- Email: [email protected]
New normal limits for pediatric ECG in childhood obesity? Influence of childhood obesity on the ECG
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
Contents lists available at ScienceDirect
Progress in Pediatric Cardiology journal homepage: www.elsevier.com/locate/ppedcard
New normal limits for pediatric ECG in childhood obesity? Influence of childhood obesity on the ECG ⁎
C. Paecha, , M. Anhalta, R.A. Gebauera, F. Wagnera, M. Vogelb, T. Kirstenc, M. Weidenbacha, W. Kiessb, I. Dähnerta, A. Körnerb a
Department for Pediatric Cardiology, University of Leipzig - Heart Center, Strümpellstr. 39, 04289 Leipzig, Germany Hospital for Children and Adolescents, Center for Pediatric Research, University of Leipzig, Philipp-Rosenthal-Straße 27, 04103 Leipzig, Germany c LIFE Research Center for Civilization Diseases, University of Leipzig, Philipp-Rosenthal-Straße 27, 04103 Leipzig, Germany b
A R T I C L E I N F O
A B S T R A C T
Keywords: ECG Obesity Children Reference value
Introduction: Studies demonstrated abnormal ECG phenomena in adult obese patients. Although some of these phenomena are clearly pathologic, for others the clinical relevance is less clear. In children this conflict is even harder to address as there are only scarce specific reference data on ECG in childhood obesity. The aim of this study was to investigate the influence of childhood obesity on distinct ECG parameters of cardiac activation and repolarization in a cohort of otherwise healthy obese volunteers and compare these with lean controls. Methods: We prospectively enrolled 53 otherwise healthy obese children (BMI (mean/SD) 2.35 (1.39–3.56)) and 43 lean controls (BMI (mean/SD) − 0.243 (−2.02–1.25)) from the LIFE Child Study. All probands underwent a thorough cardiac evaluation including a 12‑lead ECG. Results: Obese children showed a more left sided QRS axis (p < 0.01). This effect was independent from age (p = 0.28) or sex (p = 0.3). Otherwise there were no major differences between the groups. Most importantly, there were no pathologic phenomena recorded in otherwise healthy, obese children. Conclusion: In healthy children, obesity does not result in pathologic ECG phenomena. Therefore pathology has only to be suspected in case of clearly abnormal ECG findings even in severely obese children.
1. Introduction With the increasing prevalence of childhood obesity a number of comorbidities, especially cardiovascular complications ensue. The well described association with elevated blood pressure and structural cardiac alterations is relevant in the obese child with hypertension [1–3]. Whether these are accompanied by alterations in the ECG, and whether these are of clinical relevance for cardiovascular risk stratification for example in the ECG evaluation prior to a scheduled medical or surgical therapy is less clear. It is well known from adult studies that there are various ECG changes that are associated with obesity. These include left axis deviation, signs of left ventricular hypertrophy, bradycardia and alterations of cardiac repolarization like ST–segment depression, T-wave inversion, increased electrical inhomogeneity and QT interval prolongation [4]. In children there are only scarce data. Some studies imply there are abnormalities in the ECG of obese children related to their obesity alone [3,5]. As these ECG findings are particularly evident
⁎
in severely obese patients they are challenging for the pediatric cardiologist in the judgement of whether a distinct ECG alteration represents a variation of the normal or an underlying pathologic medical condition. Hitherto data imply that there are some changes associated with pathologic conditions like left ventricular hypertrophy in arterial hypertension and others lack evidence of pathology despite being atypical like left axis deviation or relative QTc interval prolongation [4]. The aim of this study was to investigate the influence of childhood obesity on distinct ECG parameters of cardiac activation and repolarization in a cohort of otherwise healthy obese volunteers and compare these with lean controls. 2. Methods 2.1. Study Sample A total of 96 consecutive healthy, Caucasian pediatric volunteers at the age of 6 to 18 years, who participated in the LIFE Child Study at the
Corresponding author. E-mail address: [email protected] (C. Paech).
https://doi.org/10.1016/j.ppedcard.2017.11.002 Received 7 May 2017; Received in revised form 1 November 2017; Accepted 27 November 2017 1058-9813/ © 2017 Elsevier B.V. All rights reserved.
Please cite this article as: Paech, C., Progress in Pediatric Cardiology (2017), https://doi.org/10.1016/j.ppedcard.2017.11.002
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
LIFE Leipzig Research Center for Civilization Diseases from 2011 to 2014 were prospectively enrolled in the study [5]. All probands underwent a thorough cardiac evaluation including past medical history, physical examination, anthropometric evaluation, 12 lead ECG and echocardiography. Written informed consent of the parents was obtained. The study was approved by the ethics committee of the University of Leipzig (reg. no: 264-10-19042010) and is registered NCT02550236. Exclusion criteria were gross pathology, electrolyte disturbances, arterial hypertension or structural heart disease and marked ventricular hypertrophy but none of these was present in any patient. All anthropometric parameters were adjusted for age and sex based on national reference values of German children from KromeyerHauschild et al. [6] and accordingly are given in standard deviation score (SDS). Probands were stratified into overweight/obese and lean children applying an adjusted BMI 1.28/1.88 SDS as cut off according to current German guidelines [6].
Table 1 Patient characteristics. Lean (mean ± SEM)
Obese (mean ± SEM)
N Age (years) Sex (m/f) Height (cm) Height SDS Weight (kg)
43 11.34 (7.33–17.71) Male 31/female 12 148.5 (122.5–179.6) 0.07 (− 1.57–2.48) 37.00 (19.90–71.70)
BMI BMI SDS
17.47 (13.26–23.75) − 0.24 (− 2.02–1.25) 74.20 (56.6–101) − 0.27 (− 2.57–1.18) 60.00 (48.80–74.50)
53 11.48 (6.54–16.49) Male 37/female 16 154.9 (126.1–185.1) 0.94 (− 1.00–2.96) 65.80 (33.50–135.50) 26.89 (20.11–40.59) 2.35 (1.39–3.56)
Hip circumference (cm) Hip circumference adj. Waist circumference (cm) Waist circumference adj. Syst. BP (mm Hg)
2.2. ECG Analysis For each child, a 12‑lead ECG was recorded using an electrocardiograph (General Electrics, MAC 5000). The frequency response of this recorder is flat to 150 Hz. A paper speed of 50 mm/s and an amplitude of 10 mm/mV was used. The ECGs were recorded by the same technician throughout the study. All ECGs were anonymized by pseudonymization and analyzed blinded by two independent physicians with extensive experience in the analysis of pediatric ECGs.
Diast. BP. (mm Hg)
− 0.36 (− 2.28–1.13) 105.00 (86.67–125.33) 65.67 (54.33–77.67)
p value
0.284 0.55 0.084 < 0.01 < 0.01 < 0.01 < 0.01
97.70 (70.2–138) 1.75 (0.41–2.65)
< 0.01 < 0.01
84.80 (63.00–107.50) 1.66 (0.93–2.33)
< 0.01
111.30 (93.00–132.67) 69 (51.67–80.00)
< 0.01
< 0.01
0.07
SDS = standard deviation score; adj. = adjusted; BP = blood pressure. Table 2a Influence of obesity on ECG parameters (all ages) timing intervals.
2.3. Statistics ECG HR QRS axis P axis ECG lead II
Statistical analysis was carried out with SPSS 21.0 software. Continuous data were assessed for normality and the Student's t-test was used for normally distributed data. To characterize the influence between continuous variables bivariate correlation was used and Pearsons correlation coefficient (r) is reported. For this study, α was set at 0.05; thus p-values < 0.05 (two-sided) were required for statistical significance. The entire study cohort was analyzed as a single cohort. In addition, analyses were performed after subdivision of patients into three age groups as previously suggested by Davignon et al. and Rijnbeek et al., that are acknowledged to represent key studies in defining the limits of normal in pediatric ECG [7,8].
P PQ QRS QT
ECG lead V5
P PQ QRS QT
Lean (n = 43) (mean ± SEM)
Obese (n = 53) (mean ± SEM)
p value
75.72 (63.46–87.98) 78.37 (58.29–98.45) 48.49 (20.19–76.77) 71.86 (58.54–85.18) 130.93 (110.02–151.84) 78.84 (64.01–93.67) 355.58 (327.19–383.97) 68.84 (50.43–87.25) 127.44 (104.96–149.92) 78.84 (66.65–91.03) 352.56 (326.28–378.82)
75.58 (62.31–80.85) 61.60 (40.23–82.97) 40.28 (16.49–64.07) 77.36 (62.93–91.79) 128.87 (112.04–145.7)
0.96 < 0.01 0.13 0.06 0.59
81.13 (67.03–95.23) 352.26 (329.59–374.93) 70.00 (52.70–87.10) 124.04 (106.08–142.00) 83.96 (73.16–94.76) 355.28 (330.90–379.67)
0.44 0.53 0.75 0.41 0.32 0.60
SR = sinus rhythm; HR = heart rate.
