Download Right Precordial T-Wave Inversion in Healthy Endurance Athletes

JACC: CLINICAL ELECTROPHYSIOLOGY
VOL. 1, NO. 1-2, 2015
ª 2015 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
ISSN 2405-500X/$36.00
PUBLISHED BY ELSEVIER INC.
http://dx.doi.org/10.1016/j.jacep.2015.03.007
Right Precordial T-Wave Inversion in
Healthy Endurance Athletes Can Be
Explained by Lateral Displacement
of the Cardiac Apex
Maria J. Brosnan, MBBS,*y Guido Claessen, MBBS,z Hein Heidbuchel, MBBS, PHD,x David L. Prior, MBBS, PHD,*y
Andre La Gerche, MBBS, PHD*zk
ABSTRACT
OBJECTIVES The objective of this study was to test the hypothesis that T-wave inversion in the right precordial leads
(TWIV2-3) reflects lateral displacement of the heart such that the surface electrocardiographic (ECG) leads overlie a
greater proportion of the right ventricle (RV).
BACKGROUND TWIV2-3 on ECG is more frequently observed among endurance athletes (EAs) than in the general
population, the underlying mechanism for which is unclear.
METHODS Sixty-eight EAs and 41 nonathletic control subjects underwent ECG and cardiac magnetic resonance imaging
(CMRI). In addition to standard measurements of biventricular function and volume, novel measurements of cardiac
displacement and orientation were analyzed from horizontal long-axis images. These included RV wall thickness in
diastole (RVd), cardiac-to-hemithorax area ratio (CHTx%), percentage of circumferential displacement of the RV apex
toward the axilla (%LatD), and the angle of interventricular septum with respect to the thoracic midline (:septal).
RESULTS All cardiac volume, RVd, CHTx%, %LatD, and :septal values were greater in EAs than in controls. Compared to
EAs without TWIV2-3, EAs with TWIV2-3 (n ¼ 26) did not have greater RV wall thickness or cardiac volumes (RVd ¼ 4.9 vs.
4.8 mm, p ¼ 0.695; LVEDV ¼ 231 vs. 229 ml, p ¼ 0.856; RVEDV ¼ 257 vs. 254 mL, p ¼ 0.746), but all measurements of
cardiac displacement toward the axilla were greater (%LatD ¼ 45.6% vs. 37.9%, respectively, p < 0.0001; :septal ¼
54.23 vs. 48.63 , respectively, p ¼ 0.001; and CHTx% ¼ 46.3% vs. 41.9%, respectively, p ¼ 0.048).
CONCLUSIONS In healthy EAs, TWIV2-3 is associated with displacement of the RV toward the left axilla rather than RV
dilatation or hypertrophy. TWIV2-3 may be explained by the position of the RV relative to that of the surface ECG leads.
(J Am Coll Cardiol EP 2015;1-2:84–91) © 2015 by the American College of Cardiology Foundation.
R
ight precordial T-wave inversion in leads V 2
to exclude structural heart disease when found in
to V 3 (TWI V2-3) is uncommon in the general
athletes (3,4). TWI V2-3, however, may be more preva-
population but is observed in up to 85% of
lent among highly trained endurance athletes (EAs)
subjects with confirmed arrhythmogenic right ven-
(5,6) and some ethnic athletic populations (7) than
tricular cardiomyopathy (ARVC), a genetically deter-
among nonendurance athletes and the general popu-
mined cardiomyopathy which is associated with an
lation (8,9).
increased risk of sudden cardiac death (1,2). Thus,
The mechanisms underpinning the greater preva-
current guidelines consider TWIV2-3 an abnormal
lence of TWI V2-3 among EAs have not been elucidated.
finding, which should prompt further investigation
Zaidi et al. (10) investigated the logical hypothesis
From the *Department of Cardiology, St. Vincent’s Hospital, Fitzroy, Australia; yDepartment of Medicine, St. Vincent’s Hospital
and University of Melbourne, Fitzroy, Australia; zDepartment of Cardiovascular Medicine, University Hospitals Leuven, Leuven,
Belgium; xHasselt University and Heart Center, Jessa Hospital, Hasselt, Belgium; and the kBaker IDI Heart and Diabetes Institute,
Melbourne, Australia. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Manuscript received December 17, 2014; revised manuscript received January 30, 2015, accepted February 16, 2015.
