploring electrode was placed over the Vs position. The negative electrode was placed in the fourth intercostal space at the right sternal border and the ground electrode was placed at the manubrium sterni. The complex obtained closely resembled Lead Vs of the conventional ECG. The tapes were screened for possible ECG abnormalities on the Electrocardioscanner, and the suspicious segments seen on the screen were printed out on regular ECG paper,

From

the Cardiology Service and Department of Physical Medicine and Rehabilitation and Medicine A, Hadassah ITniversity Howital and Hebrew University-Hadassah Medical School, Jerusalem. Israel. Sur:llorted by the Joint Fund of the Hebrew University and the Hadassah Medical Organization (Mr. N. Caon. Switzerland). Received for publication Dec. 6. 1972. Rwrint requests to: S. Stern. M.D., Hadassab University Hospital. P.O.B. 499. Jerusalem. Israel. *Avionics. Los Angeles. Calif.

b’ol. 86. hid. 4, fip. 501-507

October,

1973

American Heart

Tournal

501

7’oble 1. Dclaiis of 7 ptrtic’ds 2-G12011~ monitoring

vith

fret risic*nf S-7’ f~lrzufiopz tlc[Prfui? II? (.o)i/ip111011.y

!

I

Patient No. and initials

;Ige (yr.)

Sex

1. B. Y.

18

M

Normal

Normal

2.

c. A.

28

M

T wave inversion

3.

I;. c.

61

hl

.4nteroseptal infarction

T wave inversion more marked -

4.

H. A.

56

1’1

Anteroseptal

infarction

Positive

5.

M. B.

54

M

Anteroseptal

infarction

6.

H. Y.

66

M

7. B. 2.

47

M

Right B.B.B. ventricular premature beats Right B.B.B.

Rest

Jfaster twn-step test

irlg E L‘G

/ / I

HI‘c~yc-ie exercise test

Normal -S-T depression of 1 mm. in i’s and ventricular premature beats S-T depression of 3 mm. in 1’;

-

-

-

Normal

1 mV

0

0.2

OA

0.6

0.8

1.0

1.2

1.c

1.6

1.8

SEC

Fig. 1. Step voltage decay curve of a Sanborn 100 ECG machine (solid line) and of the Holter-Avionics system (interrupted line). It can be seen, that after 200 msec. both systems have similar decay. A 90 per cent decay is reached in the Sanborn 100 machine after 300 mser. and in the Holter-Avionics system after 240 msec. using an improved method of operation.* The reliability of the system as to reproduction of S-T segment was tested earlier by comparing the tracings of individuals with normal ECG pattern and of others with pathological ST-T changes recorded through a conventional ECG machine \vith that obtained through the Avionics Electrocardiocorder E and its interpreting equipment; the results demonstrated identity of the tracings.g Furthermore, the Electrocardiocorder and reproduction system have a correction network for improving its low frequency response which is not a simple RC netlvork. Therefore, \ve compared the low frequency response of a conventional ECG machine (Sanborn 100) and the Electrocardiocorder E, by applying to both of them a step voltage. Fig. 1 shows that the step voltage decays to 90 per cent of its original value in the conventional

ECG machine after 300 msec. and in the Avionics system after 240 msec. Since the duration of the S-T segment is not longer than 200 msec. and after this interval the decay in the step voltage in the Avionics system is similar to that of the conventional ECG (92 per cent and 93 per cent, respectively), \ve conclude that for clinical purposes this system is satisfactory for reproducing the S-T segment. The patients lvere requested to keep a record of their activities and symptoms Ivhile being taped, so that these could he subsequently correlated with EC(i findings. S-T elevation ~vas regarded as significant if the folto\ving conditions xvere fulfilled: it occurred for at least 12 seconds, the ECC strip had a stable isoelectric line (defined as txing a straight line dralvn through three subsequent T-P segments), the S-T segment being 1.5 mm. or more above that line, the

l’ransient

Reason

for

pain

Chest

pain,

Chest

asthenia

Post

myocardial

infarction

Post

myocardial

infarction

palpitations,

Post myocardial m

infarction

breathlessness

S-T elevation

of 3-4 mm.

