Transient ST segment depression during

Holter monitoring: How to avoid false positive

findings
To increase the specificity of 24-hour Holter monitoring in detecting transient myocardial
ischemia, we separated genuine ST deviations from those dependent on artifacts by adding a
detailed shape analysis of real-time printouts to the usual criteria of significant ST segment
depression. We screened 116 apparently healthy subjects; 31 had to be excluded, because of
pathologic findings in preliminary examinations. The remaining 65 (49 women and 36 men; mean
age, 43.1 years) underwent Holter monitoring for assessment of the extent, frequency, and
duration of episodes of horizontal and descending ST segment depression of at least 0.1 mV
that persisted for at least 60 msec after the J point and that were at least 1 minute apart. On the
basis of these criteria, six subjects (7.1%) showed 24 episodes of horizontal or descending ST
segment depression with a mean of 0.2 mV (range, 0.15 to 0.25 mV), a frequency of four
episodes per 24 hours (one to nine), and a duration of 12.2 minutes (range 3-range 41 minutes).
Supplementary criteria-e.g., sudden onset of ST segment depression, identical orientation of
PQ and ST segments, or simultaneous increase in R and P wave amplitude-made it possible to
identify ST changes caused by artifacts in four volunteers. In only two subjects (2.4%) could true
silent ischemia not be differentiated from false positive results. Thus consideration of only the
extent, frequency, and duration of episodes does not permit a differentiation between true silent
ischemia and false positive results. A supplementary shape analysis increases the specificity of
ST segment analysis in detecting transient myocardial ischemia during 24-hour Holter monitoring.
(AM HEART J 1992;124:622.)

Heinz Viiller, MD, Dietrich Andresen, MD, Thomas Brdggemann, MSc,

Matthias Jereczek, MD, Bernd Becker, MD, and Rolf SchrGder, MD
Berlin, Germany

Holter monitoring has been suggested for the detec- of an accurate definition of pathologic ST segment
tion of transient symptomatic and asymptomatic is- depression. The aim of this study was to determine
chemia.lW4 However, ST segment changes are often whether the application of a more precise definition
difficult to evaluate: the transient ones occur not only of pathologic ST depression in an accurately selected
in patients with myocardial ischemia but also in per- “normal” population could increase the specificity of
sonswithout coronary heart disease. Previous studies Holter monitoring in detecting myocardial ischemia.
in normal subjects have shown ST depression in up
METHODS
to 30%. 5-10Such a high proportion of false positive
findings might make Holter monitoring seem inap- We screened116 apparently healthy normal volunteers
propriate for evaluating myocardial ischemia in pa- (67 women and 49 men; age 21 to 60 years; mean age,
tients with coronary heart disease, but the studies 43.7 I 9.2 years) by physical examination, a questionnaire
on personaland familial history, electrolyte determination,
just cited had serious limitations, particularly insuf-
blood pressuremeasurement at rest, 12-lead electrocar-
ficient definition of a “normal” population and lack diography, and symptom-limited bicycle exerciseelectro-
cardiography (ECG) with patients in the supine position
with blood pressure measurement. We used the supine
From the Department of Cardiopulmonology, Klinikum Steglitz der Freien
Universitlt Berlin. rather than the upright position because it seems to be
Received for publication Sept. 26, 1991; accepted March 16, 1992.
more sensitive and equally specific for detecting coronary
Reprint requests: Dr. Heinz VGller, Department of Cardiopulmonology, artery disease. I1 We excluded postural ST segment shifts
Klinikum Steglitz der Freien Universitlt Berlin, Hindenburgdamm 30, D on the basis of orthostatic tests in the supine, prone, lateral,
1000 Berlin 45, Germany. sitting, and standing positions.
4l1l38900 Particular attention was directed to the exclusion of left

622
Volume 124
Number 3 Shape analysis of ST depression on Holter 623

116 volunteers
I
19 mitral valve prolapse
r

I
85 normal subjects
L 1 abnormal exercise test

I
ST normal
I
T inversion
I
ST depression
I
ST elevation
53 (62.3%) 25 (29.4%) 6 (7.1%) 1 (1.2%)