Brosnan et al.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
MARCH/APRIL 2015:84–91
that TWI V2-3 might be associated with right ventric-
ventricular (LV) hypertrophy (S V1 þ R V5, mV)
ABBREVIATIONS
ular (RV) dilation and hypertrophy but found little
and RV hypertrophy (R V1 þ SV5, mV) were
AND ACRONYMS
relationship between TWI V2-3 and RV dimensions.
recorded as continuous variables. The pres-
One possible explanation could be the modest accu-
ence of incomplete right bundle branch block
racy of 2-dimensional echocardiographic measure-
(RBBB)
ments of RV mass and volumes (11).
morphology in V 1 with a QRS duration of
toward the left axilla
<120 ms. The R/S transition zone was defined
:septal = angle of
SEE PAGE 92
was
noted,
defined
as
an
rSR 0
as the precordial lead where R-wave ampli-
We formulated an alternative hypothesis. Exercise-
tude exceeded S-wave amplitude. TWI was
induced cardiac remodeling (“the athlete’s heart”)
measured
can be profound (12), and, given the anatomical con-
considered significant if deeper than 0.1
in
each
lead
separately
and
%LatD = percentage of
circumferential displacement
of the right ventricle apex
interventricular septum with
respect to the thoracic midline
CMRI = cardiac magnetic
resonance imaging
CTHx% = cardiac to left
straints imposed by the thorax, the heart is displaced
mV. TWI V2-3 was defined as T-wave inversion
hemithorax area
progressively along the left anterior chest wall toward
in lead V 2 or in V2 and V 3 . The presence of
EA = endurance athlete
the axilla. As a result, it might be expected that a
bifid T waves was also noted and considered
larger proportion of the RV lies adjacent to the right
to represent TWI V2-3 if the negative portion
precordial electrocardiographic (ECG) leads. Thus, it
was deeper than 0.1 mV in leads V 2 and V 3.
may be that TWI V2-3 may be better explained by the
anatomical position of the RV within the thorax than
the size or structural characteristics of the RV. In
other words, the normal TWI observed in V1 may be
observed in lower and more lateral ECG leads simply
because these leads are now overlying the body of the
RV rather than being in proximity to the cardiac apex.
To address this hypothesis, we investigated whether
greater lateral cardiac displacement was associated
with TWI V2-3 in EAs and nonathletic controls using
cardiac magnetic resonance imaging (CMRI).
TWIV2-3 = right precordial
T-wave inversion
CARDIAC MAGNETIC RESONANCE IMAGING. CMRI
was performed with a 1.5-T scanner (Signa Excite, GE
Healthcare, Waukesha, Wisconsin; or Achieva, Philips
Medical Systems, Best, the Netherlands), using a
dedicated cardiac multiphased array coil and cardiac
gating during breath-hold. Cine imaging was used to
obtain a contiguous short-axis stack (8-mm slice
thickness without gaps) covering the LV and RV from
the apex to a level well above the atrioventricular
groove. Endocardial and epicardial borders were
manually traced with customized software (RightVol,
Leuven, Belgium) to quantify volumes at end-diastole
METHODS
(EDV) and end-systole (ESV).
SUBJECTS. Sixty-eight elite endurance athletes (EAs)
volunteered to participate. EAs were defined as individuals participating in more than 10 h of intense
exercise per week, and all were participating in longdistance events ranging from the marathon to the
ultraendurance triathlon. All athletes were healthy
and asymptomatic. Other than TWIV2-3, there was no
clinical evidence of ARVC in any athlete after thorough investigations.
A nonathletic control cohort consisted of 20
healthy volunteers and 21 subjects who underwent
CMRI for clinical indications but in whom no cardiac
pathology was identified. Written informed consent
was obtained from all subjects, and the protocol was
approved by the St. Vincent’s Hospital Human
Research Ethics Committee in accordance with the
declaration of Helsinki.
Measurements of RV displacement were performed, as shown in Figure 1. The end-diastolic frame
was selected from a horizontal long-axis cine acquisition, and analysis was performed using open-source
DICOM
version
4.1.2
viewing
software
(OsiriX,
Geneva, Switzerland). The following linear planes
were defined and are illustrated in Figure 1: an
anteroposterior mid thorax line passing through the
mid-point of the sternum and thoracic vertebrae
(Figure 1, line A), and a line orthogonal to and
bisecting line A, passing through the axilla (Figure 1,
line B). The angle of the interventricular septum
(:septal ) was then measured with respect to line A, in
a plane passing through the atrioventricular crux and
the cardiac apex (Figure 1, line C). The point at which
line C crossed the internal thoracic wall was labeled
RV apex. The distance from the sternum (Figure 1,
line A) to the RV apex was then manually traced,
12-
following the bony thorax, and defined as L1 (in cm).
lead ECG was performed with all subjects at rest, in
This line was then extended, following the thorax, to
12-LEAD
ELECTROCARDIOGRAPHY. Standard
the supine position, at 10 mm/mV and 25 mm/s.
meet line B, and defined as L2 (cm). This lateral
Measurements were made with digital calipers and
displacement (L1:L2) ratio was then calculated and
included heart rate, QRS axis, and QRS duration.
expressed as a percentage (%LatD). Finally, the area
Sokolow-Lyon
of the left hemithorax was traced (HTx), as was the
s
85
Cardiac Displacement Causing TWI in Athletes
Sokolow-Lyon
scores
for
left
86
Brosnan et al.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
MARCH/APRIL 2015:84–91
Cardiac Displacement Causing TWI in Athletes
F I G U R E 1 Methods for Measuring Lateral Cardiac Displacement and Angle of Rotation
on CMRI
of variances for continuous variables, and chi-square
or Fisher’s exact test for categorical variables. Univariate binary logistic regression analysis was performed to test for characteristics associated with
presence or absence of TWI V2-3. From this analysis,
covariates identified as having significant association
with TWI V2-3 were entered into a multivariate model
(with forward stepwise selection) to determine predictors of TWI V2-3 . Linear regression analysis was
used to test for an association between QRS axis and
cardiac volumes. A 2-tailed p value of <0.05 was
considered significant throughout. All statistical analyses were performed using SPSS version 21 software
(IBM, Armonk, New York).