Variant

angina

pectoris

S-T elevation

of 4-5 mm.

Variant

angina

pectoris

dizzy

pain

Fig. 2. Lovrer

spells

Upper

@neL,

@aneZ, ECG S-T elevation

tracing of patient observed during

asthenia,

No. 1, as recorded during most of the 24-hour monitoring sleep, lasting for 5 minutes and not causing him to awake.

strip jvith S-T elevation showed QRS complexes identical or closely resembling, for direction and amplitude, those of the preceding strip without the S-T elevation, and the amplitude of the QRS closely approximated the amplitude of L’s in the standard ECCi.

Results 7‘he seven patients who showed transient elevation on 24 hour monitoring were invarial)ly male and their age varied from 18 to 66 years (‘Table I). In view of their clinical background and subsequent ECG findings, the patients were divided into three groups:

S-T

Diagnosis

monitoring

Neurocirculatory suspected Neurocirculatory

Chest pain and palpitations Chest pain, syncope Chest pain,

during

Abrupt changes in rate from 84 to 170; inversion of T waves; S-T elevation of 2 mm. Repeated S-T elevation of 2 mm.; T wave inversion S-T elevation of 2 mm.; S-T depression of 1 mm.; supraventricular tachycardia; ventricular premature beats S-T elevation of 1.5 mm.; S-T depression and T wave inversion; atria1 premature beats and atrial tachycardia S-T elevation of 2 mm.

Palpitations Chest

Findings

monitoring

503

S-l’ elevation

1. Patients with neurocirculatory

period.

asthenia:

CASE 1. B. Y., 18-year-old male, referred because of palpitations which troubled him at rest and during exercise. Physical examination was negative. The resting ECG showed a single atrial premature beat, A Master test showed no ST-T changes, but several atrial premature beats were recorded, some of which were blocked. On ergometric examination’0 at a load of 100 \Vatts per minute and at a heart rate of 160 per minute, inverted T waves in [
504

Gelding

et ni.

Fig. 3. U@er panel, ECG tracing of patient Tw ;L\‘E: inversion. Lower panel, I,onger period

Fig. 4. lipper S-T ele vation

panel, ECG tracing observed intermittently

of patient during

No. I’, demonstrating hhort period5 of more marked S-T elevation and

-No. 3, during most of the 24-hour recording the day, accompanied by chest pain.

CASE 2. C. A., aged 28, complained of stabbing chest pain, not related to exercise. On physical examination he wns noted to be \-cry anxious. His resting ECG showed biphasic T wa\es in I,:{, a\‘~, and V1, V:, and Ve, which became negative on stnnding. Twenty-four hour monitoring showed repented periods of S-T elevation up to 2 mm. during ordinary daily activities lasting from 1 to 5 minutes (Fir. 3). T wave inversion was also observed at other periods. The patient felt subjertivtly impro\-ed after institution of therapy with bet:i-blocking agents. A diagnosis of neurocirculatory asthenia was made.

2. Patients

after myocclrdid

infarction:

3. I;. C., aged 61, was referred because of dizzy spell+.;. Four months previously he suffered a myocnrdial infarction. The resting ECG showed signs of a healed anteroseptal infarction. On ergometric examination, at a load of 82 \\~atts per minute and at a heart rate of 130 per minute, S-T depression of 1 mm. was recorded in I,ead V: and xrentricular premature beats were noted. At the same time the patient complained of chest pain. Twenty-four-hour monitorinK showed periods of S-T elevation of 2 mm. CASE

of blight S-T elevation T have changes.

period.

Lcwer

and

p anel,

during usual daily activities. Furthermore, S-T elevation during sleep with short runs of supraventricalar tachycnrdia and numerous x-entricular premature bents, were noted (Fig. 4). The patient did not awake during these episodes and did not complain later of nightmares. nuring the day S-T depression of 2 mm. as well ns T wave flattening were also observed. CASE 4. I-I. A., aged 56 years, suffered from an acute myocnrdinl infarction two months previously. He was referred because of palpitations and chest pain not related to exercise. The ECG showed a healed anteroseptal infarction. During ergometry, S-T depression of 3.5 mm. developed at a heart rate of 120 per minute while working at a load of 75 \\‘atts per minute and was accompanied by chest pain. Monitoring during a 24-hour period revealed S-T elevation of 1.5 mm. during sleep, lasting seven minutes (Fig. 5). Durin!: the day T wave inversion and S-T depression of 1 mm. were noted as well as atria1 premature beats and short runs of atrial tachycardia. CASE 5. M. B., aged 54 years, was referred because

