Published online before print December 26, 2006, doi: 10.1161/01.HYP.0000254947.07458.90
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(Hypertension. 2007;49:e7.)
© 2007 American Heart Association, Inc.
Letters to the Editor |
Letter to the Editor
Ambulatory Arterial Stiffness Index Is Not a Stiffness Parameter But a Ventriculo-Arterial Coupling Factor
Laboratory for Physiology, and Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands
Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands
BMEYE BV, Amsterdam, the Netherlands
Recent hypertension research has shown that large artery compliance is an important determinant of systolic pressure, pulse pressure, and cardiovascular disease. Many methods exist to determine compliance or its inverse, arterial stiffness; the time constant of the aortic pressure decay in diastole, the ratio of stroke volume over pulse pressure, and pulse wave velocity are among the most used. These methods require either invasive measurements or 2 simultaneous measurements and are not practical to use in epidemiological studies or in night–day variations. Dolan et al1 recently suggested the use of the Ambulatory Arterial Stiffness Index (AASI), defined as 1 minus the slope of the (linear) relation between diastolic and systolic pressure, as a measure of arterial stiffness. The AASI is easy to measure noninvasively and over long time periods. The AASI, although associated with pulse pressure, augmentation index, and other measures of arterial stiffness, was criticized by Laurent,2 Benetos and Lacolley,3 and Gavish4 and defended by Dolan et al.1 Thus, the question of whether AASI is a proper arterial stiffness parameter has not been answered.
Here we derive the AASI from basic principles. The ratio of stroke volume, SV, over pulse pressure, PP, is a measure of total arterial compliance: C=SV/PP, or PP=SV/C. The ratio of mean pressure, Pm, and cardiac output, Q, is a measure of systemic vascular resistance, R. With SV times heart rate, HR, being cardiac output, it follows that Pm=QxR=SVxHRxR or SVxR/T, with T heart period (R–R interval). Thus, PP/Pm=T/RC=T/
with =RC, the characteristic decay time of aortic pressure in diastole.
We approximate mean pressure by Pm=(Ps+2Pd)/3, and pulse pressure is PP=Ps–Pd, with Ps and Pd systolic and diastolic pressure. Inserting this into PP/Pm, we obtain the following: (Ps–Pd)/(Ps/3+2Pd/3)=T/; rearrangement gives the following: Pd=Ps (3–T/)/(3+2T/). Thus, 1 minus the slope of the relation between diastolic and systolic pressure equals the following: 
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Taking =1.5s and T=0.86s (70 bpm), we obtain AASI=0.41 (experimental data 0.33 to 0.561). A stiffer arterial system, that is, decreased compliance and, thus, smaller , results in an increased AASI. If we assume that compliance depends on pressure, the ratio T/ appears again in the formula, together with pressure, and, thus, the AASI depends not only on total arterial compliance or its inverse, arterial stiffness, but also systemic vascular resistance, heart period, and on pressure.
T is the characteristic time determined by the heart, and is the characteristic time of the arterial system.5 Therefore, the AASI depends on both the heart and the arterial system. The ratio T/ is a (temporal) ventriculo-arterial coupling factor; it has been shown that T/ is similar in mammals at rest, resulting in similar systolic and diastolic pressures in mammals.5 Thus, the AASI is a coupling factor as well.
Increased arterial stiffness (with R, T, and pressure constant) results in an increase in both AASI and pulse pressure, and, therefore, AASI correlates with indicators of arterial stiffness but is not a measure of arterial stiffness: it is a measure of ventriculo-arterial coupling.
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Acknowledgments |
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Source of Funding
This study was funded, in part, by grant NHS2003B274 from the Netherlands Heart Foundation.
Disclosures
B.E.W. has ownership interest of >$10 000 in BMEYE BV. The remaining authors report no conflicts.
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References |
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 Top References |
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1. Dolan E, Thijs L, Li Y, Atkins N, McCormack P, McClory S, O’Brien E, Staessen JA, Stanton AV. Ambulatory arterial stiffness index as a predictor of cardiovascular mortality in the Dublin Outcome Study. Hypertension. 2006; 47: 365–370.
2. Laurent S. Surrogate measures of arterial stiffness: do they have additive predictive value or are they only surrogates of a surrogate. Hypertension. 2006; 47: 325–326.
3. Benetos A, Lacolley P. From 24-hour blood pressure measurements to arterial stiffness: a valid short cut. Hypertension. 2006; 47: 327–328.
4. Gavish B. Correlating ambulatory blood pressure measurements with arterial stiffness: a conceptual inconsistency? Hypertension. 2006; 48: e108.
5. Westerhof N, Elzinga G. Normalized input impedance and arterial decay time over heart period are independent of animal size. Am J Physiol. 1991; 261: R126–R133.[Medline] [Order article via Infotrieve]
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  B. Gavish, I. Z. Ben-Dov, and M. Bursztyn Ambulatory Arterial Stiffness Index Is Not a Specific Marker of Reduced Arterial Compliance Hypertension, August 1, 2007; 50(2): e18 - e18. [Full Text] [PDF]
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Y. Li, J.-G. Wang, E. Dolan, E. O'Brien, T. W. Hansen, H. Ibsen, M. Kikuya, Y. Imai, T. Richart, L. Thijs, et al. Letter to the Editor: Response to Arterial Stiffness Index Is Not a Stiffness Parameter But a Ventriculo-Arterial Coupling Factor Hypertension, February 1, 2007; 49(2): e8 - e9. [Full Text] [PDF]
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