RESULTS
Demographic, morphometric, electrocardiographic,
and CMRI characteristics of EAs and controls are shown
in Table 1. Compared to controls, EAs were younger
Measurements as shown were made with a horizontal long-axis acquisition at end diastole.
and taller, and a smaller proportion of the group was
%LatD ¼ percentage of circumferential displacement of the right ventricle apex toward
female.
the left axilla; :septal ¼ angle of interventricular septum with respect to the thoracic
midline (degrees). L1 ¼ distance from Line A to the cardiac apex along the internal thoracic
ELECTROCARDIOGRAPHIC FINDINGS. Compared to
cage; L2 ¼ distance from the cardiac apex to Line B along the internal thoracic cage; Line A
controls, EAs had slower heart rates, a more right-
¼ passing through the mid-point of the sternum and thoracic vertebrae; Line B ¼
ward QRS axis, larger scores for LVH and RVH, and a
orthogonal to and bisecting Line A, passing through the axilla; Line C ¼ passing through
the atrioventricular crux and the cardiac apex.
greater prevalence of incomplete RBBB (Table 1). In
EAs, the R/S transition zone was later than that of
controls, and right precordial TWIs and bifid T waves
area of the whole heart (Figure 1, line C) within the
left hemithorax. The cardiac area/hemithorax area
ratio was then calculated and expressed as a per-
were far more prevalent. No control subject displayed
TWI beyond lead V 2.
CMRI FINDINGS IN ENDURANCE ATHLETES VERSUS
centage (CHTx%). The thickness of the RV free wall
NONATHLETIC
was measured in the short axis view from an end-
cardiac volumes were larger, and the RV free wall
CONTROLS. Right-
diastolic frame at the level of the papillary muscles.
was thicker in EAs than in controls (Table 1). Com-
All measurements were performed blinded to subject
pared to controls, EAs had a larger left hemithorax
identity or ECG findings.
area, and the heart occupied a relatively larger per-
REPRODUCIBILITY OF CMRI MEASURES. Measure-
centage of this area (expressed as CHTx%). Further-
ments of LV and RV volumes were performed by 2
more, in EAs, the RV and cardiac apex were displaced
blinded interpreters (A.L.G. and G.C.). Measurements
farther toward the left axilla, represented by greater
and left-sided
of RV displacement were performed by a single blin-
L1, %LatD, and :septal than those of controls.
ded interpreter (M.B.) and repeated by a second
CMRI FINDINGS AND ASSOCIATED ELECTROCARDIO-
blinded observer (A.L.G.), using a subset of 25
GRAPHIC FEATURES IN ENDURANCE ATHLETES
randomly selected subjects. Interobserver reproduc-
WITH RIGHT PRECORDIAL T-WAVE INVERSION.
ibility of measurements of RV volume and displace-
Electrocardiographic and CMRI characteristics of EAs
ment were assessed using intraclass correlation
with and without right precordial TWI are presented
coefficient analysis and are reported as coefficients
in Table 2. QRS axis, RVH score and R/S transition
(95% confidence interval [CI]).
zone were similar in EAs with and without TWI V2-3, as
STATISTICS. Values are means SD or percentages,
were right and left sided cardiac volumes and RVd
as appropriate. Group differences between EA and
wall thickness. On the other hand, as compared
controls as well as those between EA with TWI V2-3 and
with EAs without TWI V2-3, EAs with TWI V2-3 had
those EA without TWI V2-3 were analyzed using inde-
a larger CHTx%, %LatD and :septal representing
pendent sample t tests with Levene’s test for equality
greater displacement of the RV toward the axilla.
Brosnan et al.
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MARCH/APRIL 2015:84–91
87
Cardiac Displacement Causing TWI in Athletes
Examples of 2 representative athletes are presented
in Figures 2A and 2B.
T A B L E 1 Baseline Characteristics and Electrocardiographic and CMRI Measurements of
Endurance Athletes and Controls
CMRI FINDINGS IN ATHLETES WITH BIFID T-WAVES
Endurance Athletes
Controls
IN THE RIGHT PRECORDIAL LEADS. CMRI and other
Age, yrs
35.0 8.1
39.6 12.6
0.023
ECG findings in the 10 athletes with bifid right pre-
Males (% of total)
63 (92.6%)
28 (68.3%)
0.0014
cordial TWI were similar to those with deep TWI V2-3.