3. Results Table 2b Influence of obesity on ECG parameters (6–8 years) timing intervals.
3.1. Patients Characteristics Table 1 shows the patients basic characteristics of the stratified groups lean and overweight/obese including anthropometric measurements. Obese children did not differ from lean children with respect to age and sex distribution, but expectedly had higher BMI SDS and were taller. The systolic blood pressure was higher in obese compared to lean children, although still within normal limits. All study participants showed serum electrolyte levels within age and sex appropriate limits at the time the ECG was performed. Each had a normal echocardiography and a negative family history.
HR QRS axis P axis ECG lead II
ECG lead V5
3.2. Basic ECG Characteristics The basic ECG characteristics and timing intervals are summarized in Tables 2a–2d. Heart rate was not elevated in obese children, hence making autonomic activation unlikely. The QRS axis was slightly but significantly shifted to the left side in the obese children, whereas the Paxis remained indifferent (Table 2a). This effect was particularly apparent in the younger children aged 8–12 years as opposed to the group of adolescents (Tables 2c, 2d). Data showed a highly significant
P PQ QRS QT P PQ QRS QT
Lean (n = 1) (mean ± SEM)
Obese (n = 6) (mean ± SEM)
p value
101 (101) 90 (90) 30 (30) 80 (80) 130 (130) 90 (90) 320 (320) 70 (70) 130 (130) 80 (80) 320 (320)
81.67 (66.50–96,88) 65 (49.83–80.17) 41.67 (13.09–70.25) 75 (64.51–85.49) 118.33 (103.61–133.05) 85 (68.47–101.43) 320 (301.02–338.97) 66.67 (58.51–74.84) 115 (104.51–125.49) 81.67 (77.59–85.75) 328.33 (311.11–345.55)
0.29 0.19 0.72 0.68 0.50 0.79 1.00 0.72 0.24 0.72 0.67
SR = sinus rhythm; HR = heart rate.
correlation between the QRS axis and the waist to hip ratio (r = − 0.35/p = 0.001) with more left sided QRS axis for higher values of waist to hip ratio. Regarding time intervals, we did not see significant differences between obese and lean children when looking at all
2
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
Table 2c Influence of obesity on ECG parameters (8–12 years) timing intervals.
HR QRS axis P axis ECG lead II
Table 3a Influence of obesity on ECG parameters (all ages): amplitudes.
Lean (n = 24) (mean ± SEM)
Obese (n = 22) (mean ± SEM)
p value
78.75 (66.68–90.82) 85.42 (75.76–95.08) 51.88 (31.73–72.03) 70.83 (54.70–86.96) 130.42 (111.66–149.18) 76.25 (62.17–90.33) 347.92 (318.14–377.70) 66.25 (45.02–87.48) 124.58 (105.35–143.23) 76.67 (64.99–88.34) 347.92 (319.18–367.6)
76.27 (66.23–86.30) 62.95 (0.18–85.71) 41.14 (14.33–67.95) 73.18 (59.59–86.77) 129.55 (112.24–146.86) 78.64 (64.07–93.12) 353.18 (32.85–373.51)
0.46 < 0.01 0.13 0.60 0.87
68.18 (55.59–80.77) 125.91 (110.28–141.54) 82.73 (70.32–95.14) 356.36 (331.19–381.54)
0.71 0.80
ECG lead I
Q
ECG lead AVR
R S P Q R S Q R S Q R
SR = sinus rhythm; HR = heart rate.
ECG lead AVL
S Q R
Table 2d Influence of obesity on ECG parameters (12–18 years) timing intervals.
ACG lead AVF
P PQ QRS QT
ECG lead V5
P PQ QRS QT
HR QRS axis P axis ECG lead II
P PQ QRS QT
ECG lead V5
P PQ QRS QT
ECG lead II
0.58 0.49 ECG lead III
0.09 0.30
Lean (n = 18) (mean ± SEM)
Obese (n = 25) (mean ± SEM)
p value
70.28 (42.12–94.50) 68.3 (42.12–94.5) 45 (7.86–82.14) 72.78 (63.83–81.73) 131.67 (107.12–156.23) 81.67 (65.86–97.48) 367.78 (345.94–389.62) 72.22 (57.85–86.59) 131.11 (103.69–158.53) 81.67 (68.73–95.62) 360.56 (339.85–381.27)
73.52 (58.32–88.72) 59.6 (37.71–81.49) 39.20 (18.60–59.79) 81.60 (66.41–96.79) 130.80 (114.24–147.36) 82.4 (69.08–95.72) 359.20 (33.97–378.33)
0.43 0.24 0.52 0.33 0.89
72.40 (50.74–94.06) 124.58 (103.52–145.64) 85.6 (75.16–96.04) 360.8 (339.41–382.19)
0.98 0.39
ECG lead V1
0.87 0.18
0.28 0.97
SR = sinus rhythm; HR = heart rate.
S Q R S P Q R S
ECG lead V2
Q R S
ECG lead V3
Q R S
ECG lead V4
Q R S
ECG lead V5
Q R S
participants (Table 2a). ECG lead V6
3.3. Amplitudes
Q R S
ECG U wave ECG R/S
The measurements of amplitudes are summarized in Tables 3a–3d. Data show nearly no differences in the bipolar or unipolar limb leads. Concordant with the QRS type, there were significant differences in the Q and R wave amplitudes in left sided leads (I and aVL) with greater amplitudes in the obese participants when looking at the entire group (Table 3a). Again this effect is most evident in the group of younger children aged 8–12 years but could also be demonstrated in the group of adolescents (Tables 3c, 3d). In addition slightly more negative S waves could be demonstrated in lean compared to obese participants in leads V2 and V3 (p = 0.02) in the entire group (Table 3a). The effect could not be demonstrated in the adolescents (Table 3d). Despite differences in S wave negativity there was no statistically significant difference in R/S progression between lean and obese children, neither in the entire group (p = 0.14) nor in young children (p = 0.21) or adolescents (p = 0.8).
Lean (n = 43) (mean ± SEM)
Obese (n = 53) (mean ± SEM)
p value
− 0.05 (− 0.08 to − 0.02) 0.36 (0.08–0.63) − 0.12 (− 0.27–0.03) 0.12 (0.03–0.21) − 0.07 (− 0.01–0.01) 1.43 (0.90–1.97) − 0.15 (− 0.30–0.01) − 0.10 (− 0.21–0.00) 1.20 (0.64–1.75) − 0.1 (−0.04–0.04) 0.03 (− 0.01–0.07) − 0.78 (− 1.18 to − 0.39) 0.09 (− 0,09–0.27) 0.06 (− 0.02–0.15) − 0.43 (− 0.90–(− 0.01)) 0.01 (− 0.12–0.14) − 0.07 (− 0.18–0.02) 1.32 (0.82–1.82) − 0.13 (− 0.28–0.27) 0.07 (0.02–0.12) 0.03 (− 0.05–0.12) 0.27 (− 0.24–0.78) − 0.73 (− 1.21–(− 0.25)) 0.01 (− 0.05–0.07) 0.80 (0.18–1.43) − 1.61 (− 2.27–(− 0.95)) − 0.01 (− 0.09–0.07) 1.21 (0.44–1.98) − 1.06 (− 1.64–(− 0.48)) − 0.05 (− 0.13–0.03) 1.94 (1.30–2.58) − 0.49 (− 0.84–(− 0.13) − 0.11 (− 0.22–(− 0.01)) 1.85 (1.12–2.58) − 0.17 (− 0.33–(− 0.01)) − 0.13 (− 0.23–(− 0.04)) 1.35 (0.95–1.75) − 0.06 (− 0.15–0.02) 1.81 (1.42–2.20)
−0.32 (− 0.27–(−0.08))
< 0.01
0.79 (0.30–1.27) −0.20 (− 1.92–(−0.03)) 0.12 (0.07–0.17) −0.07 (−0.16–0.03) 1.41 (0.95–1.86) −0.13 (−0.26–0.00) −0.09 (−0.26–0.07) 0.84 (0.20–1.48) −0.04 (−0.23–0.10) 0.04 (− 0.01–0.09) −0.93 (− 1.43–(−0.42))
< 0.01 0.19 0.10 0.99 0.78 0.58 0.68 0.04 0.60 0.14 0.14
0.13 (0.01–0.25) 0.02 (− 0.12–0.15) 0.08 (− 0.41–0.56)
0.17 0.04 < 0.01
−0.20 (−0.45–0.05) −0.06 (−0.17–0.04) 1.05 (0.52–1.58) −0.10 (−0.22–0.027) 0.07 (0.03–0.06) 0.023 (− 0.06–0.10) 0.28 (− 0.13–0.69) −0.73 (− 1.20−(− 0.25)) 0.01 (− 0.07–0.10) 0.84 (0.31–1.37) −1.30 (− 1.85–(−0.75))
< 0.01 0.53 0.01 0.31 0.67 0.61 0.88 0.98
0.00 (− 0.03–0.02) 1.27 (0.73–1.82) −0.79 (− 1.27–(−0.30))
0.59 0.64 0.02
−0.03 (−0.10–0.03) 1.81 (1.21–2.41) −0.42 (− 0.74–(−0.10))
0.39 0.31 0.31
0.09 (− 0.17–0.00)
0.24
1.70 (1.22–2.18) −0.18 (−0.36–0.00)
0.24 0.75
−0.06 (−0.33–0.21)
0.10
1.31 (0.79–1.84) −0.08 (−0.20–0.03) 1.87 (1.53–2.21)
0.74 0.37 0.47
3.23 (2.59–3.87)
0.14
3.42 (2.79–4.05)
0.81 0.78 0.02
there were no major differences in the ECG parameters and most important there were no pathologic phenomena recorded in otherwise healthy, obese children. 4. Discussion Obese patients have an increased risk for various comorbidities, particularly cardiovascular complications. Studies in adults have reported that there are several ECG phenomena associated with obesity, but there is only scarce data in children. The aim of this study was to investigate the influence of childhood obesity on various ECG parameters in a cohort of otherwise healthy individuals. The main conclusion drawn from the data of the current study is that childhood obesity has no clinically relevant effect on ECG parameters in children, even though we did see a slight, yet non-pathologic, left shift of the QRS axis. These findings are in contrast to the findings in the adult population that included clinically insignificant findings like left axis deviation and
3.4. Main Results We found a slight left-sided shift in QRS axis and increased amplitudes of the left sided leads in obese children, although all measured parameters remained within normal limits for age and sex. Otherwise, 3
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
Table 3b Influence of obesity on ECG parameters (6–8 years) amplitudes.