2 “sudden onset”
6 shape analysis

2 positive by 2 increase in R-wave

shape analysis amplitude

thallium 201 imaging

+
I I
1 normal 1 pathologic

1 norhal
Fig. 1. Pattern of the study with stepsof subject selection on the basisof pathologic findings in prelim-
inary examinations, resultsof ST segmentanalysisduring 24-hour Holter monitoring, and additional shape
analysis.

ventricular hypertrophy. The following criteria were used
for its ECG diagnosis:(1) Sokolow and Lyon12precordial
voltage criteria = Svi + Rv5 or Rvs > 35 mm and (2)
RI + SIII > 25 mm.13 Left ventricular (LV) hypertrophy
was assumedif at least one parameter was positive.
Two-dimensional and two-dimensionally guided
M-mode echocardiography wasperformed with a Toshiba
SSH I60A unit (Toshiba Corp., Tokyo, Japan) using a 2.5
MHz transducer. Measurements of the internal diameter
and wall thickness of the left ventricle were performed at
end diastoleaccordingto the Penn convention describedby
Devereux and Reichek.14Left ventricular mass(LVM) was
calculated using the following formula: LVM (in
grams) = 1.04 [(LVID + IVST + PWT)3 - (LVID)3] -
13.6, where LVID denotesthe left ventricular internal di-
ameter, IVST the interventricular septal thickness, and
PWT the posterior wall thickness. LV hypertrophy was
defined asa ratio of ventricular massto body surface area
(LVM/BSA) exceeding 132gm/m2 in men and 109 gm/m2
in w0men.l”
If theseinvestigations did not indicate underlying heart
disease,they were followed by 24-hour Holter monitoring.
We useda direct-recording two-channel Holter monitoring
system(Mark 4, Cardio Data Services,Haddonfield, N.J.).
In preliminary experimental and clinical studies,lsl7 the
accuracy of the system in analyzing ST segmentchanges
was shown to be comparable to that achieved with fre-
quency-modulated systems.
 September 1992
624 Vdler et al. American Heart Journal

Ml M2 M,

~ 0 mV
~ 0.1 mV
~ 0.2 mV
Fig. 2. Principle of automatic ST segment measurement, based on analysis of difference in voltage between
measuring point Mr on PQ segment (zero voltage) and measuring point Ms on ST segment 60 msec after
the J point. Point M3 is at a fixed distance of 60 msec from Mz. Difference between Mr and Mz indicates
extent of ST segment depression; difference between M:, and Ms describes slope (ascending or descending)
of ST segment.

time 5.00 a.m. 5.30 a.m.

+ 0.2 mV
ST-trend LYYYhLyWyqiw;w -
i - - 0.2 mV

--
HR=62 4.53 a.m.
I
II : I A‘ : : .’ 1
lead CM5
1 1.0 mV

HR=59 5.05 a.m.

lead CM5
1 l.OmV

Fig. 3. Example of position-dependent repolarization disturbances with sudden onset of descending ST

depression during the night in a 4%year-old woman (subject No. 1) despite no postural ST segment shifts
in preliminary examinations.

Of the 116 original subjects, 31 (26 % ) were not included range: 143.4 to 339.8 gm/m2); two subjects showed ST seg-
in the study because of pathologic findings in the prelim- ment depression in response to orthostatic testing and one
inary examinations (Fig. 1). Mitral valve prolapse was doc- had positive findings in the exercise ECG. The remaining
umented in 19 cases by auscultation and by echocardi- 85 healthy volunteers underwent 24-hour Holter monitor-
ography. Nine subjects had arterial hypertension with LV ing. There were 49 women with a mean age of 43.7 k 8.6
hypertrophy (mean LVM/BSA = 196.4 + 63.7 gm/m”; years and 36 men with a mean age of 43.6 + 9.8 years.
Volume 124
Number 3 Shape analysis of ST depression on Holter 625

time 10.00 a.m. 10.30 a.m.

ST-trend

heart rate

HR = 101 9.56 a.m.

1.0 mV
lead CM5

HR = 140 10.13 a.m.

Fig. 4. Episode of descendingST depressionof 0.2 mV in a 39-year-old woman (subject No. 34). PQ and
ST segmentsdisplayed a parallel course and an identical extent becauseof exaggeratedatria1 repolariza-
tion waves.

