Published online before print March 19, 2007, doi: 10.1161/HYPERTENSIONAHA.106.082248
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(Hypertension. 2007;49:986.)
© 2007 American Heart Association, Inc.
Original Articles |
Ambulatory Arterial Stiffness Index Is Not a Specific Marker of Reduced Arterial Compliance
From the Unit of Internal Medicine (G.S., M.P., G.Pucci, M.R.M., L.S., E.M.), Angiology and Arteriosclerosis, University of Perugia, Perugia, Italy; the Department of Clinical Medicine and Prevention (G.Parati), University of Milano-Bicocca, Milan, Italy; and the Department of Cardiology (G.Parati), San Luca Hospital, IRCCS, Istituto Auxologico Italiano, Milan, Italy.
Correspondence to Giuseppe Schillaci, Unit of Internal Medicine, Angiology and Arteriosclerosis, University of Perugia Medical School, Hospital "Santa Maria della Misericordia," Piazzale Menghini, 1, IT-06129 Perugia, Italy. E-mail skill{at}unipg.it
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Abstract |
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Ambulatory arterial stiffness index (AASI), a measure based on the relative behavior of 24-hour systolic and diastolic blood pressure (BP), has been suggested as a marker of arterial stiffness and a predictor of cardiovascular mortality. However, a narrow range of diastolic BP values over the 24 hours tends to flatten the regression slope and to artificially increase AASI. We explored the possible influence of different ranges of 24-hour diastolic BP fluctuations, such as those related to nocturnal BP fall, on AASI, and on its relationship with target organ damage. In 515 untreated hypertensive patients, AASI was directly related to age (r=0.30) and 24-hour systolic BP (r=0.20), whereas it was inversely related with nocturnal systolic and diastolic BP reduction (r=–0.28 and –0.46, respectively; all P<0.001). A direct relationship was found between AASI and left ventricular mass index (r=0.17; P<0.001), but this relation was no longer significant after adjustment for age, sex, body mass index, daytime systolic BP, and day-night systolic BP reduction (all P<0.05). AASI was directly related to carotid-femoral pulse wave velocity, an intrinsic measure of aortic stiffness (r=0.28; P<0.001), but no independent relation was found in a multiple linear regression. Our conclusions are as follows: (1) AASI is strongly dependent on the degree of nocturnal BP fall in hypertensive patients; (2) there is no significant relation between AASI and left ventricular mass after proper adjustment for confounders; and (3) the relation between AASI and a widely accepted measure of aortic stiffness, such as pulse wave velocity, is weak and importantly affected by other factors.
Key Words: ambulatory blood pressure monitoring • arteries • blood pressure • arterial stiffness • left ventricular hypertrophy
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Introduction |
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A novel index, based on the relative behavior of systolic and diastolic blood pressure (BP) over 24 hours, has been recently suggested by Li et al1 as an easily obtainable marker of arterial stiffness. By plotting the individual values of systolic and diastolic BP measurements obtained through 24-hour noninvasive ambulatory BP monitoring, the authors calculated the regression slope of diastolic BP on systolic BP. The slope was assumed as a global measure of arterial compliance, and its reciprocal (1 minus the slope), named ambulatory arterial stiffness index (AASI), was taken as a measure of arterial stiffness. The rationale underlying this assumption is that, for any given increase in distending arterial pressure, systolic and diastolic pressures tend to increase in a parallel fashion in a compliant artery, whereas in a stiff artery, the increase in systolic pressure is accompanied by a lesser increase, or even by a decrease, in diastolic pressure. In an analysis of the Dublin Outcome Study, Dolan et al2 showed that the AASI is able to predict cardiovascular mortality in hypertensive patients. Other studies have also shown recently that this index is associated with preclinical target organ damage in hypertension.3,4
However, several factors other than arterial stiffness may affect the regression slope of diastolic on systolic BP, and among them the range of variation in diastolic BP levels over the 24 hours may play an important role. Because of mathematical reasons, in a regression model, the range of the dependent variable (in this case, 24-hour diastolic BP) influences the regression slope. For narrow ranges of the dependent variable, B unavoidably tends to 0, thus increasing AASI. As shown by Dolan et al (see Figure 1 in their article),2 patients with a steeper slope (and a smaller AASI) were also characterized by a greater range of variation in diastolic BP over the 24 hours. In contrast, individuals with a narrower distribution of BP values over the 24 hours tended to have a flatter slope and a greater AASI. In particular, AASI values appear to be inversely associated with the degree of nocturnal BP fall, that is, with a parameter that was found to importantly influence 24-hour BP variability5,6 and that has been reported to bear some relationship not only with arterial stiffness,7 but also with several other factors, including neural cardiovascular regulation.8
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Based on these considerations, the aim of the present study was to explore the determinants of AASI more in depth. This was done through the following: (1) the identification of possible correlates of AASI in a hypertensive population; (2) the assessment of the relation between AASI and left ventricular (LV) mass index after accounting for confounders; and (3) the assessment, in a large subgroup of the same population, of the relationship occurring between AASI and a widely used measure of aortic stiffness, namely, carotid-femoral pulse wave velocity.
