Download "Nonspecific" ST Segment and T-Wave Changes

Effect of Propranolol on "Nonspecific" S-T
Segment and T-Wave Changes:
Differentiation of Coronary from Noncoronary
ECG Changes*
S . Behar, M.D., and I . Kariu, M.D.
Thii study evaluates the effect of propranolol 10 to 20 mg per os, on so-called
nonspecific S T segment and T-wave changes in patients suspected of having
coronary insufficiency. One hundred forty three subjects were tested. Of these, 41
patients with definite heart disease (31 coronary patients and ten with left heart
hyperlrophy and strain) served as a control. One hundred two patients with noospecific ST-T changes to be evaluated were divided into two subgroups according
to their clinical history: 53 of these patients had no clinical history of heart
disease and had precordial pain clinically n d suggestive of coronary insufficiency;
49 patients, in whom, on clinical grounds, the diagnosis of coronary insufficiency
remained doubtful and angina pectoris could not be definitely excluded. No
patients in the contrd group reverted to normal ECG patterns after propanolol.
In most subjects in whom, on clinical grounds, angina pectoris could be excluded,
the ECG pattern reverted to normal. In the doubtful cases, both clinically and
electrocardiographically, a good separation of coronary from noncoronary could
be established. The mode of action and the rationale of this test, as well as its
clinical significance, are discussed.
onsiderable importance is ascribed to the ECG in
determining the diagnosis of ischemic heart
disease. A horizontal depression of the S-T segment
and negative, symmetrical T-waves are considered
characteristic of coronary heart disease; however,
doubts remain concerning the interpretation of S-T
segment and T-wave deviations from normal when
they are not clear-cut coronary, namely flat or even
slight negative T-wave and mild not horizontal S-T
depression changes, the so-called nonspecific S-T
changes.'
Several tests (hyperventilation, administration of
glucose and KCl) in addition to the classic Master's
test are in clinical use to clarify this point, but with
uncertain results and difficult interpretati~n.~"Recently, a new test has been introduced by Furberg
whose aim is to evaluate the nonspecific ECG
'From the Institute of Cardiolo , Chaim Sheba Medical
iv
Medical
Center, Tel-Hashomer; and ~ e y ~ v University
School, Israel.
Reprint requests: Dr. Behar, Sheba Medical Center, TelHashomer, Israel
376
changes through administration of pr~pranolol.'.~
The basic assumption is that in the majority of
noncoronary cases, nonspecific ECG changes are a
result of imbalance in the autonomic system.
We present the results of a study of this test that
we performed during the last year.
Our series consisted of 143 patients: 41 controls who had a
definite clinical and electrocardiographic pathologic diagnosis
(anginal syndrome, state after myocardial infarction, left
heart hypertrophy) and 102 patients who complained mostly
of chest pain whose ECG showed nonspecific S-T segment
and T-wave changes. The patients include 62 men and 40
women; 75 percent of them were over 40 years old. For investigation these patients were divided into two groups according
to clinical impression and our interpretation of their chest
pain, when present: group 1 consisted of 53 patients who
either had no complaints at all or whose complaints were
clearly nonanginal chest pain. Group 2, was composed of 49
patients with chest pain. Although the pain was not typical,
it was not possible to rule out with certainty angina pectoris
(AP). Both groups showed nonspecific S-T segment and Twave changes.
CHEST,
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VOL. 63, NO. 3, MARCH, 1973
PROPRANOLOL EFFECT ON NONSPECIFIC S-T SEGMENT AND T-WAVE CHANGES
-
Table 1 - 4 - T and T Waves Changes of the ECG and
Propranold Test
Reapom to Propranolol
Return
Material
ControI+l
Diagnosis
ptienta
Definite Cardiac
Pathology
to
No Partial
Normal Change C b e
0
5
36
Study group-102 ptienta
No angina pectoris
53
T Changea 46
41
S T Changeg 7
7
49
-
-
Angina pectoria
T Change8 43
19
15
9
-- -
S T Changea 6
3
2
1
R d t a of the propranolol test in 143 caees: 41 controla with definite clinical
and electmcardiographic pathology and 102 c a m with nonspecific S-T
segment and T-wave chmgw for evaluation.
After the basic ECC was performed at rest, the patients
were given propranolol orally in doses according to their
weight: 10 milligrams if weight was under 60 kilograms and
20 milligrams to patients who weighed over 60 kilograms.
