Functional and Myocarditis-induced T-wave Abnormalities

Functional and Myocarditis-induced T-wave Abnormalities* Effect of Orthostasis, J3-blockade, and Epinephrine

]ouko Karjalainen, M.D.

Negative T waves in the ECG during an acute infection may be due purely to functional variations, making the diagnosis of acute myocarditis difficult. The effects of orthostasis, 13-blockade, and intravenous epinephrine infusion (0.070. 211Lg/kglmin) on T waves and the Q-T interval was studied in 28 young men with acute myocarditis, in 29 persons with functional T-wave abnormalities, and in 30 healthy subjects. Myocarditis-induced negative T waves were never normalized by 13-blockade. FUnctional T-wave inversions were normalized by 13-blockade in 22 subjects (76 percent). Orthostasis always augmented the T-wave abnormalities that were normalized by 13-blockade. Functional T-wave

abnormalities responding to 13-blockade were augmented by epinephrine in 17 subjects (77 percent); but those unresponsive to 13-blockade were normalized in six of seven subjects. The Q-T. interval was significantly (p<0.01) lengthened in subjects with myocarditis (410 ± 36 ms) compared with controls (384 ± 27 ms~ The 13-blockade test is useful in differentiating between functional T-wave inversions and acute myocarditis. However, functional T-wave abnormalities are not constantly abolished by 13-blockade but may then be normalized by epinephrine. A clearly prolonged Q-T. interval speaks for a diagnosis of myocarditis.

T-wave abnormalities are ECG findings characteristic of acute infectious myocarditis. 1 However, "functional" or "nonspecific" repolarization changes causing a similar appearance of the T waves are encountered in routine ECGs of apparently healthy, asymptomatic people. AtterhOgl recently reported notched T waves in 4. 4 percent and inverted T waves in 0. 9 percent of asymptomatic young men. During acute infection, fever, tachycardia, hypoxia, electrolyte disturbances, the autonomic nervous sytem, and drugs may further influence the T waves. 3 Thus, ECG abnormalities noted in connection with acute infectious diseases should not be explained solely as indicating acute myocardial involvement. In fact, in clinical practice the nonspecific nature of such T-wave inversions makes it difficult to assess the possible existence of simultaneous acute myocarditis. Functional T-wave abnormalities are normalized by ~-adrenergic blockade, while those of organic origin persist. 4 On the other hand, functional-type T-wave inversions could be reproduced by epinephrine infusion after their normalization by rest. 5 The present study concentrates on the differential diagnosis of myocarditis-induced T-wave abnormalities.

previous heart disease or other major medical problems. They were divided into 28 myopericarditis and myocarditis patients (group M), 29 subjects with functional T-wave abnormalities (group F), and 30 control subjects (group C) as follows.

SUBJECfS AND METHODS

The study population consisted of 87 young men in military service, aged 18 to 38 years (median 20 years), without a history of *From the Central Military Hospital1, Helsinki, Finland. Supported by a grant from the Signe and Ane Gyllenberg Foundation. Manuscript received October 21; revision accepted January 18. Reprint requests: Dr: Karjalalnen, Central Military Hospital I, PL5, 00281 Helsinki 28, Finlaiul 888