Height, cm
180 7
174 9
Compared to athletes with no TWI, all cardiac vol-
Weight, kg
76 8
77 13
0.602
1.9 0.1
1.9 0.2
0.441
Heart rate, beats/min
55 9
69 15
<0.0001
QRS axis
74 21
47 37
<0.0001
umes were similar, but :septal (56 vs. 49 , respectively, p ¼ 0.001) and %LatD (47% vs. 38%,
respectively, p < 0.0001) were larger.
CMRI FINDINGS IN NON-ATHLETIC CONTROLS WITH
RIGHT PRECORDIAL T-WAVE INVERSION. Only 1
nonathletic control subject demonstrated right pre-
Characteristic
BSA, cm2
p Value
<0.0001
RVH score, mV
6.6 3.3
3.8 2.7
<0.0001
LVH score, mV
22.3 6.3
16.8 5.8
<0.0001
R/S zone beyond V3
61 (89.7%)
33 (80.5%)
0.0014
R/S zone beyond V4
37 (54.4%)
10 (24.4%)
0.0042
T-wave inversion, V2 only
16 (23.5%)
1 (2.4%)
T-wave inversion, V2-3
7 (10.3%)
0
Compared to the remainder of the nonathletic control
Bifid T-waves, V2-3
10 (14.7%)
0
0.0125
group, this subject demonstrated larger cardiac vol-
T-wave inversion or bifid T-waves, V2-3
27 (39.7%)
1 (2.4%)
<0.0001
umes (LVEDV of 178 vs. 159 ml, respectively; RVEDV
Incomplete RBBB
31 (45.6%)
10 (24.4%)
of 212 vs. 167 mL, respectively), and larger mea-
LVEDV, mL
230 31
159 43
<0.0001
RVEDV, mL
256 37
167 50
<0.0001
RV:LV
1.1 0.1
1.0 0.1
0.006
L1, cm
(45% vs. 35%, respectively). As expected with only 1
9.0 1.7
7.1 1.7
<0.0001
L2, cm
22.1 1.8
20.4 2.7
<0.0001
subject, none of these differences reached statistical
%LatD
41 8
35 8
<0.0001
significance.
:septal
51 7
46 7
0.002
247 36
225 44
0.005
cordial
TWI,
which
was
isolated
to
leads
V2.
surements of CHTx% (44% vs. 39%, respectively),
:septal
(47 PREDICTORS
vs.
OF
40 ,
respectively),
RIGHT
and
PRECORDIAL
%LatD
T-WAVE
INVERSION IN ENDURANCE ATHLETES. Univariate
Left hemithorax, cm2
0.023
0.0436
0.0406
% of CTHx
44 7
39 8
0.001
RVd thickness, mm
4.9 1
3.6 0.7
<0.0001
predictors of TWIV2-3 are shown in Table 3. On multivariate analysis, %LatD was the only variable significantly associated with the presence of TWIV2-3, with
an odds ratio (OR) of 11.52 per 10% increment in this
ratio (95% CI: 10.59 to 12.53, p ¼ 0.001). Area under the
Values are mean SD or n (%).
%LatD ¼ lateral displacement of the RV apex (L1/L2%); :septal ¼ angle of interventricular septum with respect
to midline; BSA ¼ body surface area; CTHx ¼ cardiac to left hemithorax area; L1 ¼ distance from sternum to RV
apex; L2 ¼ distance from sternum to left axilla; LVEDV ¼ left ventricular end diastolic volume; RVd ¼ RV diastolic;
RVEDV ¼ right ventricular end diastolic volume; RVH ¼ right ventricular hypertrophy.
receiver operating curve (ROC) was 0.774 (95% CI:
0.661 to 0.887, p < 0.0001), with %LatD >42.8% predicting TWI V2-3 with 74% sensitivity and 78% specificity (Figure 3). When separately considering those
T A B L E 2 Electrocardiographic and CMRI Measurements in Endurance
Athletes With Right Precordial T-Wave Inversion Compared to Those Without
athletes with bifid T-waves in V 2-V 3, the findings
were similar, with %LatD the only variable on
Measurements
EAs With TWI V2-3
(n ¼ 27)
EAs Without TWIV2-3
(n ¼ 41)
p Value
76 19
72 22
0.492
6.2 3.6
6.9 3.2
0.406
43.2%
56.8%
0.621
multivariate analysis associated with this finding (OR:
QRS axis
12.10 per 10% increment, 95% CI: 10.54 to 13.89,
RVH score
p ¼ 0.007). Area under the ROC curve was 0.856
R/S zone after V4
(95% CI: 0.742 to 0.970, p ¼ 0.001) with %LatD >43.2%
LVEDV, ml
231 38
230 26
0.856
predicting the presence of bifid T-waves in the right
RVEDV, ml
258 45
255 32
0.746
L1, cm
9.8 1.6
8.5 1.6
0.001
L2, cm
21.5 1.9
22.5 1.7
0.027
%LatD
46 7
38 8
<0.0001
precordial leads with 90% sensitivity and 80.5%
specificity.
