V
SatktFcwmoftheTW~twinrCawd
N&y
Seibgyi,
M.D.,
and Samuel L. Solomon, M.D.,
Brooklyn,
N. Y.
Alterations in the form of the T wave with changes in the heart rate were Changes in the size, investigated in a series of cases for the first time by Scherf.’ shape, or direction of the T wave, as well as changes in the S-T segment in the absence of alterations of the QRS complex were observed following the prolonged pauses of single ventricular and auricular extrasystoles, of blocked aurirrular extrasystoles, and in partial heart block. In a third of the cases studied, a&erations of the T waves in postextrasystoiic beats were noted; but among many hundreds of cases of partial heart block, the author found only 2 cases showing the phenomenon. Later investigators dealt with T-wave changes in the postextrasystolic beat only,ZJ and a search of the available literature revealed no further report of T-wave changes in partial heart block of the type herein described. Because the occurrence of alteration of the T wave in partial heart Mock seems so rare, we felt that the report of this case, with its multiplicity of variations in the contour of the T, might be of interest. CASE
REPORT
A ‘IO-year-old Hebrew widow was admitted to the Brooklyn Hebrew Home and Hospital for the Aged for custodial care on March 30, 1957. Her significant past history was gall-bladder surgery 36 years before, and hypertension of unknown duration. The blood pressure on admission was 220/90 mm. Hg. The lungs were clear. The heart was “enlarged,” the pulse rate was 74 per minute, and the rhythm was regular. A slight “systolic murmur” was audible at the apex. Blood chemistry, blood count, urinalysis, and seroIogy were all negative. X-ray showed an enlarged left ventricle. An electrocardiogram on March 26, 1957, revealed “regular sinus rhythm, pattern of left ventricular hypertrophy, and right bundle branch block.” On Sept. 6, 1957, she had an episode of unconsciousness, which was sudden in onset and lasted for 10 minutes. The electrocardiogram at this time showed complete A-V dissociation and posterolateral wall &hernia. During the next few days the pulse rate ranged between 48 and 32 per minute. On Sept. 18, 1957, she was transferred to the Hospital Division. Her cardiic rate was now 36 per minute. She was in no distress. The ahztrccardmgram now revealed A-V Mock, Z:C, 3:1, with periods of complete A-V dissociation, ventricular bigeminy, and changes suggestive of anteroseptal wall infarction. From ths Brooldyn Hebrew Home Received for publication May 23,
and Hospital 1969.
for 687
the
Aged,
Brooklyn,
N.
Y.
638
October,
1959
OFTHE T WAVE AND DURATION UFTHE PRECEDING; DIASTOLIC PERIOD (TRACING OF SEPT. 21, 1957, CYCLES 5 TO 9) -
TABLEI.
RELATIONOFMAGNITUDI?
I
NUMBER OF CYCLE
5
Durationt of preceding diastole (l/l00 sec.)
*Beceuae
6 ES
-___
105
Voltage of T wave (mm.) Upright Inverted
the
i\m. Heart J.
S%II,.\GVI AND SOLOMON
16.25
7
--_--
8 ES
____
-
108
-
-__~-
-
--
17
9
----
108
-z __.
of a downsloping
base line the beginning of the QRg wvi18 used as the reference level for The voltage we.9 measured to the nearest 0.26 mm. are given in l/100 second.
measurements of the T in ell tracings. tTime
TABLE
measurements
II.
RELATIONOF MAGNITUDEOFTHETWAVEAND DIASTOLIC PERIOD (TRACING OF SEPT.
DURATIONOFTHE
NUMBEROF
I I
Duration of preceding diastole (l/100 sec.) Voltage of T wave (mm.) Upright Inverted
36 _. -------
37
38
i
100
70
*
28
-
17.25
12.5
CYCLE
I
35 _-
PRECEDING
21, ~~~~,CYCLES 34 ~045)
42 43 ____---92
72
*
17
16
3.5 1
28
12
44
45
16
14
-
*Not discernible. tNot
ascertainable.