The diagnosis of acute myocarditis required typical serial ECG changes of "acute pericarditis,''" where the initial ST-segment elevation of0.1 mV or more in several leads is gradually replaced by an inversion of the T-waves for several weeks before their eventual normalization. An equivalent criterion of acute myocarditis was gradually changing pattern of negative T waves in several leads, detected during or soon after an acute infection and lasting for at least two weeks, before their eventual normalization. 7 In these patients, it was also necessary to observe an unequivocal pericardia) rub and/or a transient radiologic enlargement of the heart; all had echocardiographic wall motion abnormalities. The clinical findings of these myocarditis patients were published elsewhere. 7 Functional T-wave abnormalities in subjects in group F were also first seen in connection with an acute infectious disease, and initially aroused the suspicion of acute myocarditis. No other signs of myocarditis or any other cardiac abnormality were subsequently observed, however. Physical findings, in repeated careful clinical examinations, serial serum cardiac enzymes, serum natrium and potassium levels, and serial chest x-ray film findings remained normal, and no distinct abnormalities such as mitral valve prolapse could be detected in serial echocardiograms. During a three-month follow-up, these functional or nonspecific T wave abnormalities either vacillated between normal and abnormal or remained permanently abnormal. 1 Control subjects were taken from among those who were initially hospitalized because of an acute infectious disease, but whose ECGs remained normal during and two weeks after the infection. No signs of cardiac abnormality were detected in physical examinations and chest x-ray films. Detailed ECG studies of the control subjects were made one to two weeks after the fever had subsided. By choosing the control subjects from among patients recovering from a recent acute infection, the three study groups were matched with the general circulatory and vasoregulatory effects of the infection itself. 8 T-waw Abnormalities (Jouko Katj8181nen)

Table !-Heart Rates (bpm) and Q-T. Intervals (ms) in Different Groups* Standing Resting

Standing

Myocarditis (n = 28) 14 Heart rate 73t 410t 36 QT" Functional, responsive to 13-blockade (n = 22) Heart rate 74t 13 QT, 25 401:1: Functional, unresponsive to ~-blockade (n = 7) 15 Heart rate 63 QT, 18 383 Controls (n = 30) Heart rate 61 10 QT, 27 384

~-blockade

~-blockade

102t 411

17 30

60t 377:1:

10 28

78:1: 387

10 29

101:1: 406

15 28

56 362

9 23

72 384

10 25

406

96

9 21

53 364

9 18

380

90 409

16 23

52 357

7 28

380

73

70

12 19 8 23

*Values are mean ± SD. :j: p<0.05 vs controls t p
Beta-blockade and Orthostasis Tests A 12-lead ECG at 50 mm/s paper speed was recorded at supine rest and after three minutes' free standing. Two hours after an oral dose of 100 mg metoprolol, ECGs were again recorded at supine rest and in a standing position. The tests were performed on every subject during his hospital stay.

Infusion

of Epinephrine

A dilution of epinephrine in normal saline solution was prepared just before the test. A control ECG was recorded after a rest period of five to ten minutes following the insertion of an intravenous (IV) saline drip. Then epinephrine was infused at constant rates: 0. 07 wd kg/min, 0.14 IJ.g/kg/min, and 0.21 IJ.g/kg/min. Each infusion was continued for one minute and the time required for recording the 12-lead ECG. Rhythm was monitored continuously by oscilloscope. The procedure was terminated prematurely if disturbing subjective symptoms appeared. The epinephrine infusion test was performed on every subject in groups F and C, and in 13 patients in the myocarditis group. For myocarditis patients, the test was performed during the recovery stage of the disease, the patients being symptom-free, but their ECG still showing negative T waves.

Measurement

of the Q-T Interval

The Q-T interval was measured in each subject at supine rest, after three-minute orthostasis and ~-blockade. The end of the T wave was

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Statistical Methods Statistical significances were examined using the unpaired or paired t test. RESULTS

Resting ECG in Different Groups Heart Rate: The mean heart rates were similar in subjects in group M and in subjects in group F responsive to ~-blockade, while lower resting heart rates were recorded in subjects in group F unresponsive to ~-blockade and in control subjects (Thble 1). T Waves: Figures 1 to 3 show the distribution of negative T waves in groups M and F. In both groups, T

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taken at the point where the T waves' line of most rapid descent transected the baseline in leads V2 or V3• 9 When the T wave was negative or biphasic in these leads or when there was a fusion of the T and U waves, the chest leads with most precise ending of the T wave was selected for measurements. The heart rate correction was made according to Bazett's formula10

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FIGURE 1. Effect oforthostasis and ~-blockade on the relative number of negative T waves in ECG leads in 28 myocarditis patients. Beta-blockade did not normalize T wave abnormalities caused by myocarditis. The increment of negative T waves in leads 2, 3, aV~"' Vu induced by standing was abolished by ~-blockade. CHEST I 83 I 6 I JUNE, 1983