After careful preparation of the skin, we attached the two
exploratory electrodesto V5 and to the xiphoid locations.
The two negative electrodes were positioned at the upper
sternum. A technician performed the analysis semiauto-
matically with visual control. Automatic ST segmentmea-
surement is basedon analysis of the difference in voltage
(in millivolts) betweenmeasuringpoint Ml on the PQ seg-
ment (zero voltage) and measuringpoint M2 on the ST
segment60 msecafter the J point (Fig. 2). A third point
(M3) is at a fixed distance60 msecfrom M2. The difference
in voltage between Ml and M2 indicates the extent of ST
segmentdepression,whereasthat betweenM2 and M3 de-
scribesthe slope (ascendingor descending)of the ST seg-
ment.16Ml and M2 were located by the technician before
analysisand were adjusted if necessary.Isoelectric baseline
ST segmentdisplacement was thus determined continu-
ously throughout the entire 24 hours. The ST data were
plotted asa 24-hour trend. From eachtrend-curve segment
demonstrating ST changes,a strip of the real-time ECG
(paper speed,25 mm/set) wasvisually analyzed according
to the following commonly applied criteria. A significant
episodewasdefined asa horizontal or descendingST seg-
ment depressionof at least 0.1 mV persisting for at least 1
minute, and single episodeshad to be at least 1 minute
apart-the “one-by-one-by-one rule.”
In a secondstep, ST segmentdepressionthus detected
underwent more detailed analysis.The beginning,the end,
and the time of maximal depressionwere documented on
real-time ECG (25 mm/set). In addition to the ST segment
measurement,the following additional assessments were
done. Determination of R amplitude: R amplitude deter-
mination wasachievedby calculating the mean amplitude
of 10 QRS complexesimmediately before the ST episode
and at the time of maximal ST segmentdepressionfrom
the real-time ECG recording. An R amplitude increaseof
more than 20% from immediately before the episodeto
maximal ST segment depression was assessedas not
pathologic. Temporal development of individual ST seg-
ment episode: An artifact wasassumedwhen there was a
suddenchangein the ST segmentslope (Fig. 3). Course of
PQ segment: If ST and PQ segmentsdisplayed a parallel
course and an identical slope, this was assessedas not
pathologic (Fig. 4).
RESULTS
The results of Holter monitoring are summarized
in Fig. 1. Six subjects (three men and three women)
had a total of 24 episodes of transient horizontal or
descending ST segment depression of at least 0.1 mV
lasting at least 1 minute. The average number per
subject was 4.0 f 2.8 in the 24 hours, and the mean
duration was 47.0 & 44.1 minutes. The maximal ex-
tent of ST segment depression was 0.15 to 0.25 mV,
 September 1992
626 Killer et al. American Heart Journal

time 5.00 a.m. 5.30 a.m.

: i.. : ;
, - + 0.2 mV
ST-trend --, ., ----
- - 0.2 mV

- 120/
- lOO/
I ./ i. - 801
w--_- .-.... -- ~~ - -- -- -.------------~ -

--OF& 69 521 a.m.

: :.

1 1.0 mV

HR=69 5.20 a.m.

1 1.O mV

Fig. 5. Transient ST segment depression,accompaniedby simultaneousincreasein R wave amplitude

(subject No. 8).

Table I. Frequency, duration, and courseof ST segmentdepressionin six normal subjects

Subject Max ST depression Heart rate
No. Age (yr) Sex Episodes in 24 hr Duration (min) (mV) ST course (beatslmin)

1 48 M 5 6 0.20 Desc 77
8 38 M 4 58 0.15 Horiz 75
63 38 M 9 131 0.25 Desc 75
34 39 F 1 15 0.20 Desc 140
30 36 F 2 51 0.15 Desc 140
81 48 F 3 21 0.25 Desc 135

Desc, Descending; Horiz, horizontal; Max, maximal.