TABLE III.
RELATION OF MAGNITUDE OF THE T WAVE AND DURATION OF THE PRECEDING PERIOD (TRACINGOF SEPT. 21,1957,C~~~~s 17 ~021)
DIASTOLIC
I ) Duration of preceding diastole (l/100 sec.) Voltage of T wave (mm.) Upright Inverted *Not
ilscertainable.
I
NUMBEROFCYCLE
17 *
/
I
;: -
- I -I 18.5
;
19
40
1
20
21
<4
24
a
14
15
(
Elmer
“4”
VARIATIONS
IN
FORM
OF
T WAVE
IN
PARTIAL
HEART
639
BLOCK
Since there were no syncopal attacks, both Isuprel and digitalis were withdrawn after two weeks. She improved progressively, and by Oct. 31, 1957, she was ambulant, with a pulse rate of 72 per minute. On Feb. 7, 1958, she suffered another syncopal attack, with a drop of the heart rate to 40 beats per minute. She improved on Isuprel, and by Feb. 24, 1958, the extrasystoles noted previously had disappeared, but the heart rate continued at 42 per minute. On March 30, 1958, she developed sudden dyspnea and cyanosis, rallying briefly, only to expire in an episode of dyspnea the same day. A tracing taken on Sept. 19,1957 (Fig. 1) shows second degree A-V block with varying ventricular response of 2:1, 3:1, and more. Ventricular extrasystoles were recorded singly, forming ventricular bigeminy, and in series of two and more. The most prominent feature of the electrocardiogram is the presence of huge and wide inverted T waves, registered in Leads Va to Ve. The widening is accentuated by the merging of the final limb of the T wave with the U wave and the superposition of the P wave. The Q-T inter-vat is obviously and grossly prolonged. Its exact duration cannot be determined because of the distortion of its terminal portion. The extrasystoles constituting the bigeminy occur on the upstroke of the T wave, following the inscription of the P wave. The succeeding auricular impulse is usually blocked, giving rise to a 3:1 block. This suggests retrograde conduction of the extrasystole. When two and, usually, when three extrasystoles were inscribed in succession, the 3:l block persisted. suggesting retrograde conduction of only the first extrasystoles. TABLE
IV.
RELATION DIASTOLIC
OF MAGNITUDE OF THE T WAVE AND DURATION OF THE PRECEDING PERIOD (TRACING OF SEPT. 23, 1957, CYCLES 1 TO 10)
___I_--. NUMBER
--
OF CYCLE
-..-
3 2
1 dias-
Voltage of T wave (mm.) Upright Inverted -.-I_ _____ *Not
6
7
8
-.-~
--Duration of preceding tole (l/l00 sec.)
5
ES
*
128
-
56
24
12.5
15
-
15.25
13
I
-
36
124
24
15.75 ~----.
12.25
-l--
1 Y /
34
13
1 /
10 -120
15.5
ascertainable.
A tracing taken two days later (Sept. 21, 1957) shows further improvement in the function of the A-V conduction system. Periods of regular sinus rhythm, of three to six beats, alternate with periods of 3:1 and 2:l transmission. Ventricular extrasystoles are less numerous. As a consequence of these variations in rhythm the duration of the diastolic period Euctuates widely. Associated with these fluctuations are marked alterations in the amplitude, shape, and direction of the T waves. Thus, T waves ranging from 18 mm. in depth to a few millimeters in height were recorded (Figs. 2, 3, and 4). Tables I, II, and III, corresponding to these figures, show the Elationship between the amplitude of the T wave and the length of the preceding diastolic period. In connection with Figs. 2 to 4, certain observations are in order: (1) In general, in this case, giant T waves as recorded in Cycle 35 were inscribed whenever the diastole approached 100. (2) Cycles 42 to 4.5 illustrate alternation of the size of the T wave and corresponding alternation in the duration of the Q-T interval. Such alternations were noted whenever series of sinus rhythm of more than four beats were recorded. (3) In each series of sinus rhythm the T wave of the second beat was most strongly affected by the sudden change in the cardiac rate. The degree of change in the configuration depends on the duration of the preceding diastolic period. Whenever a giant T wave (Cycle 35 in Fig. 3) precedes a series, the T wave of the first beat fills the entire
640
SZILAGYI
AND
Am. Heart 1. Oatober. 1959
SOLOMON
cycle from the S-T junction to the onset of the subsequent QRS complex, leaving only a minimal diastolic period, if any. The T wave of the second beat shows the pattern of ischemia-injury (Cycle 37 or 41); its QRS is slightly modified. In those instances in which the sinus series is preceded by the compensatory pause of a ventricular extrasystole, the T wave of the first beat is of somewhat shorter duration, leaving a discernible diastole. The T wave of the second beat is small and of the coronary type (Cycle 20). Another two days later (Sept. 23, 1957) regular sinus rhythm block were encountered only rarely. On one occasion several
was established.