868

BETA BLOCKADE

FIGURE 2. Effect of orthostasis and P-blockade on the relative number of negative Twaves in 22 subjects with functional T-wave abnormalities responsive to P-blockade.

wave inversions were most common in inferoapical leads 2, 3, aVF, V4-6. In myocarditis patients, the T wave was also often negative in lead 1 (43 percent) and occurred in anterolateral leads 1, aVL, and Vu in 29 percent of the 28 patients. In group F, the T wave was negative only once in lead 1 in resting ECG; also in that subject, the T-wave negativity was most prominent in inferoapicalleads. Functional T-wave abnormalities (group F) were usually most prominent in the first recorded ECG, as hospital rest tended to normalize these T waves in the majority of cases. Q-T Interval: Myocarditis patients had the longest Q-T. interval: 410±36 ms (mean± SD) (Table 1). It was clearly lengthened (over 450 ms) in fuur patients. The Q-T. interval was also almost significantly lengthened in subjects in group F responsive to P-blockade when compared with controls. The longest Q-T. interval in group F was 440 ms. Effect of Standing Heart Rate: Three minutes' standing increased the heart rate very similarly in different groups (Thble 1). T Waves: The effect of standing on the relative

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number of negative T waves in groups M and F are shown in Figures 1 to 3. If bedrest reverted the inverted T waves to normal in group F, standing always reproduced them again. Standing without exception augmented those group F T-wave inversions that subsequently were normalized by P-blockade. The Twave abnormalities in leads 2, 3, aVF, and V4--6 tended to become more marked in the standing position in myocarditis patients as well. Three minutes' standing induced T wave inversions in inferior leads 3 and aVF in 20 percent of control subjects, while leads 1 and aVL were not affected by the body position. Q-T Interval: Standing did not affect the Q-T. interval in myocarditis patients or group F subjects with P-blockade responsive T-wave inversions (Table 1). In contrast, the groups with lower heart rates showed an increase in the Q-T. interval. Lengthening of the Q-T. interval induced by standing probably is related to the fact that despite attempting to correct by Bazett's fOrmula fur heart rate, the Q-T. obviously is still rate dependent (Fig 4).

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870

T-waw Abnormalities (Joulco Katjalainen)

QTC (ms) 420

• Myocarditis patients I} Healthy subjects

410 400

390 380

370 360

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80

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HEART RATE (bpm)

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FIGURE 4. Relation between the Q-T, interval and heart rate in resting ECG (R) after three minutes' standing (S), after Ji-blockade (B), and after Ji-blockade and three minutes' standing (B + S) in 28 myocarditis patients and in 30 control subjects. (Other subgroups followed the same pattern; Thble 1). For a reference, a normal relationship between the Q-T, interval and heart rate (triangles) is calculated from the QT interval/heart rate nomogram published by Boudoulos et al. u It shows that the QT, interval is still heart rate-dependent despite the attempt by Bazett's formula to correct for heart rate. Acute Ji-blockade induces an apparent real shortening of the Q-T interval, while the effect of standing on the Q-T interval is explained by changes in heart rate.

Q-T Interval: Acute 13-blockade highly significantly (p<0.001) shortened the Q-T. interval in every group (Table 1); this was most conspicuous in subjects in group F responsive to 13-blockade, while there was less shortening in the myocarditis patients. The shortening of the Q-T. interval is still apparent, although the heart rate dependence of the Q-T. is taken in account (Fig 4). Effect of Epinephrine Infusion Hearl Rate: Epinephrine infusion increased the mean heart rates by 18 to 23 beats per minute in different groups. A junctional slow rhythm was induced by epinephrine in four subjects in group F (three unresponsive to 13-blockade), in one myocarditis patient, and in three control subjects. Ventricular extrasystoles were induced only once in a subject in group F unresponsive to 13-blockade who also had transient junctional rhythm during epinephrine infusion and transient atrial fibrillation thereafter. T wave: The effect of epinephrine on negative T