Transient

Fig. 5. Upper panel, ECG Loser puanel, S-T elevation

tracing during

of patient No. 4, as recorded during most sleep, lasting 7 minutes and not awakening

Fig. 6. Upper panel, ECG tracing of patient No. Lower panel, Repeated periods of S-T elevation, accompanied by chest pain

5, as recorded during lasting up to several

of chest pain, palpitations, and two episodes of syncope. Seven years before he had suffered from a myocardial infarction. The ECG at rest showed evidence of healed anteroseptal infarction, prolonged P-R interval, right bundle branch block, and left anterior hemiblock. Twenty-four-hour monitoring disclosed repeated S-T elevation of 2 mm. during normal daily activity lasting up to five minutes (Fig. 6). The patient felt chest pain at these times. During sleep flattening of T wave and premature ventricular beats, about 3 per minute, were recorded,

3. Patients

with “variant”

angina pectoris:

6. H. Y., aged 66, had a history of chest pain not related to effort, and was known to suffer from chronic lung disease. The resting ECG showed right bundle branch block and ventricular premature beats. Twent!;-four-hour monitoring showed 3 to 4 mm. S-T elev;ltion on walking which coincided with the periods of chest pain and breathlessness mentioned in the patient’s diarv _ (Fig.._ 7). CASE 7. B. Z., aged 47, suffered from chest pain not related to exercise. His resting ECG showed right bundle branch block. A single Master test was CASE

S-T elevation

of the 24-hour the patient.

monitoring

50.5

period.

most of the 24-hour monitoring period. minutes, during usual daily activities,

negative. Twenty-four-hour monitoring showed during the day one period of S-T elevation of 4 to 5 mm. lasting 7 minutes (Fig. 8). At that time the patient experienced chest pain, although he did not exert himself.

Discussion

In our study of 174 patients that underwent 24-hour continuous ECG monitoring, seven showed transient S-T elevation. Two of these patients suffered from neurocirculatory asthenia and though various EC{; changes have been‘ described in this syndrome,‘l the finding of transient S-T elevation has, to the best of our knowledge, not been described previously. The clinical symptoms and findings on this condition can satisfactorily be explained on the 1)asis of sympathetic overactivity and can be prevented by the institution of beta-blocker

Fig. 7. Upper panel, ECG Lower $unel, S-T elevation

tracing of patient recorded during

Nu. 5, as recorded during most walking, accompanied by chest

of the 2-Lhour pain.

monitoring

period.

Fig. 8. Upper panel, l
tr,icillg of Ixttient recorded durill%

No. 7, ;LS recorded ;I 7-minute period

of the Z&hour

monitoring

period.

therapy. I2 The detection of S-T elevation in the two cases descrilwtl above suggests the possibility of sympathetic induced coronary artery constriction. Since our patients were relatively young, \ve assume that they have normal coronary arteries; however, that vasospasm in a normal artery can result in S-T elevation remains to 1~ proved. The second group of patients consisted of three who had suffered a previous myothat acute cardial infarction. It is known ischemia in cardiac muscle alongside an infarcted area may give rise to S-T elevation13 and it is thought to explain this linding in the patients of this group. The third group had atypical chest pain, and S-T elevation at rest or during ordinary physical activity. All these findings are

during most of chest IAn.

compatil)le \vith the tliagnosis of Prinzmetal’s \.ariant angina pectoris.’ This condition implies the presence of a high grade localizetl occlusion in the proximal part of one of the three main coronary arteries. l’rinzmetal and co-xvorkers’ mention three such cases. I’eretz,2 and .Silverman and I~lanim7 tlescril)e one case each, \\-ho at postmortem examination slio\\- severe localized stenosis at the proximal end of one of the three main coronary arteries. Alamlpin and Krattus14 performed coronary arteriography on six cases and found a single major stenotic lesion in five. They suggested the possibility of surgery in these patients, \vhich \vould seem reasonaMe on the Ijasis of the poor prognosis in this syndrome.’ This step was taken by Silverman and Flanim7 in a patient \~ho slio\ved a seg-