One hour later the ECG was repeated and compared with
the basic tracing. None of the patients was fasting nor had
they received any medication (in particular, digitalis) that
might affect the ECG.
No side-effects were noted in any of the patients
after administration of the drug.
The results were classified as follows: ( I ) no
correction and sometimes worsening of the S-T-T
changes after administration of propranolol; (2)
partial correction; ( 3 ) reversion to normal.
The propranolol test gave the following results
(Table 1).
Control Group: There were 41 patients with
definite heart pathology. In 36 of these no change
or worsening occurred (Fig 1); in the remaining
five patients some mild changes were pen but in all
1 1 E P O R E
41, the ECG remained pathologic.
Patients for Znuestigatwn: These 102 patients had
nonspecific S-T-T changes.
Group 1 consisted of patients who definitely did
not have stenocardia. The ECG retumed to normal
in 48 persons (Fig 2,3). In four patients the tracing
remained unchanged, and in one only partial
changes were evident.
Group 2 was composed of 49 doubtful cases. In
22 patients the ECG returned to normal after
propranolol ingestion; in 17, no change occurred
and in 10, the ECG changes were partial only.
As shown in Table 1the pathologic ECG findings
are related in most cases to T-wave inversion with
or without some associated nonspecific S-T segment
changes. Thirteen patients showed principally S-T
segment depression. It is worthwhile mentioning
that in all the seven belonging to group 1 the S-T
segment became normal (Fig 4 ) but did so only in
three of the six patients belonging to group 2.
The frequency of nonspecific changes in the ECG
is estimated between 1 percent to 5 percent in a
normal population. This percentage increases greatly when an aged population is st~died.'.~
Disturbances of the electrolyte balance, in particular of potassium, is an accepted mechanism in
explanation of this phenomenon especially during
digitalis and diuretic treatment or in the postprandial ECG. Some attribute the nonspecific S-T-T
changes to the position of the heart.2.8*6
Another probable more frequent mechanism that
may explain nonspecific ECG changes is the dysfunction of the autonomic system caused by increased sympatheti~otonia.~
Since adrenergic stimulation of the heart is transmitted via the p-receptors,
it is assumed that depression of these receptors by 8blockers will bring about balance of the autonomic
system and in this way correct the electrocardiographic findings that are caused by adrenergic
hyperactivity. Consequently, the disappearance of
the S-T-T changes and the emergence of a normal
P R O P R A ' N O L O L
FIGURE
1. Typical history of stenocardia with
pathologic ECG changes which became more
pronounced and clear-cut after propranolol.
CHEST, VOL. 63, NO. 3, MARCH, 1973
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BEHAR, KARlV
-- .
-
- -
--
-
--
,
- ---
-
?--
,
I
r
v.
I
i
.
II
I
F
V.
tracing- would indicate no coronary heart disease
while the persistence or worsening of the ECG
changes could not be attributed to syrnpatheticotonia and is most probably a sign of coronary
involvement. Partial changes are difficult to evaluate and remain doubtful.
In our study, in those diagnosed definitely
pathologic, the ECG did not return to normal in
any patient. Among the 53 in whom we could
clinically rule out coronary heart disease, 48 reverted to normal. It would therefore appear that
there is a good agreement between the clinical
impression and the propranolol test results.
There remains the doubtful group of 49 cases in
whom it was difficult for us to decide clinically
whether or not ischemic heart disease was present.
This group showed mixed results. Therefore, if one
assumes that a good agreement exists between the
influence of propranolol and the clinical assessment,
it may be seen that this borderline group is not
homogenous and includes both coronary and noncoronary cases.
It is obvious that, in the absence of a definite
criterion for coronary heart disease, such as anatomic verification, or at least cine-coronary angiography, evaluation is made on the basis of comparison
with a test that is itself still being verified (the
propranolol test) with criteria whose value are
uncertain (clinical impression). This is, however,
the weak point of the entire ECG evaluation. On
the other hand, it is d a c u l t to ignore the clear
parallelism existing between pathologic and normal
cases both according to clinical evaluation and
according to the propranolol test.
4
FIGURE2. NO history of chest pains in an 18year-old boy.
V.
EFFEC~
OF HEART
RATE
Table 2 shows the range of heart rate in both the
control and study group before and after propranolol administration as well as the mean pulse
rate as related to the results obtained: reversion to
normal ( + ) or no change ( - ) of the ECG tracing.