Periods
of
periods of block were recorded at short intervals. This is shown in Fig. 5 and Table IV. As can be seen, the T waves of the regular beats are sharply inverted, the Q-T interval smaller than in cycles with comparable T waves on the previous record. The T waves following the periods of block, and those following the shorter compensatory pause of a ventricular extrasystole are of identical contour and deeper than the T waves of the other regular beats. This is in distinct contrast to the marked variation in the size 2:l
of the T waves record.
with
varying
duration
of the preceding
diastolic
period
observed
in the previous
continuous strip of Lead V4 of the tracing taken on Sept. 19, 1957. The tracing shows T waves in sinus beats. The P w&ves me regularly spaced at an interval of 82 (l/lo0 sec.), c01~t3sponding to a rate of 73 per minute. A ventricular extmsystole follows the first conducted sinus beat, and two successive extrasystoles follow the second one. No extrasystole is interposed between the third and fourth conducted sinus beats. The R-R intervals of the siuus beats measure 254 (3 X 82), 254 (3 X 82), and 168 (2 X 82). respectively, indicating the presence of 3:l block when a single extrasystole and two successive extrasystoles occurred, and 2:l block in the absence of an extrasystole.
giant
Fig. I.-A negative
COMMENT
Massive T-wave inversion in coronary heart disease has been the subject of various reports. Huge T waves were observed in cases with slow ventricular rate, and the possibility
that
increased
and varying
vagal
tone plays
a role in the
mechanism of massive inversion was considered.4 Some casesdid not show slowing of the ventricular rate.6 The authors felt that ischemia may have been a precipitating factor. In our case the huge inverted T waves shown in Fig. 1 occur at a slow ventricular rate resulting from myogenic disturbance in the A-V system. The fact that huge T waves occur only after long diastolic periods, and the orderly and related manner of their variation, suggest that the extent of the prolongation of diastole increased filling of the heart is a determining factor in the and the consequently production
of the T-wave
changes.
In the opinion
of Scherf’
“alterations
of the
T waves seem to be chiefly connected with changes in the filling of the heart,” metabolic processes accompanying alteration of the and again, “the different contractility seem to be the most probable explanation for the changes in the T
VARIATIONS
IN FORM
OF T WAVE
IN PARTIAL
HEART
641
BLOCK
waves as described. It is conceivable that changes in the strength of systote are unaccompanied by changes in the form of the T wave under normal conditions, but appear if the”..heart is in some way ‘damaged’.” As observed in this case, the giant T waves-in the second electrocardiogram (Figs. 2-4) appear to have been merely’s specific alteration which occurred in the then existing state of the myo-
Fig.
2.-A
strip
of Lead V4 of the tracing taken on Sept. 21, 1867. The figure shows T waves in sinus beat8 when following prolonged diastolic periods.
giant
negative
Fig. 3.-The two strips are continuous records of Lead V4 of the same tracing shown in Fig. 2. The last beat-Cycle 39-of the upper strip is reproduced at the start of the lower strfp. The figure illustrates the marked alterations of the T waves subsequent to diastolic periods of various duration, and the almost identical contour when they follow diastolic periods of the eame duration.