ASSOCIATION BETWEEN QRS AXIS AND RIGHT
VENTRICULAR VOLUMES. QRS axes did not differ
between those subjects with and those without
TWIV2-3; however, linear regression analysis demon-
:septal
Left hemithorax, cm2
% of CTHx
RVd thickness, mm
54 2
49 6
0.001
236 36
254 34
0.048
46 7
42 6
0.009
4.9 1.3
4.8 0.9
0.149
strated a significant association between QRS axis and
Values are mean SD or %.
RV volume, with each 10 increment in axis associ-
%LatD ¼ lateral displacement of the RV apex (L1/L2%); :septal ¼ angle of interventricular
septum with respect to midline; CTHx ¼ cardiac to left hemithorax area; L1 ¼ distance from
sternum to RV apex; L2 ¼ distance from sternum to left axilla; LVEDV ¼ left ventricular end
diastolic volume; RVd ¼ RV diastolic; RVEDV ¼ right ventricular end diastolic volume; RVH ¼ right
ventricular hypertrophy; TWI ¼ T-wave inversion.
ated with a 4.4-ml increase in RVEDV in athletes
(p ¼ 0.036) and a 5.9-ml increase in nonathletes
(p ¼ 0.005).
88
Brosnan et al.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
MARCH/APRIL 2015:84–91
Cardiac Displacement Causing TWI in Athletes
F I G U R E 2 Lateral Cardiac Displacement, but Not RV Volumes Explain Right Precordial T-Wave Inversion
(A) Horizontal long-axis CMRI images of 2 endurance athletes, athlete A (left) and athlete B (right). Although both athletes had almost
identical cardiac volumes, athlete A demonstrated less lateral displacement of the RV than athlete B (%LatD ¼ 36.7 vs. 59.7%, respectively).
The resultant ECG appearances are shown in B. (B) Precordial ECG leads V1 to V6 have been transposed onto the CMRI images of athletes A and
B in approximate standard positions. The corresponding appearances of leads V1 to V6 of the athletes’ ECGs are shown at the bottom right of
each image. In the athlete A, the body of the right ventricle overlies the sternum, between V1 and V2 (mid-RV axis). T-wave inversion is seen in
lead V1 but not in V2 or V3. In athlete B, the body of the right ventricle is displaced laterally, lying to the left of the sternum at the position of
lead V3, and the RV apex (apical axis) is displaced laterally toward lead V5. T-wave inversion is seen in leads V1 and V2. Also note the bifid
appearance of lead V4. %LatD ¼ lateral displacement of the RV apex (L1/L2%); CMRI ¼ cardiac magnetic resonance imaging; ECG ¼ electrocardiography; L1 ¼ distance from sternum to RV apex; L2 ¼ distance from sternum to left axilla; LVEDV ¼ left ventricular end-diastolic
volume; RVEDV ¼ right ventricular end-diastolic volume.
REPRODUCIBILITY OF CMRI MEASUREMENTS BETWEEN
(95% CI: 0.971 to 0.992), and RVEDV was 0.982 (95% CI:
INTERPRETERS. There was excellent agreement be-
0.965 to 0.991).
tween interpreters for measurements of cardiac displacement and cardiac volumes, with intraclass
DISCUSSION
correlation coefficients as follows: :septal was 0.938
(95% CI: 0.53 to 0.973), L1 was 0.958 (95% CI: 0.889 to
Lateral displacement of the cardiac apex was first
0.982), L2 was 0.933 (95% CI: 0.849 to 0.971), %LatD
described in endurance athletes more than a century
was 0.932 (95% CI: 0.837 to 0.971), LVEDV was 0.985
ago by the Swedish physician Henschen (13), who
Brosnan et al.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
MARCH/APRIL 2015:84–91
Cardiac Displacement Causing TWI in Athletes
T A B L E 3 Univariate Predictors of Presence of Right Precordial
T-Wave Inversion in Endurance Athletes
displaced inferiorly and laterally relative to the sternum means that a greater proportion of the RV is
positioned under ECG leads that have been placed
Predictor
OR (95% CI)
p Value
L1, per cm increase
1.707 (1.193–2.444)
0.003
L2, per cm increase
0.727 (0.543–0.974)
0.033
%LatD, per % increase
1.152 (1.059–1.253)
0.001
occasionally in V 3 in athletes. We demonstrated a
:septal, per degree of increase
1.150 (1.049–1.259)
0.003
strong association between the extent of leftward
0.985 (0.970–1.000)
0.054
cardiac displacement and the extent of TWI in the
1.105 (1.021–1.195)
0.013
Left hemithorax, per cm2 increase
CTHx %, per % increase
more inferiorly and laterally. Thus, the TWI normally
observed in V1 is frequently observed also in V 2 and
precordial leads. Thus, it seems that TWIV2-3, which is
usually associated with pathological changes in the
%LatD ¼ lateral displacement of the RV apex (L1/L2%); :septal ¼ angle of
interventricular septum with respect to midline (degrees); CI ¼ confidence
interval; CTHx% ¼ cardiac to left hemithorax area; L1 ¼ distance from sternum to
RV apex; L2 ¼ distance from sternum to left axilla.