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FIGURE 5. Effect of intravenous adrenaline (epinephrine) infusion (0.07 to 0.2lJLg/kglmin) on the relative number of negative T waves in ECG leads. Symbols: 4 = 22 subjects with functional T-wave abnormalities responsive to Ji-blockade, • = seven subjects with functional T-wave abnormalities unresponsive to Ji-blockade. CHEST I 83 I 6 I JUNE, 1983

871

waves in the 13 myocarditis patients was diverse. There was no effect in three, the negativity increased in six, while it tended to lessen in four subjects. The net effect in all of group M was slight worsening of abnormalities. In group F, epinephrine produced effects opposite those of~-blockade. A greater negativity of the Twaves occurred in 17 of the 22 subjects responsive to ~-blockade, four showed no effect, and in only one subject did the negative T waves normalize. In turn, epinephrine normalized negative T waves in six of the seven subjects unresponsive to ~-blockade, while there was no effect in one (Fig 5). Seventeen percent of the control subjects showed Twave inversion after adrenaline infusion; this occurred in inferior leads 3 and/or aVF in three cases and twice in leads VS-4· Early repolarization-type ST-segment elevation was reduced by epinephrine. Epinephrine caused higher U waves and earlier beginning of the U wave, causing a partial fusion of the T and U waves. 12 DISCUSSION

Clinically mild or asymptomatic myocarditis frequently occurs in connection with various acute infections. 1•7 Although its acute course and late prognosis are usually favorable, 13-1.5 there is still a danger of sudden cardiac death16 or insidiously congestive cardiomypathy17 in these patients. Furthermore, because of the detrimental effect of physical exercise during the first days of the disease, 18 hard physical exercise must be avoided during myocarditis. Thus, it is necessary to recognize even mild myocarditis, particularly in physically active young people. In mild acute infectious myocarditis, T-wave abnormalities of the ECG are often the only detectable abnormalities. 1•7 This study shows that myocarditisinduced negative T waves are not normalized by ~-blockade. In contrast, functional T-wave abnormalities were abolished by ~-blockade in 76 percent of the 29 subjects without any demonstrable cardiac abnormality. In those subjects whose functional T-wave abnormalities were unresponsive to ~-blockade, epi-

nephrine infusion usually normalized T waves; myocarditis-induced T-wave abnormalities were only rarely normalized by epinephrine. Functional T-wave abnormalities unresponsive to ~-blockade and those induced by myocarditis were also differentiated by follow-up: the former persisted, while the latter were usually normalized gradually within a few weeks. 7 The differential diagnosis of functional T-wave negativity and Twave inversions due to acute myocarditis are summarized in Table 2. Furbert first showed that ST-T abnormalities of organic origin were unresponsive to ~-blockade while functional changes were abolished. His series included patients with coronary heart disease and myocarditis. Since then, ~-blockade has been used increasingly to confirm the innocence of nonspecific functional T-wave abnormalities. 19' 20 Not all T-wave aberrations in apparently healthy subjects are normalized by ~-blockade, however. Atterh0g2 found notched T waves in 4.4 percent and inverted T waves in 0. 9 percent of asymptomatic young men in leads 2, V4 , or V6 , and 11 percent were Chronic ~-blockade has unresponsive to ~-blockade. even been shown to be the occasional cause ofT-wave inversions. 111 Thggart et al5 found that inverted T waves unresponsive to ~-blockade could be normalized by IV epinephrine infusion. On the other hand, epinephrine reproduced T-wave inversions in subjects responsive to ~-blockade after their normalization by rest. They suggested a bimodal response of myocardium to epinephrine. The present study confirms the existence of two types of functional T-wave aberration that behave in opposite manners during ~-blockade and ~-stimulation. Isoprenaline also may normalize T-wave abnormalities in apparently healthy subjects, while abnormalities due to pericarditis persisted. 22 The precise physiologic mechanisms responsible for the functional T-wave abnormalities are obscure. Atterhog et al23 provided evidence of increased sympathoadrenergic activity in these subjects. Plasma norepinephrine but not epinephrine concentration

Table 2-Diffenmtial Diagnoaia of Myocarditis-induced T Wave Abnonnalities* Functional Myocarditis

