Published online before print October 16, 2006, doi: 10.1161/01.HYP.0000248121.29383.6e
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(Hypertension. 2006;48:e109.)
© 2006 American Heart Association, Inc.
Letters to the Editor |
Response to Correlating Ambulatory Blood Pressure Measurements With Arterial Stiffness: A Conceptual Inconsistency
Shanghai Institute of Hypertension, Shanghai Jiaotong University Medical School, Shanghai, China
Cambridge University Hospitals, Addenbrook’s Hospital, Cambridge, United Kingdom
Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland
Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium
We defined the ambulatory arterial stiffness index (AASI) as unity minus the regression slope of diastolic on systolic blood pressure, as measured at the brachial artery by ambulatory monitoring.1,2 AASI reflects the dynamic relation between diastolic and systolic blood pressure during the day. Conceptually consistent with a hypothesis put forward in 1914,3 the stiffer the arterial tree, the closer the regression slope and AASI are to 0 and unity, respectively. We concede that AASI is an indirect measure of arterial stiffness and must be influenced by other hemodynamic factors, such as wave reflections originating from peripheral sites, stroke volume, and peripheral resistance. The range of systolic and diastolic blood pressure values, which itself depends on the duration of the awake and asleep periods and on the intensity of physical activity during daytime, might additionally influence AASI. Nevertheless, in collaboration with the Ohasama investigators,4 we demonstrated recently that random exclusion of readings from ambulatory recordings with measurements programmed at 30-minute intervals did not significantly change the average value of AASI until 
7 readings were omitted.
We validated AASI in terms of established indexes of arterial stiffness. Among 166 healthy volunteers, the correlation between AASI and aortic pulse wave velocity was 0.51 (P<0.001).1 As illustrated in Figure 1 of the Irish study, the slope of diastolic on systolic blood pressure can be similar in individual recordings with differences in 24-hour systolic pressure or 24-hour pulse pressure as large as 40 or 25 mm Hg, respectively. However, across individual subjects, as other measures of arterial stiffness, AASI increased with age and mean arterial pressure.1 Furthermore, both before and after adjustment for arterial wave reflections by considering height and heart rate as covariates and for mean arterial pressure, AASI correlated more closely with the central and peripheral systolic augmentation indexes than 24-hour pulse pressure did.1
The discussion on what AASI means exactly in terms of arterial regulation5 might continue for some time until appropriate experimental studies in animals or human volunteers have been completed. However, as of to date, 1 cross-sectional analysis6 and 3 prospective cohort studies2,4,7 demonstrated significant association of AASI either with signs of target organ damage in never-treated hypertensive patients6 or with the incidence of cardiovascular mortality and morbidity2,4,6 in representative population samples randomly recruited in Western Europe2,7 or Japan.4 AASI seems to be especially predictive of stroke,2,4,7 even at levels of blood pressure within the normotensive range.2,7 AASI retains it prognostic significance, over and beyond 24-hour pulse pressure, a static surrogate measure of arterial stiffness throughout the day.2,4,6 Additional adjustment for any component of clinic or 24-hour blood pressure did not remove the prognostic significance of AASI.4,7 Abstraction made of the physiological interpretation of the novel index, AASI, allows noninvasive risk stratification beyond anthropometric characteristics, classic cardiovascular risk factors, lifestyle, and other measures derived from blood pressure measurement in the clinic environment or under ambulatory conditions. In our opinion, this represents the ultimate validation and added value of AASI.
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Acknowledgments |
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Disclosures
None.
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References |
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 Top References |
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1. Li Y, Wang JG, Dolan E, Gao PJ, Guo HF, Nawrot T, Stanton AV, Zhu DL, O’Brien E, Staessen JA. Ambulatory arterial stiffness index derived from 24-hour ambulatory blood pressure monitoring. Hypertension. 2006; 47: 359–364.
2. 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.
3. MacWilliam JA, Melvin GS. Systolic and diastolic blood pressure estimation with special reference to the auditory method. Br Med J. 1914; 2: 693–697.
4. Kikuya M, Staessen JA, Ohkubo T, Thijs L, Metoki H, Asayama K, Obara T, Inoue R, Li Y, Dolan E, Hoshi H, Hashimoto J, Totsune K, Satoh H, Wang JG, O’Brien E, Imai Y. Ambulatory arterial stiffness index and 24-hour ambulatory pulse pressure as predictors of mortality: results from the Ohasama study. Stroke. In press.
5. Gavish B. Correlating ambulatory blood pressure measurements with arterial stiffness: a conceptual inconsistency. Hypertension. 2006; 48: e108.
6. Leoncini G, Ratto E, Viazzi F, Vaccaro V, Parodi A, Falqui V, Conti N, Tomolillo C, Deferrari G, Pontremoli R. Increased arterial stiffness index is associated with target organ damage in primary hypertension. Hypertension. 2006; 48: 397–403.
7. Hansen TW, Staessen JA, Torp-Pedersen C, Rasmussen S, Li Y, Dolan E, Thijs L, Wang JG, O’Brien E, Ibsen H, Jeppesen J. Ambulatory arterial stiffness index predicts stroke in a general population. J Hypertens. In press.
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