Fig. 4.-A strip of Lead V4 of the same tracing shown in Figs. 2 and 3. The flgnre pause of a ventricular tions of the T waves subsequent to the COmpenmtOw
Riuatra~ &he a&era. extraay&&.
642
SZILAGYI
AND
SOLOMON
cardium in response to marked lengthening of the diastole and increased filling of the heart. It is generally accepted that in ischemia of the subepicardial myocardium the electrical activity is prolonged in these layers, resulting in inversion of the T wave and prolongation of the Q-T interval.s Since the T waves are less wide and deep in the third electrocardiogram (Fig. 5) that in the previous one, it may be assumed that the circulation in the vicinity of the infarcted area had improved when this tracing was recorded. The uniformity of the T waves following diastolic periods of markedly varying prolongation suggests that with a lesser degree of &hernia the myocardium became less susceptible to variations in the diastolic filling. This is in accordance with the concept of Levine and associates2 that alterations in postextrasystolic beats suggest “ischemia” or “ischemia-like changes.”
Fig. 5.-The two strips The last cycle of the upper illustrates the alterations of following the compensatory
are continuous records of Lead V5 of the tracing taken on Sept. 23. 1957. strip-Cycle 6-is reproduced at the start of the lower strip. The figure the T waves following each of the prolonged periods of block, and those pause of B ventricular extrasyetole.
As was noted, alternate changes in the size of the T waves in regular sinus rhythm occurred whenever sinus series of more than four beats were recorded. Alternans of the T wave per se is physiologic. It occurs when the cardiac rate is suddenly accelerated, and is the effect of the sluggish adaptation of the recovery phase to the new rate. ‘,* Under physiologic conditions the T wave maintains its contour, while its duration undergoes variations-as evidenced by the alternate shortening and lengthening of the Q-T interval-until equilibrium is reached. In our case, alternation is not confined to the Q-T interval, but extends to the size of the T. Table V presents data (taken from Tables I-III) for cycles with diastolic periods of from 12 to 28, on the one hand, and cycles with diastolic periods of from 92 to 108 and more, on the other. This juxtaposition hints at a relatively much greater increase in voltage in the diastolic periods in the range between 12 and 28 than for a similar increase in voltage in the diastolic periods in the range of values above 92. This may be explained by the rapid filling of the ventricles in early diastole, in which a small increment in duration is associated
VoIume
58
Num!w
4
VARIATIONS
1N
FORM
OF
T WAVE
IN
PARTIAL
HEART
643
BLOCK
with a large increase in filling, whereas at the end of a prolonged diastole the opposite occurs. This would support the viewpoint that the variations in the T waves are the response of the ischemic myocardium to changes in filling. The strikingly small T wave, of the coronary type (as illustrated in Cycle 20)‘ measures half the voltage of the T’s almost adapted to the new rate. The Q-T interval is shorter than that of the subsequent beat by one fifth. The pronounced reduction in the Q-T interval in our case is not merely part of the adaptation process. s Such shortening has been attributed to marked acceleration in the electrical activity in both the subendocardial and subepicardial layers, and has been observed in experimental asphyxia in cats and during pure nitrogen breathing.1° The ventricular complex following an imperceptible diastolic period (illustrated in Cycles 39 or 41) shows, in addition to the disproportionally short Q-T interval, elevation of the S-T segment and terminal inversion of the T wave. The QRS complex is slightly modified. Although restricted to three cycles only, the change has the earmarks of alternans of the S-T segment. This phenomenon is thought to be due to failure of parts of the ventricular muscle to depolarize. Alternation of the S-T segment is commonly observed in experimental occlusion and indicates severe myocardial damage.7 Experimental findings and clinical experience point up the fact that transient displacement of the S-T segment,11J2 even with transient modification, simulating myocardial infarction may result from extreme coronary insufficiency. The changes in the T wave, and those of the entire ventricular complex observed in the second cycle of each sinus series may be analogously related to extreme reduction in the coronary flow. TABLEV.