the heart rate at that time being 98 f 30.2 beats/min No. 8, but revealed an exercise-induced reversible
(Table I). perfusion defect in the inferior segment in subject
Detailed analysis of the individual ST depression No. 81, a 48-year-old woman. After she gave her in-
episodes yielded the following findings. A sudden formed consent, she underwent a right and left heart
onset of ST segment depression was seen in all 14 catheterization with exercise testing and coronary
episodes of subjects No. 1 and 63 (Fig. 3). Subjects angiography, which yielded normal results.
No. 30 and 34 had three episodes of marked descend-
DISCUSSION
ing ST depression of 0.15 to 0.20 mV. However, these
ST courses were identical with the PQ segments (Fig. Several studies have called attention to the occur-
4). The two other subjects (No. 8 and 81) had seven rence of transient ST segment depression in healthy
episodes of ST depression; two were accompanied by subjects. Those results conflict with reports of sig-
a simultaneous increase in R wave amplitude (Fig. 5) nificant ST segment depression in 2.5 ‘% to 30% of
and the other five episodes were defined as true pos- normal subjects. 2,5 In our own study, we detected
itive (Fig. 6). Those two subjects underwent exercise significant episodes of ST segment depression in
thallium-201 imaging, which was negative in subject 7.1% of 85 normal subjects. There are several possi-
Volume 124
Number 3 Shape analysis of ST depression on Holter 627

time 3.00 p.m. 3.30 p.m.

., .(
..1 - +0.2 mV

- 60/

HR=80 14.44 p.m.

HR=94 15.02 p.m.

Fig. 6. Presentation of gradual ST trend depressionin a 48-year-old woman (subject No. 81) with normal
findings in bicycle exercise stresstest, exercisethallium-201 imaging, and right and left heart catheteriza-
tion. DescendingST depressionof 0.25 mV cannot be consideredasfalse positive, becauseall criteria of
transient myocardial ischemiawere fulfilled by both semiautomatic and shape analysis.

ble reasons for this wide variation in results. An es- could be the reason for the comparatively high per-
sential factor obviously is subject selection, especially centage of subjects with ST segment depression
with respect to age and sex.5pg ST segment changes (30%) observed by those authors.
have been observed in connection with other influ- Even with extensive preliminary investigations
ences: hyperventilation, hypokalemia, the use of and stringent exclusion criteria, there is still ST seg-
drugs (particularly cardiac glycosides), and mitral ment depression of up to 10 So. It must be stated,
valve prolapse.6, 7, syl8 The percentage of volunteers however, that the interpretation of ST segment
with mitral valve prolapse in our population, accord- depression has so far not been carried out with
ing to physical examination and two-dimensional enough emphasis on accuracy. The difficulties in in-
echocardiography, was a surprisingly high 16.4 5%. terpreting ST segment depression in Holter moni-
Mitral valve prolapse can lead to ST segment de- toring lie in the investigative tool itself4: 24-hour
pression, lg so we had to exclude a considerable num- Holter monitoring is more prone to artifacts than
ber of subjects from our study. These findings show routine and exercise ECG. Most importantly, respi-
that such preliminary screening is indispensable, al- ration- and position-dependent changes cause R and
though it had not been done by several other inves- P wave alterations.
tigators. To eliminate such false positive ST segment de-
The results of studies are influenced by disagree- pression, we submitted all 24 significant episodes
ment as to the duration of episodes of ST segment that were detected by conventional criteria (the one-
depression. Most studies considered an ST segment by-one-by-one rule) to an additional formal analysis.
depression of at least 0.1 mV to be significant only if The position-dependent repolarization disturbances
it lasted for more than 1 minute, but a duration of 30 play a particularly important role in Holter monitor-
seconds was already regarded as pathologic by Arm- ing. Up to 15 % of all ST segment depressions are the
strong et a1.5 Such a difference in definition alone result of postural changes.20 Such false positive ST