Responsive to ~-blockade

T wave pattern

Gradual change

Vacillating

Standing Beta-blockade

No effect No effect/or augmented Usually augmented Inferoapical, anterolateral, or general

Augmented Normalized

Epinephrine ECG leads

*Inferoapical

m

Augmented Inferoapical

Unresponsive to ~-blockade

Persisting/or vacillating No effect No effect/or augmented Normalized Inferoapical, or septal

= leads 2, 3, aVF, Vl-'1; anterolateral = leads 1, aVL, Vl-'1; septal = leads Vu; general = leads 1, 2, 3, aVF, aVL, Vl-'1.

T-- Abnormalities (Jou/co Katja/8/nen)

correlated with the degree of the T-wave aberration. Taggart et al, 5 on the other hand, showed that these Twave abnormalities could not be produced by norepinephrine infusion, while epinephrine infusion was effective. They supposed that an altered P-adrenoreceptor responsiveness in the heart is more relevant than any catecholamine hypersecretion. The present study also concurs with the concept of an unusual responsiveness of cardiac P-adrenoceptors in these subjects: the same concentrations of epinephrine infusions induced T-wave abnormalities in group F but not in control subjects. If unusual end-organ responsiveness is more relevant than catecholamine hypersecretion in creating "functional" ECG changes, there remains the question of the reason for this altered sensitivity. Strenuous endurance training leads to sport heart syndrome, often expressed by negative T waves in the ECG. These T waves may be normalized by isoprenaline. 24 Marked myocardial hypertrophy in some cases of sport heart naturally provides an anatomic cause for negative T waves. 25 In the present series, three of the seven subjects with functional negative T waves unresponsive to P-blockade regularly engaged in sport. On the other hand, physical inactivity may be expressed as Twave abnormalities of "vasoregulatory asthenia," which can be normalized by physical training. 26 Patients with mitral valve prolapse syndrome typically have inferoapical T-wave inversions responsive to Pblockade.27 Functional ST-T abnormalities are also often added to those of coronary insufficiency and are frequently seen during convalescence after myocarditis. 7,14,15 Thus, while catecholamine hypersecretion may explain functional T-wave abnormalities in some subjects, the adaptation of P-receptor responsiveness to an altered level may be responsible in others, and an organic cause may even be incriminated as a trigger. These factors may lead to local changes in action potential duration and an altered sequence of ventricular repolarization. The relationship of T wave form, action potential durations, and sympathoadrenergic activity has been comprehensively discussed elsewhere. 2.5,22.28

Q-T Interval Gittlemann et al 29 found a prolonged Q-Tc interval in 63 percent of patients with fatal myocarditis verified by autopsy. The present study also discloses a prolonged Q-Tc in patients with mild myocarditis compared with control subjects. However, because the Q-Tc interval was also somewhat lengthened in subjects with functional T-wave aberrations, a mildly prolonged Q-Tc interval cannot be used as a differential diagnostic clue. A markedly prolonged Q-T interval somewhat favors the diagnosis of myocarditis: in 14 percent of the

myocarditis patients the Q-Tc interval was at least 450 ms, while the longest Q-Tc interval in group F was 440 ms. Beta-blockade significantly shortened the Q-Tc interval in all groups, and this effect was most conspicuous in subjects with functional T-wave abnormalities. This is partly explained by the changes in heart rate, since the Q-Tc interval calculated by Bazett's formula is still heart rate-dependent. There is evidence, however, that acute and chronic P-blockade have contrasting effects on the ventricular repolarization time. 30 A prolongation of the Q-T interval reflects inhomogeneity of the ventricular refractory periods and plays a role in arrhythmia vulnerability. 28 A high incidence of sudden death in patients with a prolonged Q-T interval is well known. Since this is also a most serious, although fortunately rare, complication of acute myocarditis, patients with myocarditis-induced lengthening of the Q-T interval warrant special attention. REFERENCES

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26 27 28 29 30

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T._ Abnormalities (Joulro Kllt/tllllinen)