ECG lead I
ECG lead II
ECG lead III
ECG lead AVR
ECG lead AVL
ACG lead AVF
ECG lead V1
ECG lead V2
ECG lead V3
ECG lead V4
ECG lead V5
ECG lead V6
ECG U wave ECG R/S
Q R S P Q R S Q R S Q R S Q R S Q R S P Q R S Q R S Q R S Q R S Q R S Q R S
Table 3c Influence of obesity on ECG parameters (8–12 years) amplitudes.
Lean (n = 1) (mean ± SEM)
Obese (n = 6) (mean ± SEM)
p value
0 0.7 −0.4 0.15 −0.1 2.15 0 −0.25 2.15 0 0 −1.2 0 0.25 −1.2 0 −1 2.1 0 −1 0 0.6 −1.5 0 1.35 −2.6 0 1.6 −0.5 0 2.3 −0.15 −0.15 2.2 0 −0.2 1.9 0 1 3
− 0.03 (− 0.07–0.01) 0.81 (0.53–1.09) − 0.25 (− 0.49–(−0.01) 0.1 (0.03–0.17) − 0.12 (− 0.22–(−0.02) 1.76 (1.55–1.97) − 0.09 (− 0.32–0.13) 0.23 (− 0.34–(− 0.13)) 1.23 (1.00–1.45) − 0.04 (− 0.13–0.05) 0.08 (0.03–0.12) − 1.2 (−1.50–(− 0.89)) 0.12 (− 0.11–0.35) 0.12 (− 0.12–0.35) 0.25 (− 0.30–0.70) − 0.3 (−0.66–0.06) − 0.15 (− 0.24–(−0.06)) 1.47 (1.35–1.59) − 0.07 (− 0.23–0.10) 0.08 (0.06–0.11) 0 0.55 (0.2–0.91) − 1.06 (− 1.87–(−0.25)) 0 1.2 (0.77–1.63) − 1.58 (− 0.41–(−1.17)) − 0.01 (− 0.03–0.01) 1.55 (1.03–3.07) − 0.7(− 1.08–(− 0.32)) − 0.09 (− 0.18–(−0.01)) 2.14 (1.68–2.57) − 0.32 (− 0.59–(−0.04)) 0.18 (− 0.26–(− 0.09)) 1.9 (1.63–2.17) − 0.11 (− 0.18–(−0.03)) −(0.18 (− 0.26–(−0.11)) 1.53 (1.45–1.60) − 0.07 (− 0.3–0.10) 2 2.83 (2.422–3.24)
0.48 0.73 0.59 0.54 0.88 0.15 0.72 0.89 0.01 0.70 0.16 1.0 0.53 0.62 0.05 0.48 0.63 0.01 0.72 < 0.01
ECG lead I
Q R S
ECG lead II
ECG lead III
R S Q
ECG lead AVR
R S Q R
ECG lead AVL
0.90 0.63
ACG lead AVF
0.76 0.07 0.72 0.93 0.65 0.37 0.76 0.60 0.80 0.36 0.52 0.85 < 0.01 0.72
ECG lead V1
S Q R S Q R S P Q R S
ECG lead V2
P Q R S
ECG lead V3
Q R S
ECG lead V4
Q R S
ECG lead V5
Q
0.72
major pathology like signs of left ventricular hypertrophy, bradycardia and alterations of cardiac repolarization like ST – segment depression or T-wave inversion [9,10]. There are several hypotheses concerning possible influencing factors of obesity on ECG parameters. Beside easy determinable factors like arterial hypertension or left ventricular hypertrophy, mainly hormonal and autonomic nervous system influences are reported [11–13]. In addition it is well known that electrolyte disturbances may influence the ECG tracing [14]. It also needs to be considered that adults have a longer exposure time to obesity (and potentially related arterial hypertension) that eventually result in morphological and electrical cardiac alterations, which are not yet identifiable in children. This study included only healthy participants as confirmed by an intensive cardiac work up including echocardiography and laboratory findings. This excluded patients with arterial hypertension, left ventricular hypertrophy or electrolyte imbalances and may be a main reason for the almost normal ECG findings present in our cohort. Also, heart rate was similar in both groups hence not pointing to an autonomic nervous system effect. Nevertheless the presented data show at least some minor differences between lean and obese participants. The slightly more left sided axis may be simply due to anatomical differences like increased abdominal fat deposits, as substantially differing waist and hip circumferences between the groups imply a significantly increased abdominal fat in the obese participants. However, it needs to be considered that in children an increased waist-to-hip ratio not
P Q
R S ECG lead V6
Q R S
ECG U wave ECG R/S
Lean (n = 24) (mean ± SEM)
Obese (n = 22) (mean ± SEM)
p value
− 0.08 (− 0.11–(− 0.05)) 0.30 (0.06–0.54) − 0.15 (− 0.31–0.00)
−0.02 (−0.07–0.03)
0.22
0.88 (0.19–1.57) −0.22 (− 0.37–(−0.08) 0.12 (0.08–0.55) −0.08 (−0.20–0.04)
< 0.01 0.12 0.91 0.85
1.47 (0.98–1.96) −0.14 (−0.27–(0.01)) −0.11 (−0.30–0.08)
0.73 0.80 0.69
0.89 (0.09–1.69) −0.05 (−0.31–0.07) 0.03 (− 0.01–0.06) −0.94 (− 1.48–(−0.40)) 0.14 (0.03–0.26) 0.03 (− 0.10–0.15) 0.08 (− 0.54–0.70) −0.21 (−0.46–0.04) −0.05 (−0.18–0.22) 1.06 (0.38–1.74) −0.10 (−0.25–0.04) 0.68 (0.02–0.11) 0.023 (− 0.07–0.12) 0.26 (− 0.20–0.72) −0.75 (− 1.18–(−0.32)) 0.08 (0.05–0.11) 0.005 (− 0.02–0.03) 0.75 (0.14–1.37) −1.29 (− 2.02–(−0.55)) 0.00 (− 0.01–0.01) 1.24 (0.75–1.73) −0.88 (− 1.45–(−0.31)) −0.02 (−0.08–0.05) 1.93 (1.26–2.61) −0.47 (− 0.84–(−0.10)) 0.09 (− 0.17–(−0.01))
0.22 0.44 0.48 0.31
1.80 (1.24–2.47) −0.19 (− 0.37–(−0.02)) −0.10 (− 0.18–(−0.02)) 1.42 (0.97–1.88) −0.08 (−0.16–0.00) 1.77 (1.43–2.20) 3.27 (2.64–3.90)
0.21 0.95
0.12 (0.05–0.19) − 0.09 (− 0.17–(− 0.01)) 1.52 (1.92–1.12) − 0.15 (− 0.32–0.01) − 0.13 (− 0.23–(− 0.02) 1.32 (0.94–1.70) − 0.08 (− 0.21–0.04) 0.04 (− 0.01–0.08) − 0.81 (− 1.15–(− 0.46)) 0.1 (− 0.13–0.33) 0.08 (0.01–0.14) − 0.53 (− 0.8–(− 0.25)) 0.01 (− 0.11–0.13) 0.09 (− 0.20–0.01) 1.43 (1.04–1.81) − 0.10 (− 0.23–0.03) 0.09 (0.05–0.22) 0.04 (− 0.07–0.14) 0.28 (− 0.31–0.86) − 0.73 (− 0.13–(− 0.18)) 0.08 (0.05–0.11) 0 0.99 (0.55–1.43) − 1.88 (− 2.41–(− 1.35)) 0.00 (− 0.02–0.03) 1.34 (0.50–2.18) − 1.33 (− 1.87–(− 0.79)) − 0.06 (− 0.15–0.02) 2.12 (1.61–2.62) − 0.62 (− 1.00–(− 0.24)) − 0.15 (− 0.25–(− 0.05)) 2.07 (1.26–2.88) − 0.19 (− 0.36–(− 0.02)) − 0.17 (0.26–(− 0.08)) 1.36 (0.97–1.75) − 0.06 (− 0.57–0.03) 1.71 (1.25–2.17) 3.5 (2.91–4.09)
0.43 0.10 < 0.01 < 0.01 0.22 0.29 0.96 0.11 0.66 0.92 0.90 0.96 0.31 0.13 < 0.01 0.97 0.64 0.01 0.04 0.30 0.18 0.03
0.01 0.61 0.58 0.63 0.21
necessarily means intraabdominal fat accumulation as also subcutaneous fat is centered to the mid of the body. As younger children naturally tend to have rather right sided QRS axis this effect is more evident in younger children than in the adolescents. The differences in S waves in the precordial leads V2 and V3 seem to be of no clinical importance as the R/S progression was not different between the groups, implying balanced right and left ventricular forces.
