M L Marcovecchio1,2, M Gravina3,4, S Gallina5,6, E D'Adamo7, R De Caterina8,9, F Chiarelli10,11, A Mohn12,13, G Renda14,15. 1. Department of Paediatrics, University "G. d'Annunzio", Chieti-Pescara, Via dei Vestini 5, 66100, Chieti, Italy. m.marcovecchio@unich.it. 2. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. m.marcovecchio@unich.it. 3. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. gravina.mari@libero.it. 4. Institute of Cardiology, "G. d'Annunzio" University, Chieti, Italy. gravina.mari@libero.it. 5. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. sgallina@unich.it. 6. Institute of Cardiology, "G. d'Annunzio" University, Chieti, Italy. sgallina@unich.it. 7. Department of Paediatrics, University "G. d'Annunzio", Chieti-Pescara, Via dei Vestini 5, 66100, Chieti, Italy. ebe.dadamo@yahoo.com. 8. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. r.decater@unich.it. 9. Institute of Cardiology, "G. d'Annunzio" University, Chieti, Italy. r.decater@unich.it. 10. Department of Paediatrics, University "G. d'Annunzio", Chieti-Pescara, Via dei Vestini 5, 66100, Chieti, Italy. chiarelli@unich.it. 11. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. chiarelli@unich.it. 12. Department of Paediatrics, University "G. d'Annunzio", Chieti-Pescara, Via dei Vestini 5, 66100, Chieti, Italy. amohn@unich.it. 13. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. amohn@unich.it. 14. Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy. grenda@unich.it. 15. Institute of Cardiology, "G. d'Annunzio" University, Chieti, Italy. grenda@unich.it.
Abstract
Subclinical cardiac abnormalities represent predisposing factors for cardiovascular disease (CVD) in obese subjects. The aim of this study was to evaluate early cardiac abnormalities in obese youth and the potential association with insulin resistance (IR). Thirty obese (12 males (M)/18 females (F); age = 11.5 ± 2.4 years; body mass index (BMI)-standard deviation score (SDS) = +2.1 ± 0.5) and 15 normal weight (10 M/5 F; age = 12.8 ± 3.1 years; BMI-SDS = +0.3 ± 0.9) children and adolescents underwent Doppler two-dimensional echocardiographic assessments of left atrial (LA) and ventricular (LV) geometry and LV diastolic function (peak early [E] and late waves, E wave deceleration time, myocardial flow velocities). Homeostasis model assessment of IR (HOMA-IR) was used as an IR index. LA size was increased in obese children, as indicated by higher LA diameter (4.9 ± 0.5 vs 4.1 ± 0.4 cm, p < 0.001), area (14.3 ± 2.5 vs 10.7 ± 2.0 cm(2), p < 0.001), and volume (33.8 ± 10.6 vs 23.7 ± 6.4 ml, p = 0.003). LV mass was also increased in obese children (87.0 ± 16.6 vs 68.8 ± 13.2 g, p = 0.003), who also showed subtle diastolic dysfunctions, as indicated by higher values of E (97.1 ± 14.3 vs 86.2 ± 11.9 cm/s, p = 0.02). All the above parameters were significantly associated with BMI-SDS (p < 0.05). In addition, HOMA-IR was independently associated with LA diameter, area, and volume (β = 0.314, p = 0.040; β = 0.415, p = 0.008; β = 0.535, p = 0.001). CONCLUSION: Obese children feature increased LA size, which emerged to be mainly correlated to, and possibly driven by IR, suggesting an increased CVD risk. WHAT IS KNOWN: Left atrial and ventricular alterations have been reported in obese adults, and they represent predisposing factors for cardiovascular disease. There is some evidence suggesting that obese children show increased left ventricular mass and also increased atrial size, although with conflicting results. WHAT IS NEW: Obese normotensive children showed a moderately increased atrial size, subtle alterations in left cardiac diastolic function, and ventricular mass. An association between insulin resistance and left cardiac changes was found, although its mechanism remains to be determined.
Subclinical cardiac abnormalities represent predisposing factors for cardiovascular disease (CVD) in obese subjects. The aim of this study was to evaluate early cardiac abnormalities in obese youth and the potential association with insulin resistance (IR). Thirty obese (12 males (M)/18 females (F); age = 11.5 ± 2.4 years; body mass index (BMI)-standard deviation score (SDS) = +2.1 ± 0.5) and 15 normal weight (10 M/5 F; age = 12.8 ± 3.1 years; BMI-SDS = +0.3 ± 0.9) children and adolescents underwent Doppler two-dimensional echocardiographic assessments of left atrial (LA) and ventricular (LV) geometry and LV diastolic function (peak early [E] and late waves, E wave deceleration time, myocardial flow velocities). Homeostasis model assessment of IR (HOMA-IR) was used as an IR index. LA size was increased in obese children, as indicated by higher LA diameter (4.9 ± 0.5 vs 4.1 ± 0.4 cm, p < 0.001), area (14.3 ± 2.5 vs 10.7 ± 2.0 cm(2), p < 0.001), and volume (33.8 ± 10.6 vs 23.7 ± 6.4 ml, p = 0.003). LV mass was also increased in obese children (87.0 ± 16.6 vs 68.8 ± 13.2 g, p = 0.003), who also showed subtle diastolic dysfunctions, as indicated by higher values of E (97.1 ± 14.3 vs 86.2 ± 11.9 cm/s, p = 0.02). All the above parameters were significantly associated with BMI-SDS (p < 0.05). In addition, HOMA-IR was independently associated with LA diameter, area, and volume (β = 0.314, p = 0.040; β = 0.415, p = 0.008; β = 0.535, p = 0.001). CONCLUSION: Obese children feature increased LA size, which emerged to be mainly correlated to, and possibly driven by IR, suggesting an increased CVD risk. WHAT IS KNOWN: Left atrial and ventricular alterations have been reported in obese adults, and they represent predisposing factors for cardiovascular disease. There is some evidence suggesting that obese children show increased left ventricular mass and also increased atrial size, although with conflicting results. WHAT IS NEW: Obese normotensive children showed a moderately increased atrial size, subtle alterations in left cardiac diastolic function, and ventricular mass. An association between insulin resistance and left cardiac changes was found, although its mechanism remains to be determined.
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