Author + information
- Published online December 3, 2018.
- Sandra Erbs, MD,
- Henriette Broniecki, Cand Med,
- Kathrin Scheuermann, BS,
- Ephraim Winzer, MD,
- Jennifer Adam, MA,
- Ulrike Spielau, MD,
- Felix Woitek, MD,
- Marcus Sandri, MD,
- Marion Zimmer, MD,
- Christian Besler, MD,
- Wieland Kiess, MD,
- Axel Linke, MD,
- Antje Körner, MD and
- Norman Mangner, MD∗ ()
- ↵∗Heart Center Dresden, Technical University of Dresden, Fetscherstrasse 76, D-01307 Dresden, Germany
Childhood obesity is associated with changes in myocardial geometry and function indicating early onset of unfavorable alterations of the myocardium (1,2). The value of those studies is limited by a cross-sectional study design. We aimed to assess the impact of weight reduction on temporal changes of geometric and functional parameters of the myocardium in obese children and adolescents.
Thirty-four lean (LC), 15 obese (OC), and 15 children reducing their standardized body mass index (BMI-SDS) by at least 0.25 units (RC) were examined at baseline and after a median follow-up of 3.2 years (interquartile range: 3.0 to 3.4) assessing anthropometric parameters, measures of glucose and insulin metabolism, and applying echocardiography including a 2-dimensional speckle-tracking analysis.
Results are summarized in Table 1. Subjects were well matched (p > 0.05) with regard to age and sex distribution. During follow-up, LC showed a stable BMI-SDS, whereas OC had an increased, and RC a reduced, BMI-SDS (p < 0.01). At baseline and follow-up, systolic blood pressure was significantly higher in OC and RC (p < 0.01), and increased equally in all groups during follow-up (p = 0.29). Fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR) were significantly higher in OC and RC at baseline (p < 0.01). At follow-up, insulin (p = 0.08) and HOMA-IR (p = 0.10) tended to lower values in RC but increased in OC.
At baseline and compared with LC, OC and RC were characterized by a higher left ventricular (LV) mass index (LVMI) (p < 0.01). At follow-up, LVMI decreased significantly in RC, but increased in OC, whereas it remained stable in LC (p < 0.01). At baseline, the number of children diagnosed with LV hypertrophy according to a z-score >1.64 was 0 (0%), 4 (26.7%), and 2 (13.3%) for LC, OC, and RC, and were 0 (0%), 6 (40%), and 1 (6.7%) at follow-up, respectively. Left atrial volume index (LAVI) was enlarged in OC and RC compared with LC at baseline (p < 0.01). At follow-up, LAVI significantly decreased in RC, but increased in OC, whereas it remained stable in LC (p = 0.03). Right atrial area (p = 0.02) and right ventricular diameter (p < 0.01) were also enlarged in OC and RC at baseline and did not change during follow-up.
Both at baseline and follow-up, no difference was detected in global LV ejection fraction. Global longitudinal LV strain and strain rate were significantly reduced in OC and RC obese as compared with LC at baseline (p < 0.01). At follow-up, global longitudinal LV strain significantly improved to lower values in RC, but attenuated to higher values in OC, whereas it remained stable in LC (p = 0.01). Global longitudinal LV strain rate followed the same pattern (p = 0.07). LV circumferential strain was blunted in OC and RC compared with LC at baseline, but it disproportionately improved to lower values in OC compared with LC and RC at follow-up (p < 0.01). This change was also observed for circumferential strain rate (p = 0.01).
Correlation analysis revealed that the change in LVMI was predicted by a change in HOMA-IR (beta 0.292; p = 0.02) and low-density lipoprotein cholesterol (beta −0.262; p = 0.04), whereas the change in longitudinal strain was predicted by the change in BMI-SDS (beta −0.274; p = 0.04) and HOMA-IR (beta −0.302; p = 0.02). The change in LAVI was solely predicted by the change in BMI-SDS (beta 0.343; p < 0.01).
Previous studies evaluating the effect of diet (3) or exercise training (4) on geometric LV parameters could not show a significant decrease of those parameters. A potential explanation for our positive result might be the longer follow-up, whereas the previous studies only observed their subjects for 3 to 9 months. Enlargement of the left atrium is in line with the pathophysiological model suggesting that obesity is associated with a higher blood volume, cardiac output, and peripheral resistance leading to cardiac chamber dilatation, which is, at least at this time, reversible by weight reduction. Previous studies (1,2) documented decreased longitudinal deformation in obese children and adolescents. Data on reversibility of those changes are scarce. A study showing restored global strain and strain rate after a lifestyle intervention program based on exercise and diet (5) is in line with our results.
In conclusion, weight reduction during adolescence is associated with an improvement of obesity-induced structural and functional cardiac alterations. The voluntary aspect of weight reduction indicates that it is not the method of body weight reduction that is important, but simply the weight loss per se.
Please note: This work was performed at Heart Center Leipzig, University Hospital, and University Hospital for Children and Adolescents, Leipzig, Germany. This work was supported by research grants to Drs. Erbs and Körner by the German Research Foundation for the Clinical Research Center “Obesity Mechanisms” CRC1052/1 C05 and by LIFE Child (Leipzig Research Center for Civilization Diseases, Universität Leipzig), funded by the European Union, by the European Regional Development Fund (ERFD) by means of the Free State of Saxony within the framework of the excellence initiativeClinical. Dr. Linke has received grants from Medtronic and Claret Medical; and personal fees from St. Jude Medical, Medtronic, Claret Medical, Boston Scientific, Bard, and Edwards Lifesciences, outside the submitted work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Erbs and Broniecki contributed equally to this work and are joint first authors.
- 2018 American College of Cardiology Foundation