Transient

mental obstruction of 7.5 per cent in his right main coronary artery. We believe that with the development of selective coronary arteriography and bypass surgery, the exact diagnosis of a condition with the above mentioned pathological associations and a poor prognosis has special importance. !%nce the history in this syndrome is atypical and both the resting and the exercise ECG are usually normal, continuous ECG monitoring under dynamic conditions as described above is of particular assistarnce in diagnosing these cases. Summary

3.

4.

5.

6.

Seven out of 174 patients subjected to continuous 24-hour ECG monitoring because of atypical chest pain and/or palpitations were found to have transient S-T elevation. Two were diagnosed as suffering from neurocirculatory asthenia, three had myocardial infarction, and two suffered, most probably, from Prinzmetal’s variant angina pectoris. We believe that the finding of transient S-T elevation is of special significance, because of the pathological and therapeutic implications, and that continuous ECG monitoring during unrestricted daily activities provides a unique opportunity to detect this condition more frequently. We are greatly indebted to Prof. J. Weinmnnn of the Bioengineering Dept. of the Hebrew University-Hadassah Medical School, and to Dr. Y. Mahler of the Electronics Dept. of the Hadassah University Hosoital for their useful helo. The devoted technical assistance of Mrs. Batia ‘Glassman is gratefully acknowledged. REFERENCES 1. Prinzmetal, Bar, N.:

2.

M., Angina

Kennamer, pectoris

R., Wada, I. A variant

T., and form of

7.

8.

9.

10.

11.

12.

13.

14.

S-T elevation

507

angina pectoris. Preliminary report, Am. J, Med. 27~375, 1959. Peretz, D. I.: Variant angina pectoris of Prinzmetal, Can. Med. Assoc. J. 85:110, 1961. Bellet, S., Eliakim, M., Deliyiannis, S., and La Van, D.: Radioelectrocardiography during exercise in patients with angina pectoris: comparison with the postexercise electrocardiogram, Circulation 25:5, 1962. Gilson, J., Holter, N. Y., and Glasscock, W. R.: Clinical observations using the electrocardiocorder-AVSEP continuous electrocardiographic system. Tentative standards and typical patterns, Am. J. Cardiol. 14:204, 1964. Lunger, M., and Shapiro, A.: Continuous electrocardiographic monitoring in nocturnal angina (Abstr.), Am. J. Cardiol. 13:119, 1964. Whiting, R. B., Klein, M. D., Vander Veer, J., and Lown, B.: Variant angina pectoris, N. Engl. J. Med. 282:709, 1970. Silverman, M., and Flamm, M. D.: Variant angina pectoris, anatomic findings and prognostic implications, Ann. Intern. Med. 75:339, 1971. Tzivoni, D., and Stern, S.: Improved method of operating the Holter-Avionics ECG recording .. system, AM. HEART J. 83:846, 1972. Stern. S.. and Tzivoni. D.: The reliabilitv of the Halter-Avionics sys&m in reproducing the ST-T segment (Letter to the Editor), AM. HEAKT J. 84:427, 1972. Kiinig, K., and Messin, R.: Methods of evaluation of the physical capacity, Acta Cardiol. (Suppl.) 14:30, 1970. Holmgren, A., Jonsson, B., Levander, M., Linderholm. H.. Siijstrand. T.. and Striim. G.: E.C.G. chal~ges’in’vasoreg~~latbry asthenia’ and the effect of physical training, Acta Med. Stand. 165:259, 1959. Frohlich, E. D., Dustan, H. P., and Page, I. H.: Hyperdynamic beta-adrenergic circulatory state, Arch. Intern. Med. 117:614, 1966. Friedberg, C. K.: Diseases of the heart, Philadelphia and London, 1966, W. B. Saunders Company, p. 710. Macalpin, R. N., and Krattus, A. A.: Angina pectoris at rest with preservation of exercise capacity--Angina inversa (Abstr.), Circulation (Suppl. II):176, 1967.