626 Vdler et al.
segment depressions cannot be recognized by the
one-by-one-by-one rule. They can be distinguished
from true positive ST depressions only through
assessment of the temporal course of the ST depres-
sions and by concomitant measurement of the R am-
plitude.21, 22
There may also be other causes for false positive
ST segment depressions. The example in Fig. 4 shows
a false positive ST segment depression which, be-
cause of its slow course, did not differ in its trend from
a myocardial ischemia. The ST segment depression
developed in connection with a sinus tachycardia
and, in the presence of markedly downsloping PQ
segments, was probably the expression of exagger-
ated atria1 repolarization waves during exercise.23
The ST segment depression appearing here, partic-
ularly in the trend plot, could in part be the result of
a false zero line. The close proximity of the P wave to
the nadir of the R wave during a tachycardia can
cause the measuring point Ml initially set at the PQ
segment to shift into the P wave (Fig. 2). Only
detailed measurement of the real-time ECG makes it
possible to distinguish an artifact-caused change
from an ST depression consequent to myocardial is-
chemia.
It is in the nature of Holter monitoring registration
that artifacts cannot be avoided and that they com-
plicate the interpretation of ST depressions, even in
patients with coronary hearf-disease.24 The ST seg-
ment analysis in Holter monitoring should therefore
not be performed on the basis of the one-by-one-by-
one rule alone. Rather, each episode should be eval-
uated exclusively according to its original registra-
tion. The temporal course of the episode and the
baseline course and R amplitude shifts should be
considered in the evaluation.
Nevertheless, despite careful analysis of all ST
changes, two subjects had ST segment depressions
that could not be distinguished from those in coro-
nary heart disease patients. Even if neither exercise
thallium-201 imaging nor coronary angiography yield
pathologic findings in such cases, myocardial ische-
mia cannot be ruled out. An exercise-independent
vasospasm affecting the small vessels is conceiv-
able.25 Moreover, such changes could be associated
with abnormal vasomotor dilatory reserve, as well as
with cellular-dependent mechanisms.i6>27,28
In conclusion, transient ST segment depression, as
detected during Holter monitoring in patients with
coronary heart disease, can be observed in a minor
percentage in a carefully defined “normal” popula-
tion. Regular ST segment analysis with the conven-
tional one-by-one-by-one rule is not sufficient. A
shape analysis of the real-time printouts with addi-
September 1992
American Heart Journal
tional criteria is necessary to increase the specificity
of Holter monitoring as a diagnostic tool for detect-
ing transient myocardial ischemia.
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Number 3 Shape analysis of ST depression on Halter

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Adjuvant metoprolol improves efficacy of

class I antiarrhythmic drugs in patients with
inducible sustained monomorphic ventricular
tachycardia
Inducible ventricular tachycardia frequently persists despite solitary class I antiarrhythmic drug
therapy. To determine the effect of metoprolol as adjuvant therapy, 19 patients with clinical
ventricular tachycardia with baseline inducible sustained monomorphic ventricular tachycardia
and persistently inducible ventricular tachycardia despite class I drugs were evaluated. Eight of
19 patients (42%) became noninducible when metoprolol was added to class I drug therapy.
Sixteen of 19 patients (84%) were harder to induce or noninducible on a regimen of adjuvant
metoprolol therapy. In evaluating the clinical characteristics of the 19 patients, no significant
differences were found between patients who were persistently inducible and those rendered
noninducible. In evaluating the electrophysiologic characteristics, the group eventually rendered
noninducible had a significantly shorter baseline induced cycle length (259 + 27 vs 305 + 53
msec). Combination class I drug and metoprolol therapy significantly lengthened the ventricular
effective refractory period in both groups compared with baseline. The long-term follow-up was
excellent in all patients remaining on metoprolol in the noninducible group. Therefore adjuvant
metoprolol therapy creates a significant improvement in a number of patients with persistently
inducible ventricular tachycardia despite class I drug therapy. (AM HEART J 1992;124:629.)

Michael A. Brodsky, MD, Steven P. Chough, BAS, Byron J. Allen, MD,

Edmund V. Capparelli, PharmD, Mikhail V. Orlov, MD, and Gina Caudillo, RN
Orange, Calif.

From the Division of Cardiology, University of California, Irvine Medical Patients demonstrating clinical ventricular tachycar-
Center. dia or fibrillation often have inducible ventricular
Received for publication Jan. 27, 1992; accepted March 10, 1992.
tachycardia when studied with programmed electri-
Reprint requests: Michael A. Brodsky, MD, Division of Cardiology, Univer-
sity of California, Irvine Medical Center, 101 City Dr. South, Orange, CA cal stimulation. Traditionally these patients are then
92668. tested with class I antiarrhythmic drugs. However,
4/l/39278 patients with inducible sustained monomorphic ven-

629