PATHOPHYSIOLOGY AND NATURAL HISTORY

ARRHYTHW

Incidence of the coexistence of left ventricular false

tendons and premature ventricular contractions in
apparently healthy subjects
MICHIHIRO SUWA, M.D., Yuzo HIROTA, M.D., HIKARU NAGAO, M.D., MASAYA KINO, M.D., AND
KEISHIRo KAWAMURA, M.D.

ABSTRACT The incidence of the coexistence of left ventricular false tendons and premature ventric-
ular contractions (PVCs) was evaluated prospectively. Over 14 months, left ventricular false tendons
were found in 71 (6.4%) of 1 1 17 consecutive patients examined echocardiographically. Two types of
false tendons were observed: longitudinal, from the ventricular septum to the posteroapical wall (n =
62), and transverse, between the septum and the lateral wall (n = 9). Among 62 patients with PVCs
and no underlying heart disease, false tendons were detected in 35 (56%); 28 had unifocal and seven
had bifocal PVCs. Episodes of ventricular tachycardia were documented in one of the 28 patients with
unifocal PVCs and in one of the seven patients with bifocal PVCs. These PVCs were poorly controlled
by antiarrhythmic drugs but easily suppressed by exercise. Left ventricular false tendons were detected
in 36 patients on routine echocardiographic examinations performed in the other 1055 subjects, and 10
of these patients were judged to have no underlying heart disease. PVCs were detected in two (20%) of
these 10 patients. Although a definite conclusion that left ventricular false tendons are arrhythmogenic
cannot be derived from these results, the unexpectedly high incidence of the coexistence suggests that
left ventricular false tendons may be an etiologic factor in the development of PVCs, especially the rate-
dependent and medically uncontrollable PVCs seen in apparently healthy individuals.
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Circulation 70, No. 5, 793-798, 1984.

