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Q J Med 2000; 93: 441-448
© 2000 Association of Physicians

Increased augmentation index and systolic stress in type 1 diabetes mellitus

I.B. Wilkinson, H. MacCallum, D.F. Rooijmans, G.D. Murray1, J.R. Cockcroft2, J.A. McKnight3 and D.J. Webb

From the Clinical Pharmacology Unit and Research Centre, University of Edinburgh, Western General Hospital, Edinburgh, 1 Department of Community Health Sciences, University of Edinburgh Medical School, Edinburgh, 2 Department of Cardiology, University of Wales College of Medicine, University Hospital, Cardiff, and 3 Metabolic Unit, Western General Hospital, Edinburgh, UK

Received 9 March 0000 Type 1 diabetes mellitus is associated with endothelial dysfunction and increased arterial stiffness, both of which may contribute to the excess cardiovascular mortality in such patients. Arterial stiffening increases pulse wave velocity and wave reflection, which augments central systolic pressure and stress. Using the non-invasive technique of pulse wave analysis, we investigated aortic augmentation and central pressure in 35 patients with type 1 diabetes and 35 matched controls. Peripheral pulse waveforms were recorded from the radial artery. Central aortic waveforms were then generated, and augmentation index (AIx), ascending aortic pressure and tension time index (TTI), a measure of systolic load, were calculated. Peripheral and central blood pressure did not differ between the two groups. AIx was significantly elevated in the diabetic patients compared with controls (7.1±1.6% vs. 0.4±2.0%; p=0.01), as was the TTI (2307±51 mmHg.s.min-1 vs. 2010±61 mmHg.s.min-1; p<0.001). Estimated pulse wave velocity was also higher in the diabetic group. Type 1 diabetes is associated with an increased AIx and rate of wave travel, indicating enhanced wave reflection and increased systemic arterial stiffness, and elevation of the TTI. Such haemodynamic effects may contribute to the increased left ventricular mass and risk of cardiovascular disease associated with type 1 diabetes mellitus.

Address correspondence to Dr I.B. Wilkinson, Clinical Pharmacology Unit and Research Centre, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU. e-mail: i.wilkinson{at}ed.ac.uk


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