5. Conclusion In healthy children, obesity does not result in pathologic ECG phenomena. Therefore pathology has to be suspected in case of abnormal ECG findings even in severely obese children. The results of this study emphasize the importance of a thorough cardiologic work up in 4
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
Funding Source
Table 3d Influence of obesity on ECG parameters (12–18 years) amplitudes.
ECG lead I
ECG lead II
ECG lead II
ECG lead AVR
ECG lead AVL ACG lead AVF ECG lead V1
Q R S P Q R S Q R S Q R S Q R S Q R S P Q R S
ECG lead V2
P Q R S
ECG lead V3
Q R S
ECG lead V4
Q R S
ECG lead V5
Q R S
ECG lead V6
Q R S
ECG U wave ECG R/S
Lean (n = 18) (mean ± SEM)
Obese (n = 25) (mean ± SEM)
p value
0 (− 0.03–0.03) 0.04 (0.10–0.72) − 0.06 (− 0.19–0.06) 0.12 (0.11–0.22) − 0.04 (− 0.82–0.04) 1.28 (0.63–1.93) − 0.14 (− 0.29–0.00) − 0.01 (− 0.16–0.03) 0.98 (0.32–1.64) − 0.1306 (−0.301–0.04) 0.02 (−0.02–0.05) − 0.73 (–1.20–(− 0.27))
− 0.04 (− 0.09–0.01) 0.71 (0.45–0.97) − 0.17 (− 0.35–0.01) 0.12 (0.08–0.16) − 0.05 (− 0.11–0.02) 1.26 (0.85–1.68) − 0.13 (0.24–(− 0.01)) − 0.04 (− 0.18–0.09) 0.70 (0.19–1.20) − 0.04 (− 0.21–0.13)
0.01 < 0.01 0.03 0.82 0.84 0.91 0.68 0.54 0.12 0.08
0.05 (0.02–0.11) − 0.85 (− 1.35–(− 0.34)) 0.13 (0.01–0.24) − 0.01 (− 0.11–0.08) 0.09 (− 0.29–0.46) − 0.16 (− 0.39–0.07) − 0.05 (− 0.12–0.02) 0.94 (0.57–1.31) − 0.1 (−0.20–(− 0.01)) 0.07 (0.02–0.12) 0.03 (− 0.05–0.10) 0.24 (− 0.13–0.61) − 0.63 (− 1.02–(− 0.24) 0.09 (0.06–0.13) 0.02 (− 0.10–0.14) 0.82 (0.37–1.26) − 1.25 (− 1.59–(− 0.88)) − 0.00 (− 0.04–0.03)) 1.23 (0.63–1.83) − 0.73 (− 0.30)
0.09 0.45
0.08 (0.00–0,16) 0.04 (−0.05–0.13) − 0.24 (− 0.74–0.25) 0.01 (−0.14 - 0.15) − 0.05 (− 0.14–0.04) 1.24 (0.57–1.70) − 0.16 (− 0.34–0.00) 0.05 (0.00–0.10) 0.03 (−0.04–0.10) 0.24 (−0.18–0.66) − 0.68 (−1.04–(− 0.34)) 0.09 (0.06–0.12) 0.02 (−0.07–0.12) 0.51 (−0.23–1.25) − 1.19 (−1.79–(− 0.60)) − 0.02 ((−0.14–0.10) 1.01 (0.34–1.68) − 0.72 (−1.16–(− 0.28)) − 0.03 (− 0.10–0.04) 1.68 (0.94–2.49) − 0.33 (−0.58–(− 0.09)) − 0.06 (− 0.16–0.04) 1.53 (1.03–2.03) − 0.16 (− 0.27/ (−0.01)) − 0.08 (− 0.17–0.00) 1.3 (0.89–1.71) − 0.07 (− 0.14–0.01) 2.0 3.33 (2.64–4.02)
The LIFE child study is funded by means of the European Union, by the European Regional Development Fund (ERDF) and by means of the Free State of Saxony within the framework of the excellence initiative, the German Research Foundation (DFG) for the Clinical Research Center “Obesity Mechanisms” CRC1052/1 C05, and the federal ministry of education (BMBF). Financial Disclosure The authors have no financial relationships relevant to this article to disclose. Conflicts of Interest The authors have no conflicts of interest relevant to this article to disclose.
0.16 0.07 0.02 0.01 0.96 0.17 0.14 0.16 0.99 0.99 0.63
Author Statements The manuscript submitted is original, with no portion under simultaneous consideration for publication elsewhere or previously published, except for an abstract of fewer than 400 words. Only those who have made an important contribution to the study and are thoroughly familiar with the primary data are included as authors. All authors are responsible for the contents and have read and approved the manuscript for submission.
0.62 0.96 0.10 0.70
References
0.48 0.27 0.97
0.04 (− 0.10–0.03) 1.62 (1.10–2.14) − 0.40 (− 0.68–(− 0.12)) − 0.66 (− 0.08–(− 0.59)) 1.57 (1.18–1.95) − 0.19 (− 0.38–0.01)
0.71 0.77 0.42
− 0.00 (− 0.39–0.38) 1.12 (0.56–1.78) − 0.09 (− 0.22–0.04) 1.92 (1.64–2.20) 3.28 (2.60–3.96)
0.39 0.43 0.50 0.23 0.80
[1] Flechtner-Mors M, Thamm M, Wiegand S, et al. Comorbidities related to BMI category in children and adolescents: German/Austrian/Swiss obesity register APV compared to the German KiGGS Study. Horm Res Paediatr 2012;77(1):19–26. [2] Flechtner-Mors M, Thamm M, Rosario AS, et al. Hypertonie, Dyslipoproteinämie und BMI-Kategorie charakterisieren das kardiovaskuläre Risiko bei übergewichtigen oder adipösen Kindern und Jugendlichen: Daten der BZgA-Beobachtungsstudie (EvAKuJ-Projekt) und der KiGGS-Studie. Klin Padiatr 2011;223(07):445–9. [3] Mangner N, Scheuermann K, Winzer E, Wagner I, Hoellriegel R, Sandri M, et al. Childhood obesity: impact on cardiac geometry and function. JACC Cardiovasc Imaging 2014;7(12):1198–205. [4] Alpert MA, Terry BE, Cohen MV, Fan TM, Painter JA, Massey CV. The electrocardiogram in morbid obesity. Am J Cardiol 2000;85(7):908–10. [5] Poulain T, Baber R, Vogel M, Pietzner D, Kirsten T, Jurukat A, et al. LIFE Child study team. The LIFE child study: a population-based perinatal and pediatric cohort in Germany. Eur J Epidemiol 2017;32(2):145–58. [6] Kromeyer-Hauschild K, Wabitsch M, Kunze D. Monatsschr Kinderheilkd 2001;149:807–18. [7] Rijnbeek PR, Witsenburg M, Schrama E, Hess J, Kors JA. New normal limits for the paediatric electrocardiogram. Eur Heart J 2001;22:702–11. [8] Davignon A. Normal ECG standards for infants and children. Pediatr Cardiol 1979/ 80;1:133–52. [9] Fraley MA, Birchem JA, Senkottaiyan N, Alpert MA. Obesity and the electrocardiogram. Obes Rev 2005;6(4):275–81. [10] Seyfeli E, Duru M, Kuvandık G, Kaya H, Yalcin F. Effect of obesity on P-wave dispersion and QT dispersion in women. Int J Obes Relat Metab Disord 2006;30(6):957–61. [11] Sympathovagal balance, nighttime blood pressure, and QT intervals in normotensive obese women. April 2003. p. 1–7. [13] Blüher S, Petroff D, Keller A, Wagner A, Classen J, Baum P. Effect of a 1-year obestiy intervention (KLAKS Program) on preexisting autonomic nervous dysfunction in childhood obesity. J Child Neurol 2015;30(9):1174–81. [14] Wildman RP, McGinn AP, Lin J, et al. Cardiovascular disease risk of abdominal obesity vs. metabolic abnormalities. Obesity 2009;19(4):853–60.
0.77 0.80 0.53
the case that pathologic ECG features are recorded in an obese child. 6. Limitations The current study does not include an analysis of participants autonomic state by for example heart rate variability in holter ECG. The sample size is relatively small with only few young children below the age of 8 years, which might have an impact on the findings but at least have an impact on statistical analysis. Nevertheless, the inclusion of an age-matched lean control group is an advantage of this study. Acknowledgements Special thanks to Mrs. Bettina Müller for linguistic support.