THE PRESENCE of false tendons in the left ventricle
has been recognized for a long time,' and it is reported
that they are a cause of functional ejection murmurs.2
They can also cause echocardiographic observations of
the endocardium of the interventricular septum to be
misinterpreted.3 Some of them can now be easily
detected with the two-dimensional echocardiographic
technique.9 It has been generally considered that they
are a normal structural variant with no clinical
significance.
In November 1982 we had an opportunity to observe
one young male subject who was referred to us for a
thorough examination of frequent premature ventricu-
lar contractions (PVCs) (figure 1) and whose cardiac
status was normal except for the presence of a false
tendon in the left ventricle (figure 2). Cardiac exami-
nations included cardiac catheterization and coronary
cineangiography. This case made us wonder whether
false tendons might be a cause of PVCs.
From the Third Division, Department of Internal Medicine, Osaka
Medical College, Takatsuki, Osaka, Japan.
Address for correspondence: Michihiro Suwa, M.D., Third Division,
Department of Internal Medicine, Osaka Medical College, 2-7, Dai-
gaku-cho, Takatsuki City, Osaka, 569, Japan.
Received June 19, 1984; accepted July 26, 1984.
Vol. 70, No. 5, November 1984
The present study was performed prospectively to
evaluate the incidence of the coexistence of false ten-
dons and PVCs in apparently healthy individuals who
visited our cardiovascular clinic over a 14 month
period.
Methods
Study protocols. We designed two study protocols to evalu-
ate the incidence of the coexistence of left ventricular false
tendons and PVCs. In the first study, patients with PVCs on
routine electrocardiograms (ECGs) or continuous 24 hr ambula-
tory ECG monitoring but without significant heart disease were
sent to the echocardiographic laboratory to be evaluated for left
ventricular false tendon. In the second study, patients without
organic heart disease and with left ventricular false tendons
found on routine echocardiographic examination were evaluat-
ed by ambulatory ECG monitoring.
Selection of patients. From November 1982 until January
1984, echocardiographic examinations were performed in 1117
consecutive patients. Sixty-two patients underwent echocardio-
graphic examinations in a search for left ventricular false
tendons, since they had PVCs without apparent organic heart
diseases. Routine echocardiographic examinations were per-
formed in the other 1055 patients for diagnostic purposes. The
presence of organic heart disease was excluded by physical
examination, routine ECG, chest x-ray, and exercise stress tests
in addition to echocardiographic examination. Special attention
was paid to exclude patients with mitral valve prolapse. Diag-
793
 SUWA et a1.
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eVe'
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t:
--a
,~
(Crj:i
i
Vi
Vz
V4
nJy~~~~~~~~~&A~~~~~~~~~n7JKJnVx~~~~~~~~~~~~~~~~~
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M.M. 29M
11/19/82
FIGUREt 1. ECG of a 29-year-iold miani i-elici-ied to Lus tor comliplete
a
catrdioluieXic examination becauIseofC frequienit PVCs. He was comlipletely
nui rmal except for a false tendon in the left venti-ile (ligure ).
nostic caIlrdiac catheterizationi with coronary cincangiogriaphy
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was perfOrmed in seven patients with PVCs and false tendons
(includine two patients with sustained ventriculai tachycardlia).
Left ventricular false tendons and PVCs. The d'ianosis of
lett ventricular false tenldons was. imiade when a fibrous abnormal
band was inoted longitudinally, diagonally, transversely in
or
the lel't ventricular cavity by two-dimensional echocardiogiaph-
ic observations. Two dimensional echocardiograins were ob-
tamiedl with Toshiba SSH- IA with 2.4 MHZ transducer o1
a a
Toshiba SSH-40A with a : .5 MHZ transducer, and were record-
ed with Polaroid film and video recordels. Phe documentation
ot PVCs was muade with ioutine ECG and conttinuous 24 hr
ambulatory ECG monitoring with a portable two-channel ambu-
latory ECG tape recorder (Tracker T R- 1 and Pathfinder 11:
Reynolds Medical). Treadmill exercise stress tests were per-
forimied according to Bruce's protocol (stiess monitor ML-
300: Fukuda Denshi).
Results
Overall prevalence of left ventricular false tendons. In the
series of 11 17 consecutive patients, left ventricular
false tendons were seen in 71 (6.4%). The tendons
were of two types: longitudinal (or diagonal) in the left
ventricular cavity in 62 patients (8704(c) and transverse
from the ventricular septum to the free wall in nine
(1 3%c). The longitudinal type could be divided into two
subtypes morphologically: one with the ends of the
tendon attached to the base of the septum and the
posterior wall near the apex (figure 3) (this can be
794
called the long longitudinal type, which was seen in 33
patients), and the other with the ends attached to the
lower portion of the septum and the posterior wall
(figure 4) (this can be called the short longitudinal type
or diagonal type, which was seen in 24 patients).
Coexistence of these two longitudinal types was seen
in five patients. The transverse tendons are situated
horizontally from the midportion of the ventricular
septum to the lateral wall (figures 2 and 5). There
were, however, some false tendons of the longitudinal
type that could be interpreted as transverse tendons on
the transverse section of the two-dimensional
echocardiogram.
Prevalence of false tendons in subjects with PVCs. The
incidence of the coexistence of left ventricular false
tendons and PVCs is shown in figure 6. Among the 62
patients with PVCs, false tendons were detected in 35
(56%). The age range of these 35 patients (20 male and
15 female) was 12 to 70 years (mean 39). The frequen-
cy of PVCs was 10 beats to 30,300 beats (mean 8544
beats) per 24 hr. The focus of PVCs was single (unifo-
cal PVCs) in 28 patients, seven with a right bundle
branch block pattern (suggesting left ventricular ori-
gin) and 21 with a left bundle branch block pattern
(suggesting right ventricular origin) in the precordial
leads of the surface ECG. Seven patients had two foci
(bitocal PVCs) on standard ECG or ambulatory ECG
mconitoring. Bifocal PVCs seemed to originate from
both right and left ventricles in six and from two foci in
the left ventricle in one. Ventricular tachycardia was
detected in two of the 35 patients, and in both it seemed
to originate in the left ventricle. One of them had
a
bifocal PVCs originating in the left ventricle, and two
types of ventricular tachycardias were documented
corresponding to these PVCs. These two patients had
long longitudinal false tendons.
Comparison of PVCs in suibjects with and without false
tendons. The age range of the 27 patients (nine male
and 18 female) with PVCs and without false tendons
was 13 to 58 years (mean 43). The frequency of their
PVCs averaged 12,4 10 beats per 24 hr. The focus in all
cases was single; four patients showed a right bundle
branch block pattern and 23 a left bundle branch block
pattern in the precordial leads of the surface ECG.
Treadmill exercise tests were performed by 30 patients
with left ventricular false tendons and 13 patients with-
out false tendons. PVCs disappeared at heart rates of
about 90 to 150 beats/mi in both groups and were
more easily suppressed at lower heart rates during ex-
ercise in patients with false tendons than in those with-
out false tendons (112 ± 21 vs 147 ± 11/min p <
.001). There were no episodes of chest pain or isch-
CIRCULATION
 PATHOPHYSIOLOGY AND NATURAL HISTORY-ARRHYTHMIA