JUXTAPOSITIONOFSOME
DURATION OF PRECEDINGDIASTOLE (l/loo SEC.)
I
I-III,
DATAOF TABLES INCREASING MAGNITUDE
RANGEOF VOLTAGE OF T WAVE (MM.)
II II
DURATION OF PRECEDINGDIASTOLE (l/loo
ARRANGEDIN
= I
SEC.)
ORDER OF
RANGEOF VOLTAGE OF TWAVE(M?d.)
92
12 1:
1% 12.5-14
100 105
z.25 16.25
28
13-13.5
108 108
:; 18.5
>llO
CONCLUSION
AND
SUMMARY
1. Three electrocardiograms in a case of recent myocardial infarction are presented. The tracings were taken at two-day intervals. The first shows giant T waves, and the second and third show variations of the T waves in the presence of partial heart block. 2. Analysis revealed progressive enlargement of the T waves with increasing length of the preceding diastole. At one end of this progression are the small T
644
SZILAGYI
AND
SOLOMON
.\m. Heart J. October, 1959
waves of short duration, with and without displacement of the S-T segment, which follow small or imperceptible diastoles; at the other end are the giant T waves which follow long periods of block. 3. The different behavior of T waves following diastoles of similar duration in the second and third electrocardiograms suggests improvement of the circulation on the latter occasion. This different behavior supports the opinion that ih the second electrocardiogram the increase in the size of the T waves with increasing length of the preceding diastole demonstrated the response of the ischemic myocardial layers to the increased filling of the heart. 4. When the diastole was shortened to a point at which it was barely or not at all discernible, changes in the subsequent T wave or the entire ventricular complex were observed and may have been related to severe coronary insufficiency analogous to experimental and clinical experience. REFERENCES
1. Scherf, D.: HEART
Alterations J. 28:332,
in the Form of the T Waves With Changes in Heart Rate, AK 1944.
2. Levine,
H. D., Lown, B., and Strieper, R. B.: The Clinical Significance of Postextrasvstolic T-Wave Chanees. Circulation 6~538. 1952. 3. Mann, ‘R. H., and Burchell,“H.’ B.: The Si nific&ce of T-Wave Inversion in Sinus Beats Following Ventricular Extrasystoles, w M. HEART J. 47:504, 1954. 4. Ippolita ‘TT L.&her, J. S., and Fox, T. T.: Massive T-Wave Inversion, Ard. HEART J. 5. Garcia-Pilmveri, ‘M. R., Marchand, E., Diaz-Rivera, R., Santiago-Stevenson D and Rodriguez, H. : The Significance of Giant Negative T Wave in Corona’ry Artery Disease, AY. HEART J. 52:.521? 1956. 6. Ashman, R., Ferguson, F. P., Gremrllian, A. I., and Byer, E.: The Effect of Cycle-Length Upon the Form and Amplitude of the T Deflection of the Electrocardiogram, Am. J. Physiol. 143:453, 1945. 7. Leneschkin. E.: Die Aktionsdauer des Herzmuskels. Med. Wochenschrift 1:78. 1947.. 8. Lepeschkin; E.: Electrocardiographic Observations ‘on the Mechanism of the’ Electrical Alternans of the Heart, Cardiologia 16:278, 1950. 9. Lepeschkin, E.: Modern Electrocardiography, Baltimore, 1951, Williams & Wilkins Com-
pany.
10. Rothschuh, K. E.: Elektrophysiology des Herzens, Darmstadt, 1952, Dr. Dietrich Steinkopff. 11. Kisch, B.: A Contribution to the Problem of the Electrical Alternans of the Heart, Cardiologia 6:95, 1942. 12. Roesler, H., and Dressler, W.: Transient Electrocardiographic Changes Identical With Those of Acute Myocardial Infarction Accompanying Attacks of Angina Pectoris, Aba. HEART J. 47:.520, 1954.