5
Contents lists available at ScienceDirect
Progress in Pediatric Cardiology journal homepage: www.elsevier.com/locate/ppedcard
New normal limits for pediatric ECG in childhood obesity? Influence of childhood obesity on the ECG ⁎
C. Paecha, , M. Anhalta, R.A. Gebauera, F. Wagnera, M. Vogelb, T. Kirstenc, M. Weidenbacha, W. Kiessb, I. Dähnerta, A. Körnerb a
Department for Pediatric Cardiology, University of Leipzig - Heart Center, Strümpellstr. 39, 04289 Leipzig, Germany Hospital for Children and Adolescents, Center for Pediatric Research, University of Leipzig, Philipp-Rosenthal-Straße 27, 04103 Leipzig, Germany c LIFE Research Center for Civilization Diseases, University of Leipzig, Philipp-Rosenthal-Straße 27, 04103 Leipzig, Germany b
A R T I C L E I N F O
A B S T R A C T
Keywords: ECG Obesity Children Reference value
Introduction: Studies demonstrated abnormal ECG phenomena in adult obese patients. Although some of these phenomena are clearly pathologic, for others the clinical relevance is less clear. In children this conflict is even harder to address as there are only scarce specific reference data on ECG in childhood obesity. The aim of this study was to investigate the influence of childhood obesity on distinct ECG parameters of cardiac activation and repolarization in a cohort of otherwise healthy obese volunteers and compare these with lean controls. Methods: We prospectively enrolled 53 otherwise healthy obese children (BMI (mean/SD) 2.35 (1.39–3.56)) and 43 lean controls (BMI (mean/SD) − 0.243 (−2.02–1.25)) from the LIFE Child Study. All probands underwent a thorough cardiac evaluation including a 12‑lead ECG. Results: Obese children showed a more left sided QRS axis (p < 0.01). This effect was independent from age (p = 0.28) or sex (p = 0.3). Otherwise there were no major differences between the groups. Most importantly, there were no pathologic phenomena recorded in otherwise healthy, obese children. Conclusion: In healthy children, obesity does not result in pathologic ECG phenomena. Therefore pathology has only to be suspected in case of clearly abnormal ECG findings even in severely obese children.
1. Introduction With the increasing prevalence of childhood obesity a number of comorbidities, especially cardiovascular complications ensue. The well described association with elevated blood pressure and structural cardiac alterations is relevant in the obese child with hypertension [1–3]. Whether these are accompanied by alterations in the ECG, and whether these are of clinical relevance for cardiovascular risk stratification for example in the ECG evaluation prior to a scheduled medical or surgical therapy is less clear. It is well known from adult studies that there are various ECG changes that are associated with obesity. These include left axis deviation, signs of left ventricular hypertrophy, bradycardia and alterations of cardiac repolarization like ST–segment depression, T-wave inversion, increased electrical inhomogeneity and QT interval prolongation [4]. In children there are only scarce data. Some studies imply there are abnormalities in the ECG of obese children related to their obesity alone [3,5]. As these ECG findings are particularly evident
⁎
in severely obese patients they are challenging for the pediatric cardiologist in the judgement of whether a distinct ECG alteration represents a variation of the normal or an underlying pathologic medical condition. Hitherto data imply that there are some changes associated with pathologic conditions like left ventricular hypertrophy in arterial hypertension and others lack evidence of pathology despite being atypical like left axis deviation or relative QTc interval prolongation [4]. The aim of this study was to investigate the influence of childhood obesity on distinct ECG parameters of cardiac activation and repolarization in a cohort of otherwise healthy obese volunteers and compare these with lean controls. 2. Methods 2.1. Study Sample A total of 96 consecutive healthy, Caucasian pediatric volunteers at the age of 6 to 18 years, who participated in the LIFE Child Study at the
Corresponding author. E-mail address: [email protected] (C. Paech).
https://doi.org/10.1016/j.ppedcard.2017.11.002 Received 7 May 2017; Received in revised form 1 November 2017; Accepted 27 November 2017 1058-9813/ © 2017 Elsevier B.V. All rights reserved.
Please cite this article as: Paech, C., Progress in Pediatric Cardiology (2017), https://doi.org/10.1016/j.ppedcard.2017.11.002
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
LIFE Leipzig Research Center for Civilization Diseases from 2011 to 2014 were prospectively enrolled in the study [5]. All probands underwent a thorough cardiac evaluation including past medical history, physical examination, anthropometric evaluation, 12 lead ECG and echocardiography. Written informed consent of the parents was obtained. The study was approved by the ethics committee of the University of Leipzig (reg. no: 264-10-19042010) and is registered NCT02550236. Exclusion criteria were gross pathology, electrolyte disturbances, arterial hypertension or structural heart disease and marked ventricular hypertrophy but none of these was present in any patient. All anthropometric parameters were adjusted for age and sex based on national reference values of German children from KromeyerHauschild et al. [6] and accordingly are given in standard deviation score (SDS). Probands were stratified into overweight/obese and lean children applying an adjusted BMI 1.28/1.88 SDS as cut off according to current German guidelines [6].
Table 1 Patient characteristics. Lean (mean ± SEM)
Obese (mean ± SEM)
N Age (years) Sex (m/f) Height (cm) Height SDS Weight (kg)
43 11.34 (7.33–17.71) Male 31/female 12 148.5 (122.5–179.6) 0.07 (− 1.57–2.48) 37.00 (19.90–71.70)
BMI BMI SDS
17.47 (13.26–23.75) − 0.24 (− 2.02–1.25) 74.20 (56.6–101) − 0.27 (− 2.57–1.18) 60.00 (48.80–74.50)
53 11.48 (6.54–16.49) Male 37/female 16 154.9 (126.1–185.1) 0.94 (− 1.00–2.96) 65.80 (33.50–135.50) 26.89 (20.11–40.59) 2.35 (1.39–3.56)
Hip circumference (cm) Hip circumference adj. Waist circumference (cm) Waist circumference adj. Syst. BP (mm Hg)
2.2. ECG Analysis For each child, a 12‑lead ECG was recorded using an electrocardiograph (General Electrics, MAC 5000). The frequency response of this recorder is flat to 150 Hz. A paper speed of 50 mm/s and an amplitude of 10 mm/mV was used. The ECGs were recorded by the same technician throughout the study. All ECGs were anonymized by pseudonymization and analyzed blinded by two independent physicians with extensive experience in the analysis of pediatric ECGs.
Diast. BP. (mm Hg)
− 0.36 (− 2.28–1.13) 105.00 (86.67–125.33) 65.67 (54.33–77.67)
p value
0.284 0.55 0.084 < 0.01 < 0.01 < 0.01 < 0.01
97.70 (70.2–138) 1.75 (0.41–2.65)
< 0.01 < 0.01
84.80 (63.00–107.50) 1.66 (0.93–2.33)
< 0.01
111.30 (93.00–132.67) 69 (51.67–80.00)
< 0.01
< 0.01
0.07
SDS = standard deviation score; adj. = adjusted; BP = blood pressure. Table 2a Influence of obesity on ECG parameters (all ages) timing intervals.
2.3. Statistics ECG HR QRS axis P axis ECG lead II
Statistical analysis was carried out with SPSS 21.0 software. Continuous data were assessed for normality and the Student's t-test was used for normally distributed data. To characterize the influence between continuous variables bivariate correlation was used and Pearsons correlation coefficient (r) is reported. For this study, α was set at 0.05; thus p-values < 0.05 (two-sided) were required for statistical significance. The entire study cohort was analyzed as a single cohort. In addition, analyses were performed after subdivision of patients into three age groups as previously suggested by Davignon et al. and Rijnbeek et al., that are acknowledged to represent key studies in defining the limits of normal in pediatric ECG [7,8].
P PQ QRS QT
ECG lead V5
P PQ QRS QT
Lean (n = 43) (mean ± SEM)
Obese (n = 53) (mean ± SEM)
p value
75.72 (63.46–87.98) 78.37 (58.29–98.45) 48.49 (20.19–76.77) 71.86 (58.54–85.18) 130.93 (110.02–151.84) 78.84 (64.01–93.67) 355.58 (327.19–383.97) 68.84 (50.43–87.25) 127.44 (104.96–149.92) 78.84 (66.65–91.03) 352.56 (326.28–378.82)
75.58 (62.31–80.85) 61.60 (40.23–82.97) 40.28 (16.49–64.07) 77.36 (62.93–91.79) 128.87 (112.04–145.7)
0.96 < 0.01 0.13 0.06 0.59
81.13 (67.03–95.23) 352.26 (329.59–374.93) 70.00 (52.70–87.10) 124.04 (106.08–142.00) 83.96 (73.16–94.76) 355.28 (330.90–379.67)
0.44 0.53 0.75 0.41 0.32 0.60
SR = sinus rhythm; HR = heart rate.
3. Results Table 2b Influence of obesity on ECG parameters (6–8 years) timing intervals.
3.1. Patients Characteristics Table 1 shows the patients basic characteristics of the stratified groups lean and overweight/obese including anthropometric measurements. Obese children did not differ from lean children with respect to age and sex distribution, but expectedly had higher BMI SDS and were taller. The systolic blood pressure was higher in obese compared to lean children, although still within normal limits. All study participants showed serum electrolyte levels within age and sex appropriate limits at the time the ECG was performed. Each had a normal echocardiography and a negative family history.
