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Abstract 8232: Obesity-Related Arterial-Ventricular Stiffening in Children
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Background:
Obesity is associated with structural and functional changes in the heart. Increases in arterial, ventricular systolic, and ventricular diastolic elastance (stiffness) may contribute to the pathogenesis of cardiac dysfunction. However, there is little information on arterial-ventricular stiffness and coupling in obese children. The purpose of the study is to assess the relationship between body mass index (BMI) and arterial-ventricular stiffening and coupling in children.
Methods:
Echocardiography with tissue Doppler imaging was performed in 303 children aged 6 to 15 years (BMI 12 to 34kg/m2). Left ventricular (LV) end-diastolic volume, LV mass, transmitral peak flow velocity (E), and mitral annular myocardial velocity (Em) were measured. LV mass/volume ratio was calculated. Stroke volume (SV) was measured using aortic diameter and pulsed Doppler velocity profile. SV was indexed for body surface area (SVI). Effective arterial elastance (Ea) was estimated by end-systolic pressure/SVI. End-systolic elastance (Ees) was calculated by a modified single-beat method using systolic and diastolic blood pressure, stroke volume, ejection fraction, timing intervals, and an estimated normalized ventricular elastance at arterial end diastole. Operant Ed was calculated from Doppler indices reflective of atrial pressures (E/Em) and the diastolic filling volume (SV).
Results:
Ea, Ees, and Ed all increased significantly with BMI(r = 0.35, p < 0.01, 0.26, p < 0.01, and 0.15, p < 0.05, respectively). Arterial-ventricular coupling (Ea/Ees ratio) did not change with BMI. LV mass/volume ratio was positively associated with increased BMI (r = 0.48, p < 0.01). The increased LV mass/volume ratio was due to a greater increase in LV mass to LV end-diastolic volume. There were weak but significant relationships between LV mass/volume ratio and Ees (r = 0.14, p < 0.05), Ea (r = 0.18, p < 0.01), and Ed (r = 0.15, p < 0.05).
Conclusions:
The present study suggests that higher BMI is associated with increases in arterial, ventricular systolic, and ventricular diastolic stiffness in children. This combined arterial-ventricular stiffening in obese children may contribute to the increased prevalence of later cardiovascular diseases.
Ovid Technologies (Wolters Kluwer Health)
Title: Abstract 8232: Obesity-Related Arterial-Ventricular Stiffening in Children
Description:
Background:
Obesity is associated with structural and functional changes in the heart.
Increases in arterial, ventricular systolic, and ventricular diastolic elastance (stiffness) may contribute to the pathogenesis of cardiac dysfunction.
However, there is little information on arterial-ventricular stiffness and coupling in obese children.
The purpose of the study is to assess the relationship between body mass index (BMI) and arterial-ventricular stiffening and coupling in children.
Methods:
Echocardiography with tissue Doppler imaging was performed in 303 children aged 6 to 15 years (BMI 12 to 34kg/m2).
Left ventricular (LV) end-diastolic volume, LV mass, transmitral peak flow velocity (E), and mitral annular myocardial velocity (Em) were measured.
LV mass/volume ratio was calculated.
Stroke volume (SV) was measured using aortic diameter and pulsed Doppler velocity profile.
SV was indexed for body surface area (SVI).
Effective arterial elastance (Ea) was estimated by end-systolic pressure/SVI.
End-systolic elastance (Ees) was calculated by a modified single-beat method using systolic and diastolic blood pressure, stroke volume, ejection fraction, timing intervals, and an estimated normalized ventricular elastance at arterial end diastole.
Operant Ed was calculated from Doppler indices reflective of atrial pressures (E/Em) and the diastolic filling volume (SV).
Results:
Ea, Ees, and Ed all increased significantly with BMI(r = 0.
35, p < 0.
01, 0.
26, p < 0.
01, and 0.
15, p < 0.
05, respectively).
Arterial-ventricular coupling (Ea/Ees ratio) did not change with BMI.
LV mass/volume ratio was positively associated with increased BMI (r = 0.
48, p < 0.
01).
The increased LV mass/volume ratio was due to a greater increase in LV mass to LV end-diastolic volume.
There were weak but significant relationships between LV mass/volume ratio and Ees (r = 0.
14, p < 0.
05), Ea (r = 0.
18, p < 0.
01), and Ed (r = 0.
15, p < 0.
05).
Conclusions:
The present study suggests that higher BMI is associated with increases in arterial, ventricular systolic, and ventricular diastolic stiffness in children.
This combined arterial-ventricular stiffening in obese children may contribute to the increased prevalence of later cardiovascular diseases.
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