RV in nonathletes, is explained by very simple geospatial relationships in EAs.
Previous studies focusing on cardiac volumes and
dimensions as assessed by ECG have found no relationship between right precordial TWI and RV di-
used the simple technique of cardiac percussion and
mensions in athletes (10). Our observations provide a
auscultation. Our study is the first to consider this
robust
basic examination finding as a potential explanation
improved accuracy of CMRI measurements of RV di-
validation
of
these
findings,
given
the
for right precordial TWI, which is observed on the
mensions relative to that of ECG (14). We observed
ECGs of approximately 1 in 7 healthy endurance ath-
that CMRI-derived cardiac volumes, although signif-
letes in the absence of pathological electrical or
icantly larger in EAs than in controls, did not correlate
structural cardiac abnormalities (5). We extended the
directly with the presence of TWI V2-3. However, we
cardiac enlargement and displacement observed in
observed that, as a secondary result of cardiac
athletes by Henschen (13) by using modern CMRI
enlargement within the constraints of the thorax,
techniques and related these changes to the standard
lateral cardiac displacement was prominent in EAs. In
position of the ECG leads. The fact that the RV apex is
EAs with TWIV2-3 it was demonstrated that the RV was
displaced relative to the thorax such that it was
placed against the anterior chest wall with the
F I G U R E 3 Lateral Displacement of the RV Apex Predicts
apex extending closer to the left axilla. As such, this
Right Precordial T-Wave Inversion in Endurance Athletes
means that a greater portion of the RV is placed
behind the ECG leads situated on the anterior
chest wall and to the left of the sternum, namely
leads V2 and V 3. This is well illustrated by the examples in Figures 2A and 2B. Although the ventricular
volumes are similar in the 2 athletes (Figure 2A), in
athlete A, the right atrium and more than one-half of
the RV extend into the right hemithorax. In athlete B,
the heart is displaced leftward such that the entire
RV sits under the sternum or in the left hemithorax
(Figure 2B). As a result, in athlete B, much more of
the RV lies in direct proximity to the precordial
ECG markers, resulting in TWI V2-3 (Figure 2B). This
cardiac displacement is not appreciable on ECG
because the surface anatomical “window” is adjusted
to align with cardiac landmarks. In comparison, CMRI
provides accurate assessment of RV structure and
cardiac displacement can be assessed relative to the
thorax.
Receiver operating characteristic (ROC) curve shows that lateral
WE ARE LOOKING AT THE RV, BUT WHY ARE THE
displacement of the RV apex (%LatD) of greater than 42.8%
T-WAVES
predicted TWI V2-3 with 74% sensitivity and 78% specificity (red
biphasic, or notched T-waves in the right precordial
NEGATIVE? The
arrow). RV ¼ right ventricle; TWI ¼ T-wave inversion.
leads in healthy and diseased states is still not
genesis
of
negative,
completely understood. It has been demonstrated
89
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Brosnan et al.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
MARCH/APRIL 2015:84–91
Cardiac Displacement Causing TWI in Athletes
in animal and human models that epicardial activa-
abnormalities, and therefore selection bias would
tion and repolarization of an enlarged RV occurs after
not have been expected to explain the high preva-
that of the LV, and ST-T polarity is positive at the
lence of TWI V2-3. Differences in cohort demographics
earliest and negative at the latest site of epicardial
may be a more likely explanation. Compared with our
repolarization, resulting in negative or biphasic T
previous study (5), the current cohort was older
waves in the ECG leads which look at the RV (15).
(35 8 vs. 22 5 years of age, respectively), and
In subjects with ARVC, a strong correlation between
a large proportion were ultraendurance athletes
RV volumes, as assessed by ventriculography, and
participating in events such as the Ironman triathlon
the extent of right precordial TWI has been demon-
(21). Given this difference, it is perhaps reasonable
strated. Although Nava et al. (16) did not have the
to hypothesize that those who had performed the
benefit of CMRI to assess cardiac displacement,
greatest volume of training (ultraendurance athletes)
they theorized that these findings were probably due
over the longest periods of time (an average of 10 9
to RV dilatation displacing the LV backward (16).