FIGURE 2. M mode and two-dimensional echocardiograms of the left ventricular false tendon in the patient described in higure
I. Two-dimensional echocardiograms of the left ventricle from the parasternal short-axis (uipper i ig/ht) and apical four-chamber
views (lower right). A false tendon (white arrows) is seen traversing the center of the left ventricle between the ventricular septum
and the lateral free wall, pulling the ventricular septum inward in diastole to make a figure eight-shaped cavity. The tendon
appears in the center of the cavity in the M mode tracing (left, blaclk orroii and is immobile during the cardiac cycle. This case
suggested that false tendons might be a cause of PVCs. IVS - interventricuilar septum.l: RV - right ventricle; LV = left
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ventricle.

IG LIREL3. N1 cl c..d t,t) dii c c io.. ii 10. .at ai0ti u .diali ac-lt t'ciiul arf1al se teniidoni 'l'ws-dimienlsion -
at ccLhodidiogiais u1 tC[ie LIt Veiifiietliioiii
1l 1ic aptalteai-- axis (ipp)t'cr right) adt apical four-c hamiber views (lowter right). One
end of the tendon (white arrows) is attached to the base of the ventricular septum and the other to the posteroapical wall of the
ventricle. On the M mode echocardiogram (left) the tendon (black arrows) moves with the ventricular septum. AO aorta; LA
=
left atrium; RA - right atrium.

Vol. 70, No. 5, November 1984 795

 SUWA et al.

- toring. These two patients had false tendons of the

longitudinal type.
Discussion
Since about a century ago, false tendons in the left
ventricular cavity have been noted as anatomic var-
iants at autopsy. Now they can be detected easily by
two-dimensional echocardiography.4 It has frequent-
_*_ ly been emphasized that caution must be exercised in
the identification of the left ventricular endocardium of
the ventricular septum3 and in the differential diagnosis
of mural thrombus, since the echo from the tendon
might mimic these structures. Moreover, they have
been reported to be a cause of functional ejection mur-
murs.) There are no descriptions, however, of other
clinically significant features of false tendons. We ex-
amined a young man who was referred to us because of
frequent PVCs and who had no cardiac abnormalities
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FIGURE 4. Two-dimensional echocardiog,rams of a short longitudinal

left veniriculai- false tendon. Top, Apical long-axis view. bottomn apical
fouir-chamiber view. The false tendon (white arrows) is attached to the
lowei. part of the ventricular septum and the posteroapical wall of the
cavity. Abbreviations as in ligures 2 and 3.

emic ST-T changes during the exercise stress tests.