HR QRS axis P axis ECG lead II
ECG lead V5
3.2. Basic ECG Characteristics The basic ECG characteristics and timing intervals are summarized in Tables 2a–2d. Heart rate was not elevated in obese children, hence making autonomic activation unlikely. The QRS axis was slightly but significantly shifted to the left side in the obese children, whereas the Paxis remained indifferent (Table 2a). This effect was particularly apparent in the younger children aged 8–12 years as opposed to the group of adolescents (Tables 2c, 2d). Data showed a highly significant
P PQ QRS QT P PQ QRS QT
Lean (n = 1) (mean ± SEM)
Obese (n = 6) (mean ± SEM)
p value
101 (101) 90 (90) 30 (30) 80 (80) 130 (130) 90 (90) 320 (320) 70 (70) 130 (130) 80 (80) 320 (320)
81.67 (66.50–96,88) 65 (49.83–80.17) 41.67 (13.09–70.25) 75 (64.51–85.49) 118.33 (103.61–133.05) 85 (68.47–101.43) 320 (301.02–338.97) 66.67 (58.51–74.84) 115 (104.51–125.49) 81.67 (77.59–85.75) 328.33 (311.11–345.55)
0.29 0.19 0.72 0.68 0.50 0.79 1.00 0.72 0.24 0.72 0.67
SR = sinus rhythm; HR = heart rate.
correlation between the QRS axis and the waist to hip ratio (r = − 0.35/p = 0.001) with more left sided QRS axis for higher values of waist to hip ratio. Regarding time intervals, we did not see significant differences between obese and lean children when looking at all
2
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
Table 2c Influence of obesity on ECG parameters (8–12 years) timing intervals.
HR QRS axis P axis ECG lead II
Table 3a Influence of obesity on ECG parameters (all ages): amplitudes.
Lean (n = 24) (mean ± SEM)
Obese (n = 22) (mean ± SEM)
p value
78.75 (66.68–90.82) 85.42 (75.76–95.08) 51.88 (31.73–72.03) 70.83 (54.70–86.96) 130.42 (111.66–149.18) 76.25 (62.17–90.33) 347.92 (318.14–377.70) 66.25 (45.02–87.48) 124.58 (105.35–143.23) 76.67 (64.99–88.34) 347.92 (319.18–367.6)
76.27 (66.23–86.30) 62.95 (0.18–85.71) 41.14 (14.33–67.95) 73.18 (59.59–86.77) 129.55 (112.24–146.86) 78.64 (64.07–93.12) 353.18 (32.85–373.51)
0.46 < 0.01 0.13 0.60 0.87
68.18 (55.59–80.77) 125.91 (110.28–141.54) 82.73 (70.32–95.14) 356.36 (331.19–381.54)
0.71 0.80
ECG lead I
Q
ECG lead AVR
R S P Q R S Q R S Q R
SR = sinus rhythm; HR = heart rate.
ECG lead AVL
S Q R
Table 2d Influence of obesity on ECG parameters (12–18 years) timing intervals.
ACG lead AVF
P PQ QRS QT
ECG lead V5
P PQ QRS QT
HR QRS axis P axis ECG lead II
P PQ QRS QT
ECG lead V5
P PQ QRS QT
ECG lead II
0.58 0.49 ECG lead III
0.09 0.30
Lean (n = 18) (mean ± SEM)
Obese (n = 25) (mean ± SEM)
p value
70.28 (42.12–94.50) 68.3 (42.12–94.5) 45 (7.86–82.14) 72.78 (63.83–81.73) 131.67 (107.12–156.23) 81.67 (65.86–97.48) 367.78 (345.94–389.62) 72.22 (57.85–86.59) 131.11 (103.69–158.53) 81.67 (68.73–95.62) 360.56 (339.85–381.27)
73.52 (58.32–88.72) 59.6 (37.71–81.49) 39.20 (18.60–59.79) 81.60 (66.41–96.79) 130.80 (114.24–147.36) 82.4 (69.08–95.72) 359.20 (33.97–378.33)
0.43 0.24 0.52 0.33 0.89
72.40 (50.74–94.06) 124.58 (103.52–145.64) 85.6 (75.16–96.04) 360.8 (339.41–382.19)
0.98 0.39
ECG lead V1
0.87 0.18
0.28 0.97
SR = sinus rhythm; HR = heart rate.
S Q R S P Q R S
ECG lead V2
Q R S
ECG lead V3
Q R S
ECG lead V4
Q R S
ECG lead V5
Q R S
participants (Table 2a). ECG lead V6
3.3. Amplitudes
Q R S
ECG U wave ECG R/S
The measurements of amplitudes are summarized in Tables 3a–3d. Data show nearly no differences in the bipolar or unipolar limb leads. Concordant with the QRS type, there were significant differences in the Q and R wave amplitudes in left sided leads (I and aVL) with greater amplitudes in the obese participants when looking at the entire group (Table 3a). Again this effect is most evident in the group of younger children aged 8–12 years but could also be demonstrated in the group of adolescents (Tables 3c, 3d). In addition slightly more negative S waves could be demonstrated in lean compared to obese participants in leads V2 and V3 (p = 0.02) in the entire group (Table 3a). The effect could not be demonstrated in the adolescents (Table 3d). Despite differences in S wave negativity there was no statistically significant difference in R/S progression between lean and obese children, neither in the entire group (p = 0.14) nor in young children (p = 0.21) or adolescents (p = 0.8).
Lean (n = 43) (mean ± SEM)
Obese (n = 53) (mean ± SEM)
p value
− 0.05 (− 0.08 to − 0.02) 0.36 (0.08–0.63) − 0.12 (− 0.27–0.03) 0.12 (0.03–0.21) − 0.07 (− 0.01–0.01) 1.43 (0.90–1.97) − 0.15 (− 0.30–0.01) − 0.10 (− 0.21–0.00) 1.20 (0.64–1.75) − 0.1 (−0.04–0.04) 0.03 (− 0.01–0.07) − 0.78 (− 1.18 to − 0.39) 0.09 (− 0,09–0.27) 0.06 (− 0.02–0.15) − 0.43 (− 0.90–(− 0.01)) 0.01 (− 0.12–0.14) − 0.07 (− 0.18–0.02) 1.32 (0.82–1.82) − 0.13 (− 0.28–0.27) 0.07 (0.02–0.12) 0.03 (− 0.05–0.12) 0.27 (− 0.24–0.78) − 0.73 (− 1.21–(− 0.25)) 0.01 (− 0.05–0.07) 0.80 (0.18–1.43) − 1.61 (− 2.27–(− 0.95)) − 0.01 (− 0.09–0.07) 1.21 (0.44–1.98) − 1.06 (− 1.64–(− 0.48)) − 0.05 (− 0.13–0.03) 1.94 (1.30–2.58) − 0.49 (− 0.84–(− 0.13) − 0.11 (− 0.22–(− 0.01)) 1.85 (1.12–2.58) − 0.17 (− 0.33–(− 0.01)) − 0.13 (− 0.23–(− 0.04)) 1.35 (0.95–1.75) − 0.06 (− 0.15–0.02) 1.81 (1.42–2.20)
−0.32 (− 0.27–(−0.08))
< 0.01
0.79 (0.30–1.27) −0.20 (− 1.92–(−0.03)) 0.12 (0.07–0.17) −0.07 (−0.16–0.03) 1.41 (0.95–1.86) −0.13 (−0.26–0.00) −0.09 (−0.26–0.07) 0.84 (0.20–1.48) −0.04 (−0.23–0.10) 0.04 (− 0.01–0.09) −0.93 (− 1.43–(−0.42))
< 0.01 0.19 0.10 0.99 0.78 0.58 0.68 0.04 0.60 0.14 0.14
0.13 (0.01–0.25) 0.02 (− 0.12–0.15) 0.08 (− 0.41–0.56)
0.17 0.04 < 0.01
−0.20 (−0.45–0.05) −0.06 (−0.17–0.04) 1.05 (0.52–1.58) −0.10 (−0.22–0.027) 0.07 (0.03–0.06) 0.023 (− 0.06–0.10) 0.28 (− 0.13–0.69) −0.73 (− 1.20−(− 0.25)) 0.01 (− 0.07–0.10) 0.84 (0.31–1.37) −1.30 (− 1.85–(−0.75))
< 0.01 0.53 0.01 0.31 0.67 0.61 0.88 0.98
0.00 (− 0.03–0.02) 1.27 (0.73–1.82) −0.79 (− 1.27–(−0.30))
0.59 0.64 0.02
−0.03 (−0.10–0.03) 1.81 (1.21–2.41) −0.42 (− 0.74–(−0.10))
0.39 0.31 0.31
0.09 (− 0.17–0.00)
0.24
1.70 (1.22–2.18) −0.18 (−0.36–0.00)
0.24 0.75
−0.06 (−0.33–0.21)
0.10
1.31 (0.79–1.84) −0.08 (−0.20–0.03) 1.87 (1.53–2.21)
0.74 0.37 0.47
3.23 (2.59–3.87)
0.14
3.42 (2.79–4.05)
0.81 0.78 0.02
there were no major differences in the ECG parameters and most important there were no pathologic phenomena recorded in otherwise healthy, obese children. 4. Discussion Obese patients have an increased risk for various comorbidities, particularly cardiovascular complications. Studies in adults have reported that there are several ECG phenomena associated with obesity, but there is only scarce data in children. The aim of this study was to investigate the influence of childhood obesity on various ECG parameters in a cohort of otherwise healthy individuals. The main conclusion drawn from the data of the current study is that childhood obesity has no clinically relevant effect on ECG parameters in children, even though we did see a slight, yet non-pathologic, left shift of the QRS axis. These findings are in contrast to the findings in the adult population that included clinically insignificant findings like left axis deviation and
3.4. Main Results We found a slight left-sided shift in QRS axis and increased amplitudes of the left sided leads in obese children, although all measured parameters remained within normal limits for age and sex. Otherwise, 3
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
Table 3b Influence of obesity on ECG parameters (6–8 years) amplitudes.