years in the current cohort) (21) would have greater
Similarly, Awa et al. (17) theorized that, in children
cardiac remodeling and displacement, which would
with congenital heart disease, the presence of bifid
explain the higher prevalence of TWI. To address
or biphasic TWI V2-3 might be related to the proximity
this speculative hypothesis, a larger cohort with a
of the RV to the anterior chest wall as a result of
broader age range and better-defined training dura-
cardiac enlargement, with the chest leads recording a
tion would need to be studied. Nevertheless, the high
more localized epicardial deflection than would be
prevalence of TWIV2-3 in the current cohort was an
expected
Our
advantage in that it increased the statistical power
observation that it is the location of the RV with
for the comparison between athletes with and with-
respect to the anterior chest wall rather than cardiac
out TWI V2-3.
with
normal
cardiac
orientation.
dimensions per se, which result in deep or bifid
TWI V2-3, supports the theories of these authors. Our
findings also offer a possible explanation for TWI V2-3
in nonathletes who have conditions resulting in RV
displacement, such as pectus excavatum (18–20).
CLINICAL IMPLICATIONS AND FUTURE DIRECTIONS.
CMRI is increasingly used in the assessment of
asymptomatic athletes with TWI V2-3 (commonly in
the setting of preparticipation screening), in whom
underlying cardiomyopathy cannot adequately be
ASSOCIATED ECG FINDINGS. Compared to nonath-
excluded after ECG. In the absence of any clinical or
letic controls, EAs were found to have a more right-
radiological features of structural heart disease such
ward QRS axis, and the QRS transition occurred later.
as ARVC, increased lateral displacement of the RV
However, neither of these findings correlated with
apex toward the axilla may provide an explanation
the presence of TWI V2-3. Although this was perhaps
and provide reassurance regarding an expectedly
surprising, a similar lack of association between QRS
benign prognosis. Similarly, in nonathletic subjects
transition and TWI has been reported previously (16).
referred for CMRI on the basis of incidental ECG
Furthermore, we found that a more rightward QRS
findings of TWIV2-3, lateral displacement of the RV
axis was associated with bigger RV volumes in both
apex could be considered as part of the assessment.
athletes and controls, supporting the notion that a
Further studies in patients with proven ARVC
larger RV mass will result in the ECG finding of a more
would be useful to determine whether cardiac
rightward QRS axis but that the presence of TWIV2-3
displacement may contribute to the degree of
relies on other anatomical factors such as cardiac
observed TWI, or whether the ECG changes in this
displacement.
cohort represent a unique electrical substrate.
HIGHER-THAN-EXPECTED PREVALENCE OF RIGHT
STUDY LIMITATIONS. The number of nonathletic
PRECORDIAL T-WAVE INVERSION IN THE ENDURANCE
control subjects with TWI V2-3 was low, reflecting the
ATHLETE COHORT. We have previously reported that
low prevalence of TWI V2-3 in healthy, nonathletic in-
TWI V2-3 is approximately 3 times more prevalent in
dividuals. Although a trend for the same alterations
endurance athletes than in nonendurance athletes
in cardiac orientation was seen in the single control
(5). The prevalence of right precordial TWIs in the
subject with TWI V2-3, more subjects with TWI V2-3
current cohort of 68 endurance athletes was higher
would be required to determine whether the same
than that which we reported in the 251 endurance
observations hold. It is possible that other anatomical
athletes in the aforementioned study but similar to
factors which are rare in EAs, such as chest wall
that recently reported in a cohort of highly trained
adiposity, may need to be taken into consideration
endurance athletes (6). All subjects were healthy
when correlating CMRI with ECG features in nonath-
study volunteers, not included on the basis of ECG
letic subjects.
Brosnan et al.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
MARCH/APRIL 2015:84–91
Cardiac Displacement Causing TWI in Athletes
All subjects were Caucasian, thus it was beyond the
scope of this study to assess whether cardiac displacement could explain the high prevalence of right
precordial T-wave changes reported in subjects of
black African and Afro-Caribbean ethnicity (7).
endurance athletes in the absence of any clinical or radiological
features of ARVC, TWIV2-3 on 12-lead ECG may be explained by
dilatation or hypertrophy.
CMRI provides a unique opportunity to assess RV
orientation,
COMPETENCIES IN MEDICAL KNOWLEDGE: In healthy
lateral displacement of the right ventricle (RV) rather than RV
CONCLUSIONS
structure,
PERSPECTIVES
and
displacement
within
the thorax. We demonstrated that lateral displacement of the RV toward the left axilla is associated
with progressive TWI in the right precordial ECG
leads. This may explain why TWI V2-3 is more common
in EAs and may also be helpful in differentiating
athlete’s heart from ARVC in the absence of any
other clinical or radiological features to suggest this
condition.
COMPETENCIES IN PATIENT CARE: In subjects referred for
cardiac magnetic resonance imaging on the basis of ECG findings
of right precordial TWI, the extent of lateral displacement of the
RV apex toward the axilla is an important component of the
assessment. Although ECG changes may represent structural
cardiac changes, they may also reflect cardiac position within the
thorax.