PVCs could be more easily controlled by medical treat-
ment in patients without false tendons than in those
with false tendons.
Prevalence of PVCs in subjects with false tendons. Left
ventricular false tendons were detected in 36 patients
in 1055 routine echocardiographic examinations. Or-
ganic heart disease was ruled out by noninvasive diag-.......
nostic techniques in 10 patients. PVCs were detected FIGURES5 A ceft ventricular transvei-sc false tendon (white arrow) is
in two o10patient
the (20%) o repeatEGGS or observed in the cavity on parasternal lone-axis (10/)) and shoi-t-axis
ambultworyte EG montoieng. The% fnrequencat PVCGso views (bottomn) of two-dimensional echocardiogramns. On the short-axis
view the deformity of the interveIltricular. septum is appaIent at the site
pr24
24 h in
1 0beats
was 10 eats oe,
and he othr had
in on, and ifocal
he othr had ifocal of attachment of the false tendoni, which gives the cavity a higure eight
PVCs (107 beats per 24 hr) on ambulatory ECG moni- appearance.
796 CIRCULATION
J.I s_I- - -1 . -
 PATHOPHYSIOLOGY AND NATURAL HISTORY-ARRHYTHMIA
PVCs(+) PVCs(-)
n=2 n=8
FIGURE 6. Diagram of study population and incidence of false tendons and PVCs.
except false tendons on cardiac examination, including
coronary cineangiography (figure 1). The transverse
section of the left ventricle had a figure eight appear-
ance during late diastole because of the tension of the
tendon (figure 2), so we thought this mechanical force
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might be the cause of PVCs. Therefore this study was
performed prospectively to determine whether left
ventricular false tendons might be a cause of PVCs.
The frequency of left ventricular false tendons has
already been reported by some investigators using two-
dimensional echocardiography, and the incidence var-
ies from 0.5% to 46%.4 5 8, 9 Because these studies
were performed in selected groups of patients, the true
incidence of false tendons in the general population is
not known. In our laboratory, the incidence of false
tendons was 6.4%, but our observations were limited
to those patients who were referred to the echocardio-
graphic laboratory and this incidence does not reflect
that in the general population.
Relationship between PVCs and false tendons. Among
62 patients with PVCs without organic heart diseases,
left ventricular false tendons were detected in 35
(56%); PVCs were detected in two of 10 patients
(20%) with left ventricular false tendons without or-
ganic heart disease. Recently, Perry et al.' described
three cases of PVCs and no significant heart disease
among 31 pediatric patients with left ventricular false
tendons.
PVCs originated from a single focus in 29 and from
two foci in eight of the 37 patients with PVCs and left
Vol. 70, No. 5, November 1984
ventricular false tendons. Sustained ventricular tachy-
cardia was detected in two patients. There was no
definite association between PVCs and the types or
subtypes of false tendons. Unifocal PVCs were seen in
23 patients with longitudinal and six with transverse
false tendons, and bifocal PVCs were seen in eight
with longitudinal and none with transverse false ten-
dons. Both patients with ventricular tachycardia had
longitudinal false tendons.
Mechanisms of PVCs in subjects with false tendons. Two
hypotheses can be considered in the study of possible
mechanisms of the arrhythmogenesis of false tendons.
Tendons of the canine right ventricle have frequently
been used in electrophysiologic studies of the conduc-
tion system, since they contain Purkinje fibers. "' 12 It is
well known that the automaticity of Purkinje cells is
increased by mechanical stretching. 13 Furthermore,
histologic examinations have shown that human left
ventricular false tendons contain specific conduction
cells.5 14 These might become an automatic focus of
PVCs. Another possibility is that the mechanical
stretch of the left ventricular wall where the tendon is
attached triggers PVCs. A figure eight deformity of the
ventricular cavity during late diastole caused by ten-
sion due to the false tendon was frequently observed
(figures 2 and 5), especially with the transverse type of
tendon. The disappearance of PVCs on exercise might
be related to reduction of tension due to decreased left
ventricular dimension with tachycardia. Recent studies
with endocardial mapping techniques have shown that
797
 SUWA et al.
PVCs with the left bundle branch block pattern can
originate from either the right or left ventricle. 15 In 23
of 27 patients with PVCs with a left bundle branch
block pattern, the PVCs had upright QRS complexes in
the precordial leads, suggesting that these PVCs might
have originated from the ventricular septum. Some
patients had two foci corresponding to two adhesions
in the endocardium, suggesting that the mechanical
force or tension on the left ventricular wall adjacent to
the tendon might have caused the PVCs.
A definite conclusion that false tendons in the left
ventricular cavity are a cause of PVCs cannot be de-
rived from our results. Further investigations, such as
histologic examinations of the false tendons, electro-
physiologic studies of the arrhythmias, surgical inter-
vention, and surveys of PVCs, false tendons, and their
coexistence in the general population, are necessary to
establish the correlation between them. However, the
surprisingly high incidence of this coexistence (35/62
false tendons in patients with PVCs and 2/10 PVCs in
patients with false tendons) and the different responses
to exercise and medical treatment of PVCs with false
tendons and those without false tendons strongly sug-
gest that left ventricular false tendons are an etiologic
factor in the genesis of ventricular arrhythmias in ap-
parently healthy subjects.
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