ECG lead I
ECG lead II
ECG lead III
ECG lead AVR
ECG lead AVL
ACG lead AVF
ECG lead V1
ECG lead V2
ECG lead V3
ECG lead V4
ECG lead V5
ECG lead V6
ECG U wave ECG R/S
Q R S P Q R S Q R S Q R S Q R S Q R S P Q R S Q R S Q R S Q R S Q R S Q R S
Table 3c Influence of obesity on ECG parameters (8–12 years) amplitudes.
Lean (n = 1) (mean ± SEM)
Obese (n = 6) (mean ± SEM)
p value
0 0.7 −0.4 0.15 −0.1 2.15 0 −0.25 2.15 0 0 −1.2 0 0.25 −1.2 0 −1 2.1 0 −1 0 0.6 −1.5 0 1.35 −2.6 0 1.6 −0.5 0 2.3 −0.15 −0.15 2.2 0 −0.2 1.9 0 1 3
− 0.03 (− 0.07–0.01) 0.81 (0.53–1.09) − 0.25 (− 0.49–(−0.01) 0.1 (0.03–0.17) − 0.12 (− 0.22–(−0.02) 1.76 (1.55–1.97) − 0.09 (− 0.32–0.13) 0.23 (− 0.34–(− 0.13)) 1.23 (1.00–1.45) − 0.04 (− 0.13–0.05) 0.08 (0.03–0.12) − 1.2 (−1.50–(− 0.89)) 0.12 (− 0.11–0.35) 0.12 (− 0.12–0.35) 0.25 (− 0.30–0.70) − 0.3 (−0.66–0.06) − 0.15 (− 0.24–(−0.06)) 1.47 (1.35–1.59) − 0.07 (− 0.23–0.10) 0.08 (0.06–0.11) 0 0.55 (0.2–0.91) − 1.06 (− 1.87–(−0.25)) 0 1.2 (0.77–1.63) − 1.58 (− 0.41–(−1.17)) − 0.01 (− 0.03–0.01) 1.55 (1.03–3.07) − 0.7(− 1.08–(− 0.32)) − 0.09 (− 0.18–(−0.01)) 2.14 (1.68–2.57) − 0.32 (− 0.59–(−0.04)) 0.18 (− 0.26–(− 0.09)) 1.9 (1.63–2.17) − 0.11 (− 0.18–(−0.03)) −(0.18 (− 0.26–(−0.11)) 1.53 (1.45–1.60) − 0.07 (− 0.3–0.10) 2 2.83 (2.422–3.24)
0.48 0.73 0.59 0.54 0.88 0.15 0.72 0.89 0.01 0.70 0.16 1.0 0.53 0.62 0.05 0.48 0.63 0.01 0.72 < 0.01
ECG lead I
Q R S
ECG lead II
ECG lead III
R S Q
ECG lead AVR
R S Q R
ECG lead AVL
0.90 0.63
ACG lead AVF
0.76 0.07 0.72 0.93 0.65 0.37 0.76 0.60 0.80 0.36 0.52 0.85 < 0.01 0.72
ECG lead V1
S Q R S Q R S P Q R S
ECG lead V2
P Q R S
ECG lead V3
Q R S
ECG lead V4
Q R S
ECG lead V5
Q
0.72
major pathology like signs of left ventricular hypertrophy, bradycardia and alterations of cardiac repolarization like ST – segment depression or T-wave inversion [9,10]. There are several hypotheses concerning possible influencing factors of obesity on ECG parameters. Beside easy determinable factors like arterial hypertension or left ventricular hypertrophy, mainly hormonal and autonomic nervous system influences are reported [11–13]. In addition it is well known that electrolyte disturbances may influence the ECG tracing [14]. It also needs to be considered that adults have a longer exposure time to obesity (and potentially related arterial hypertension) that eventually result in morphological and electrical cardiac alterations, which are not yet identifiable in children. This study included only healthy participants as confirmed by an intensive cardiac work up including echocardiography and laboratory findings. This excluded patients with arterial hypertension, left ventricular hypertrophy or electrolyte imbalances and may be a main reason for the almost normal ECG findings present in our cohort. Also, heart rate was similar in both groups hence not pointing to an autonomic nervous system effect. Nevertheless the presented data show at least some minor differences between lean and obese participants. The slightly more left sided axis may be simply due to anatomical differences like increased abdominal fat deposits, as substantially differing waist and hip circumferences between the groups imply a significantly increased abdominal fat in the obese participants. However, it needs to be considered that in children an increased waist-to-hip ratio not
P Q
R S ECG lead V6
Q R S
ECG U wave ECG R/S
Lean (n = 24) (mean ± SEM)
Obese (n = 22) (mean ± SEM)
p value
− 0.08 (− 0.11–(− 0.05)) 0.30 (0.06–0.54) − 0.15 (− 0.31–0.00)
−0.02 (−0.07–0.03)
0.22
0.88 (0.19–1.57) −0.22 (− 0.37–(−0.08) 0.12 (0.08–0.55) −0.08 (−0.20–0.04)
< 0.01 0.12 0.91 0.85
1.47 (0.98–1.96) −0.14 (−0.27–(0.01)) −0.11 (−0.30–0.08)
0.73 0.80 0.69
0.89 (0.09–1.69) −0.05 (−0.31–0.07) 0.03 (− 0.01–0.06) −0.94 (− 1.48–(−0.40)) 0.14 (0.03–0.26) 0.03 (− 0.10–0.15) 0.08 (− 0.54–0.70) −0.21 (−0.46–0.04) −0.05 (−0.18–0.22) 1.06 (0.38–1.74) −0.10 (−0.25–0.04) 0.68 (0.02–0.11) 0.023 (− 0.07–0.12) 0.26 (− 0.20–0.72) −0.75 (− 1.18–(−0.32)) 0.08 (0.05–0.11) 0.005 (− 0.02–0.03) 0.75 (0.14–1.37) −1.29 (− 2.02–(−0.55)) 0.00 (− 0.01–0.01) 1.24 (0.75–1.73) −0.88 (− 1.45–(−0.31)) −0.02 (−0.08–0.05) 1.93 (1.26–2.61) −0.47 (− 0.84–(−0.10)) 0.09 (− 0.17–(−0.01))
0.22 0.44 0.48 0.31
1.80 (1.24–2.47) −0.19 (− 0.37–(−0.02)) −0.10 (− 0.18–(−0.02)) 1.42 (0.97–1.88) −0.08 (−0.16–0.00) 1.77 (1.43–2.20) 3.27 (2.64–3.90)
0.21 0.95
0.12 (0.05–0.19) − 0.09 (− 0.17–(− 0.01)) 1.52 (1.92–1.12) − 0.15 (− 0.32–0.01) − 0.13 (− 0.23–(− 0.02) 1.32 (0.94–1.70) − 0.08 (− 0.21–0.04) 0.04 (− 0.01–0.08) − 0.81 (− 1.15–(− 0.46)) 0.1 (− 0.13–0.33) 0.08 (0.01–0.14) − 0.53 (− 0.8–(− 0.25)) 0.01 (− 0.11–0.13) 0.09 (− 0.20–0.01) 1.43 (1.04–1.81) − 0.10 (− 0.23–0.03) 0.09 (0.05–0.22) 0.04 (− 0.07–0.14) 0.28 (− 0.31–0.86) − 0.73 (− 0.13–(− 0.18)) 0.08 (0.05–0.11) 0 0.99 (0.55–1.43) − 1.88 (− 2.41–(− 1.35)) 0.00 (− 0.02–0.03) 1.34 (0.50–2.18) − 1.33 (− 1.87–(− 0.79)) − 0.06 (− 0.15–0.02) 2.12 (1.61–2.62) − 0.62 (− 1.00–(− 0.24)) − 0.15 (− 0.25–(− 0.05)) 2.07 (1.26–2.88) − 0.19 (− 0.36–(− 0.02)) − 0.17 (0.26–(− 0.08)) 1.36 (0.97–1.75) − 0.06 (− 0.57–0.03) 1.71 (1.25–2.17) 3.5 (2.91–4.09)
0.43 0.10 < 0.01 < 0.01 0.22 0.29 0.96 0.11 0.66 0.92 0.90 0.96 0.31 0.13 < 0.01 0.97 0.64 0.01 0.04 0.30 0.18 0.03
0.01 0.61 0.58 0.63 0.21
necessarily means intraabdominal fat accumulation as also subcutaneous fat is centered to the mid of the body. As younger children naturally tend to have rather right sided QRS axis this effect is more evident in younger children than in the adolescents. The differences in S waves in the precordial leads V2 and V3 seem to be of no clinical importance as the R/S progression was not different between the groups, implying balanced right and left ventricular forces.