TRANSLATIONAL OUTLOOK: Further studies in patients with
ARVC would be useful to determine whether cardiac displace-
REPRINT REQUESTS AND CORRESPONDENCE: Dr.
Maria Brosnan, Department of Cardiology, St. Vincent’s
Hospital, Melbourne, PO Box 2900, Fitzroy, Victoria 3065,
ment may contribute to the degree of observed TWI, or whether
the ECG changes in this cohort are due to the underlying electrical substrate.
Australia. E-mail: [email protected].
REFERENCES
1. Nasir K, Bomma C, Tandri H, et al. Electrocardiographic features of arrhythmogenic right ventricular dysplasia/cardiomyopathy according to
disease severity: a need to broaden diagnostic
8. Aro AL, Anttonen O, Tikkanen JT, et al. Prevalence and prognostic significance of T-wave inversions in right precordial leads of a 12-lead
electrocardiogram in the middle-aged subjects.
criteria. Circulation 2004;110:1527–34.
Circulation 2012;125:2572–7.
2. Marcus FI, McKenna WJ, Sherrill D, et al.
9. Papadakis M, Basavarajaiah S, Rawlins J, et al.
Prevalence and significance of T-wave inversions
in predominantly Caucasian adolescent athletes.
Eur Heart J 2009;30:1728–35.
Diagnosis of arrhythmogenic right ventricular
cardiomyopathy/dysplasia: proposed modification
of the task force criteria. Circulation 2010;121:
1533–41.
10. Zaidi A, Ghani S, Sharma R, et al. Physiological
3. Corrado DAP, Heidbuchel H, Sharma S, et al.
Recommendations for interpretation of 12-lead
electrocardiogram in the athlete. Eur Heart J
2010;31:243–59.
right ventricular adaptation in elite athletes of
African and Afro-Caribbean origin. Circulation
2013;127:1783–92.
4. Drezner JA, Ackerman MJ, Anderson J, et al.
11. Lai WW, Gauvreau K, Rivera ES, Saleeb S,
Powell AJ, Geva T. Accuracy of guideline recommendations for two-dimensional quantification of
Electrocardiographic interpretation in athletes: the
“Seattle Criteria.” Br J Sports Med 2013;47:122–4.
5. Brosnan M, La Gerche A, Kalman J, et al.
Comparison of frequency of significant electrocardiographic abnormalities in endurance versus nonendurance athletes. Am J Cardiol 2014;113:1567–73.
6. Wasfy MM, DeLuca J, Wang F, et al. ECG findings in competitive rowers: normative data and the
prevalence of abnormalities using contemporary
screening recommendations. Br J Sports Med
2015;49:200–6.
7. Papadakis MCF, Kervio G, Rawlins J, et al. The
prevalence, distribution, and clinical outcomes of
electrocardiographic repolarization patterns in
male athletes of African/Afro-Caribbean origin.
Eur Heart J 2011;32:2304–13.
the right ventricle by echocardiography. Int J
Cardiovasc Imaging 2008;24:691–8.
12. Prior DL, La Gerche A. The athlete’s heart.
Heart 2012;98:947–55.
13. Henschen S. Skidlauf und skidwettlauf: eine
medizinische sportsudie (A Study in Sports Medicine, Skiing and Competitive Skiing). Mitt Med Klin
Upsala 1899;2.
14. Jurcut R, Giusca S, La Gerche A, Vasile S,
Ginghina C, Voigt JU. The echocardiographic
assessment of the right ventricle: what to do in
2010? Eur J Echocardiogr 2010;11:81–96.
15. Chen PS, Moser KM, Dembitsky WP, et al.
Epicardial activation and repolarization patterns in
patients with right ventricular hypertrophy. Circulation 1991;83:104–18.
16. Nava A, Canciani B, Buja G, et al. Electrovectorcardiographic study of negative T waves on
precordial leads in arrhythmogenic right ventricular dysplasia: relationship with right ventricular
volumes. J Electrocardiol 1988;21:239–45.
17. Awa S, Linde LM, Oshima M, Okuni M,
Momma K, Nakamura N. The significance of latephased dart T wave in the electrocardiogram of
children. Am Heart J 1970;80:619–28.
18. Quarta G, Husain SI, Flett AS, et al. Arrhythmogenic right ventricular cardiomyopathy mimics:
role of cardiovascular magnetic resonance.
J Cardiovasc Magn Reson 2013;15:16.
19. Dressler W, Roesler H. Electrocardiographic
changes in funnel chest. Am Heart J 1950;40:
877–83.
20. Kataoka H. Electrocardiographic patterns of the
Brugada syndrome in 2 young patients with pectus
excavatum. J Electrocardiol 2002;35:169–71.
21. La Gerche A, Burns AT, Mooney DJ, et al.
Exercise-induced right ventricular dysfunction and
structural remodelling in endurance athletes. Eur
Heart J 2012;33:998–1006.
KEY WORDS ARVC, athlete, cardiac
displacement, cardiac MRI, CMRI, ECG,
right ventricle
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