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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. JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015 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 90 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. 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KEY WORDS ARVC, athlete, cardiac displacement, cardiac MRI, CMRI, ECG, right ventricle 91