5. Conclusion In healthy children, obesity does not result in pathologic ECG phenomena. Therefore pathology has to be suspected in case of abnormal ECG findings even in severely obese children. The results of this study emphasize the importance of a thorough cardiologic work up in 4
Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx
C. Paech et al.
Funding Source
Table 3d Influence of obesity on ECG parameters (12–18 years) amplitudes.
ECG lead I
ECG lead II
ECG lead II
ECG lead AVR
ECG lead AVL ACG lead AVF ECG lead V1
Q R S P Q R S Q R S Q R S Q R S Q R S P Q R S
ECG lead V2
P Q R S
ECG lead V3
Q R S
ECG lead V4
Q R S
ECG lead V5
Q R S
ECG lead V6
Q R S
ECG U wave ECG R/S
Lean (n = 18) (mean ± SEM)
Obese (n = 25) (mean ± SEM)
p value
0 (− 0.03–0.03) 0.04 (0.10–0.72) − 0.06 (− 0.19–0.06) 0.12 (0.11–0.22) − 0.04 (− 0.82–0.04) 1.28 (0.63–1.93) − 0.14 (− 0.29–0.00) − 0.01 (− 0.16–0.03) 0.98 (0.32–1.64) − 0.1306 (−0.301–0.04) 0.02 (−0.02–0.05) − 0.73 (–1.20–(− 0.27))
− 0.04 (− 0.09–0.01) 0.71 (0.45–0.97) − 0.17 (− 0.35–0.01) 0.12 (0.08–0.16) − 0.05 (− 0.11–0.02) 1.26 (0.85–1.68) − 0.13 (0.24–(− 0.01)) − 0.04 (− 0.18–0.09) 0.70 (0.19–1.20) − 0.04 (− 0.21–0.13)
0.01 < 0.01 0.03 0.82 0.84 0.91 0.68 0.54 0.12 0.08
0.05 (0.02–0.11) − 0.85 (− 1.35–(− 0.34)) 0.13 (0.01–0.24) − 0.01 (− 0.11–0.08) 0.09 (− 0.29–0.46) − 0.16 (− 0.39–0.07) − 0.05 (− 0.12–0.02) 0.94 (0.57–1.31) − 0.1 (−0.20–(− 0.01)) 0.07 (0.02–0.12) 0.03 (− 0.05–0.10) 0.24 (− 0.13–0.61) − 0.63 (− 1.02–(− 0.24) 0.09 (0.06–0.13) 0.02 (− 0.10–0.14) 0.82 (0.37–1.26) − 1.25 (− 1.59–(− 0.88)) − 0.00 (− 0.04–0.03)) 1.23 (0.63–1.83) − 0.73 (− 0.30)
0.09 0.45
0.08 (0.00–0,16) 0.04 (−0.05–0.13) − 0.24 (− 0.74–0.25) 0.01 (−0.14 - 0.15) − 0.05 (− 0.14–0.04) 1.24 (0.57–1.70) − 0.16 (− 0.34–0.00) 0.05 (0.00–0.10) 0.03 (−0.04–0.10) 0.24 (−0.18–0.66) − 0.68 (−1.04–(− 0.34)) 0.09 (0.06–0.12) 0.02 (−0.07–0.12) 0.51 (−0.23–1.25) − 1.19 (−1.79–(− 0.60)) − 0.02 ((−0.14–0.10) 1.01 (0.34–1.68) − 0.72 (−1.16–(− 0.28)) − 0.03 (− 0.10–0.04) 1.68 (0.94–2.49) − 0.33 (−0.58–(− 0.09)) − 0.06 (− 0.16–0.04) 1.53 (1.03–2.03) − 0.16 (− 0.27/ (−0.01)) − 0.08 (− 0.17–0.00) 1.3 (0.89–1.71) − 0.07 (− 0.14–0.01) 2.0 3.33 (2.64–4.02)
The LIFE child study is funded by means of the European Union, by the European Regional Development Fund (ERDF) and by means of the Free State of Saxony within the framework of the excellence initiative, the German Research Foundation (DFG) for the Clinical Research Center “Obesity Mechanisms” CRC1052/1 C05, and the federal ministry of education (BMBF). Financial Disclosure The authors have no financial relationships relevant to this article to disclose. Conflicts of Interest The authors have no conflicts of interest relevant to this article to disclose.
0.16 0.07 0.02 0.01 0.96 0.17 0.14 0.16 0.99 0.99 0.63
Author Statements The manuscript submitted is original, with no portion under simultaneous consideration for publication elsewhere or previously published, except for an abstract of fewer than 400 words. Only those who have made an important contribution to the study and are thoroughly familiar with the primary data are included as authors. All authors are responsible for the contents and have read and approved the manuscript for submission.
0.62 0.96 0.10 0.70
References
0.48 0.27 0.97
0.04 (− 0.10–0.03) 1.62 (1.10–2.14) − 0.40 (− 0.68–(− 0.12)) − 0.66 (− 0.08–(− 0.59)) 1.57 (1.18–1.95) − 0.19 (− 0.38–0.01)
0.71 0.77 0.42
− 0.00 (− 0.39–0.38) 1.12 (0.56–1.78) − 0.09 (− 0.22–0.04) 1.92 (1.64–2.20) 3.28 (2.60–3.96)
0.39 0.43 0.50 0.23 0.80
[1] Flechtner-Mors M, Thamm M, Wiegand S, et al. Comorbidities related to BMI category in children and adolescents: German/Austrian/Swiss obesity register APV compared to the German KiGGS Study. Horm Res Paediatr 2012;77(1):19–26. [2] Flechtner-Mors M, Thamm M, Rosario AS, et al. Hypertonie, Dyslipoproteinämie und BMI-Kategorie charakterisieren das kardiovaskuläre Risiko bei übergewichtigen oder adipösen Kindern und Jugendlichen: Daten der BZgA-Beobachtungsstudie (EvAKuJ-Projekt) und der KiGGS-Studie. Klin Padiatr 2011;223(07):445–9. [3] Mangner N, Scheuermann K, Winzer E, Wagner I, Hoellriegel R, Sandri M, et al. Childhood obesity: impact on cardiac geometry and function. JACC Cardiovasc Imaging 2014;7(12):1198–205. [4] Alpert MA, Terry BE, Cohen MV, Fan TM, Painter JA, Massey CV. The electrocardiogram in morbid obesity. Am J Cardiol 2000;85(7):908–10. [5] Poulain T, Baber R, Vogel M, Pietzner D, Kirsten T, Jurukat A, et al. LIFE Child study team. The LIFE child study: a population-based perinatal and pediatric cohort in Germany. Eur J Epidemiol 2017;32(2):145–58. [6] Kromeyer-Hauschild K, Wabitsch M, Kunze D. Monatsschr Kinderheilkd 2001;149:807–18. [7] Rijnbeek PR, Witsenburg M, Schrama E, Hess J, Kors JA. New normal limits for the paediatric electrocardiogram. Eur Heart J 2001;22:702–11. [8] Davignon A. Normal ECG standards for infants and children. Pediatr Cardiol 1979/ 80;1:133–52. [9] Fraley MA, Birchem JA, Senkottaiyan N, Alpert MA. Obesity and the electrocardiogram. Obes Rev 2005;6(4):275–81. [10] Seyfeli E, Duru M, Kuvandık G, Kaya H, Yalcin F. Effect of obesity on P-wave dispersion and QT dispersion in women. Int J Obes Relat Metab Disord 2006;30(6):957–61. [11] Sympathovagal balance, nighttime blood pressure, and QT intervals in normotensive obese women. April 2003. p. 1–7. [13] Blüher S, Petroff D, Keller A, Wagner A, Classen J, Baum P. Effect of a 1-year obestiy intervention (KLAKS Program) on preexisting autonomic nervous dysfunction in childhood obesity. J Child Neurol 2015;30(9):1174–81. [14] Wildman RP, McGinn AP, Lin J, et al. Cardiovascular disease risk of abdominal obesity vs. metabolic abnormalities. Obesity 2009;19(4):853–60.
0.77 0.80 0.53
the case that pathologic ECG features are recorded in an obese child. 6. Limitations The current study does not include an analysis of participants autonomic state by for example heart rate variability in holter ECG. The sample size is relatively small with only few young children below the age of 8 years, which might have an impact on the findings but at least have an impact on statistical analysis. Nevertheless, the inclusion of an age-matched lean control group is an advantage of this study. Acknowledgements Special thanks to Mrs. Bettina Müller for linguistic support.
5