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(Hypertension. 2003;41:1010.)
© 2003 American Heart Association, Inc.
Editorial Commentaries |
From the Department of Therapeutics and Pharmacology, Queens University Belfast, Northern Ireland
Correspondence to Gary E McVeigh, MD, PhD, Department of Therapeutics and Pharmacology, 97 Lisburn Road, Belfast BT9 7BL, Northern Ireland. E-mail g.mcveigh@qub.ac.uk
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Risk factors for cardiovascular disease mediate their effects by altering the structure, properties, and function of wall and endothelial components of arterial blood vessels.1 The ability to detect and monitor change in the physical properties of arteries, representative of the cumulative and integrated influence of hemodynamic, metabolic, and inflammatory stimuli in impairing arterial wall integrity, holds potential to intervene at a preclinical stage to prevent or attenuate disease progression. The importance of assessing arterial wall integrity has been highlighted by recent studies demonstrating that a decrease in the pulsatile function of large arteries represents an independent predictor for future cardiovascular events.2
Information about the interaction between the left ventricle and the physical properties of the arterial circulation can be derived by the descriptive and quantitative analysis of the arterial pressure pulse waveform.3 Consistent characteristic changes in the pressure pulse waveshape have been described with aging and disease states predisposing to an increase in vascular events. One such age-related change involves a steepening of the pressure decay in diastole, largely determined by impaired buffering function of the proximal aorta.3,4 Loss of the oscillatory waveform that distorts the proximal portion of diastole from a pure exponential represents a further early and consistent finding with aging and risk factors for cardiovascular disease including hypertension, smoking, and diabetes mellitus.37 This feature arises from reflection of the incident pressure wave generated by the left ventricle from peripheral reflecting sites with a major contribution originating from impedance mismatches in small arteries and arterioles. The progressive appearance
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