Although there is a greater slowing of the heart rate
in the positive group (reverted to normal) than in
the negative group, mean decrease of 14 beats per
minute and 9 beats per minute respectively, it is
d a c u l t to ascribe the results of this decrease of
heart rate especially as there was practically no
tachycardia initially in any of these groups. In only
five patients did the initial rate exceed 110 beats
per minute. Figure 1 is illustrative in this regard.
The pulse rate decreased from 85 before propranolo1 to 60 afterwards. But the T-waves become more
negative after propranolol in spite of the bradycardia.
In all our coronary cases the S-T segment and the
T-wave inversion did not change after propranolol.
In some of them they became more pronounced.
Several authors reported relief of pain and diminishing of anginal attacks after prolonged treatment with large doses of propranolol but they do
not mention any objective electrocardiographic
changes.lO.ll
Both Rowlands12 and Goldbarg and co-workers13 note specifically the absence of any cardiographic changes in spite of relief of angina.
It is not our purpose to suggest the propranolol
test as a definitive test in cases with ambiguous
electrocardiograms. We can only point to the enBEFORE
AFTER
stenocardia in a 42-year-old woman Slinically.
PROPRANOLOL
PROPRANOLOL
F
II
vs
VI
CHEST, VOL. 6 3 , NO. 3, MARCH, 1 9 7 3
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PROPRANOLOL EFFECT ON NONSPECIFIC S-T SEGMENT AND T-WAVE CHANGES
Table W u l s e Rate Before and After Propranold
Study G r o u p
102 Patients
Control-
+
-
41 Patients
Range before propranolol
118-64
10050
10550
Range after propranolol
9651
SMiO
10550
Mean rate before propranolol
82.8
76.3
70
Mean rate after propranolol
68.6
67.7
66.5
Net Decrease in mean rate
14.2
9.6
Material
Pulae rate before and aftar propranolol in the dierent group.
couraging results. It is, of course, necessary to
perform this test on a much larger number of
patients, with long follow-up, in order to determine
to what extent it is possible to use the propranolol
test as a screening device in cases with nonspecific
electrocardiographic changes.
1 Friedberg CK, Zager A: "Nonspecific" ST and T-wave
changes. Circulation 29:655,1961
2 Sleeper JC, Orgain ES: Differentiation of benign from
pathologic T waves in the electrocardiogram. Am J Cardiol l l :338, 1963
3 Dogliotti GC, Brusca A: Cardiopathie electrocardiographique. Le Concours Medical 19-11 1177, 1966
4 Schneider RG, Lyon AF: Use of oral potassium salts in
the assessment of T-wave abnormalities in the electrocardiogram: A clinical test. Am Heart J 77:721, 1989
5 Dear HD, Buncher CR, Sawayama T: Changes in electrocardiogram and serum potassium values following glucose ingestion. Arch Intern Med 124:25, 1969
6 Kreisler B, Lapidoth E, Kariv I: Electrolyte disturbances
simulating coronary insu5ciency in healthy young adults.
Harefuah 49:225, 1965
7 Furberg C: Adrenergic beta-blockade and electrocardiographical ST-T changes. Acta Med Scand 181:21,1967
8 Furberg C: Effects of repeated work tests and adrenergic
beta-blockade on electrocardiographic ST and T changes.
Acta Med Scand 183:153,1968
9 Hiss RG, Averill HH, Lamb LE: Electrocardiographic
findings in 87,375 asymptomatic subjects-nonspecific T
wave changes. Am J Cardiol6: 178, 1960
10 Mizgala HF, Khan AS, Davies RO: Reflections on the use
of propranolol in angina pectoris. Am Heart J 80:428430,
1970
11 Grant RHE, Keelan P, Kernohan R, et al: Multicenter
trial of propranolol in angina pectoris. Am J Cardid
18:361-365, 1966
12 Rabkin R, Stables D, Levin N, et al: Prophylactic value
of propranolol in angina pectoris. Am J Cardiol 18:370383,1966 (Discussion by Rowlands DJ)
13 Coldbarg AN, Moran JF. Butterfield TR, et al: Therapy
of angina pectoris with propranolol and long acting nitrates. Circulation 40:847-853. 1969
CHEST, VOL. 63, NO. 3, MARCH, 1973
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