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Rivista di Angiologia
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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International Angiology 2006 Settembre;25(3):268-73
Effects of poor glucose handling on arterial stiffness and left ventricular mass in normal children
Khan F. 1, Kerr H. 2, Ross R. A. 3, Newton D. J. 1, Belch J. J. F. 1
1 Vascular Diseases Research Unit, The Institute of Cardiovascular Research Ninewells Hospital and Medical School, Dundee, UK
2 Department of Cardiology, Ninewells Hospital and Medical School, Dundee, UK
3 Vascular Laboratory, Department of Medical Physics, Ninewells Hospital and Medical School, Dundee, UK
Aim. Cardiovascular risk factors can be present in children and young adults. We previously found abnormal microvascular function in children who had glucose intolerance and insulin resistance. The aim of the present study was to investigate whether they also have abnormalities in left ventricular mass (LVM) and arterial stiffness.
Methods. We measured heart dimensions and LVM using echocardiography, and arterial stiffness using pulse wave analysis in 23 children with good glucose handling (postfeeding glucose: 3.9 to 5 mmol/L) and 21 with poor glucose handling (7.7 to 11.4 mmol/L).
Results. The time to pulse reflection was slightly shorter in the poorer glucose handlers (mean±SD: 143±10 vs 153±20 ms, P=0.04), suggestive of increased arterial stiffness. Also in this group, there were significant relationships between intraventricular septal thickness, blood pressure and body mass index, but not in the normal glucose handlers.
Conclusion. We have found that normal children who are in the lowest quintile of glucose tolerance in comparison with their peers are exhibiting the first signs of arterial stiffening. In addition, we have seen the beginnings of a relationship between blood pressure, body mass index and left ventricular enlargement in this group. While these changes may not yet be clinically significant, their emergence might be further evidence of early predisposition to cardiovascular disease.