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Methods |
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In our study, we recruited 515 subjects with essential hypertension who were consecutively referred to our hypertension outpatient clinic by their general practitioners for baseline, off-treatment, evaluation. All of the subjects underwent clinical examination, 24-hour ambulatory BP monitoring, and 2D targeted M-mode echocardiography. Exclusion criteria were as follows: clinical or laboratory evidence of heart failure, coronary artery disease, cerebrovascular disease, echocardiographic tracings of insufficient quality, significant valvular defects, secondary causes of hypertension, serum creatinine
1.4 mg/dL in men and 1.2 mg/dL in women, major noncardiovascular disease, known diabetes or fasting glycemia 126 mg/dL, and treatment with any cardiovascular drug, including nitrates. A subgroup of 346 patients also underwent measurement of carotid-femoral pulse wave velocity and arterial waveform analysis. Subjects who underwent arterial measurements did not differ significantly from the remaining patients in terms of age, sex, smoking habits, office and 24-hour BP values, and serum cholesterol (data not shown). Coronary heart disease risk estimation was derived from the Framingham equations for adult subjects without overt coronary heart disease,9 which take into account age, sex, systolic BP, total cholesterol, high-density lipoprotein cholesterol, smoking status, diabetes, and electrocardiographic LV hypertrophy. Written informed consent was obtained from each patient, and the study protocol was reviewed and approved by the institutional ethics committee.
Ambulatory BP was recorded using a validated oscillometric device (Spacelabs model 90207, SpaceLabs Inc) set to take a reading every 15 minutes throughout the 24 hours.10 Normal daily activities were allowed and encouraged, and patients were told to keep their nondominant arm still and relaxed to the side during measurements. Day and night subperiods were defined according to patients’ diaries. Reading, editing, and analysis of data were done as described previously.11 We had demonstrated previously that >80% of subjects in our population remained classified as dippers or nondippers in terms of 2 ambulatory BP recordings carried out 1 week apart.10 Subjects with a nocturnal reduction of systolic and/or diastolic BP 10% were arbitrarily defined "dippers," whereas those with a nocturnal BP fall smaller than this cutoff value were defined "nondippers."12 From individual 24-hour recordings, we calculated the regression slope of diastolic BP on systolic BP values. AASI was calculated as 1 minus the regression slope, as proposed by Li et al.1
Aortic (carotid-to-femoral) pulse wave velocity was calculated from measurements of common carotid and femoral artery waveforms using an automatic applanation tonometry-based device, the SphygmoCor Vx system (AtCor), as described previously.13,14 Briefly, ECG-gated pulse waveforms were obtained sequentially over the common carotid and femoral arteries. Pulse wave velocity was calculated as the distance between recording sites measured over the surface of the body, divided by the time interval between the feet of the pressure waves. All of the measurements were performed by the same observer, who was unaware of the patient’s clinical data, on the same day that the patient finished 24-hour ambulatory BP monitoring. As reported previously,15 the intraobserver coefficient of variation of aortic pulse wave velocity obtained in 50 subjects was 5.1%. Central artery waveforms were derived from the radial artery waveform and pressure by using a transfer function validated previously during catheterization studies.16,17 The point at which the central aortic pressure becomes augmented by wave reflection is recognized by a computer program, and the degree of increase is expressed as the aortic augmentation, which is quantified either in absolute term or as a percentage of aortic pulse pressure (aortic augmentation index).
Details about reading procedures and reproducibility of linear measures of LV mass in our laboratory have been reported previously.18 Linear measurements were made according to the American Society of Echocardiography.19 LV mass was calculated according to Devereux20 as follows: {0.832x[(septal thickness+LV internal diameter+posterior wall thickness)3–(LV internal diameter3)]+ 0.6 g} and corrected by height in meters at the power of 2.7.21 LV hypertrophy was defined by a LV mass index 51.0 g/m2.7.
Statistical Analysis
Continuous variables were tested to detect substantial deviations from normality by computing the Kolmogorov-Smirnov Z, and the assumption of satisfactory normal distribution was met for all of the examined variables. Pearson’s correlation coefficients were used to explore the bivariate associations between examined variables. Stepwise multiple linear regression was used to test the independent relation of several variables to LV mass index and to aortic pulse wave velocity. P<0.05 was considered statistically significant. Data are presented as mean±SD.
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Results |
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Correlates of AASI
The main clinical characteristics of the study population are displayed in Table 1. The average AASI value was 0.31±0.17 (range: –0.16 to 0.90), individual values following a Gaussian distribution. Univariate correlates of AASI are reported in Table 2. AASI had a significant direct relation with age, systolic BP, and the Framingham coronary heart disease risk score. The relation between AASI and systolic BP was stronger when BP was estimated at the aortic level according to the transfer function (r=0.29) than when it was measured at the brachial level (r=0.21; P=0.007; z test for comparison between r values). As expected, on the basis of the regression model used to generate AASI, a strong inverse relationship was found between AASI and the absolute range of diastolic BP variability over the 24 hours, expressed as absolute range (r=–0.40; P<0.001), interquartile range (r=–0.42; P<0.001), or 24-hour SD (r=–0.47; P<0.001). No significant relations were found with the corresponding systolic BP variability measures (r=0.05, 0.06, and 0.08, respectively; all P values not significant).
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A total of 70 patients (14%) were found to be nondippers. Characteristics of dippers and nondippers are reported in Table 1. As displayed in Figure 1, AASI was significantly higher in nondippers than in dippers (0.44±0.20 versus 0.29±0.15; P<0.001). A significant inverse relation was found between AASI and nocturnal systolic (Figure 2A) and diastolic (Figure 2B) BP reduction. Such associations did not change if day and night were defined by fixed time intervals (r=–0.24 for systolic BP and –0.50 for diastolic BP; both P<0.001) rather than by diary. Twenty four-hour BP profiles and AASI values in 2 representative patients with dissimilar day-night BP changes are shown in Figure 3. The close dependence of AASI on the degree of nocturnal BP fall is exemplified by the finding of an AASI as low as 0.13 in a patient with a 19%/26% awake-asleep reduction in systolic/diastolic BP, as compared with an AASI as high as 0.63 in a patient with comparable awake BP and measured aortic pulse wave velocity values but no significant nocturnal BP reduction (3%/5% awake-asleep reduction in systolic/diastolic BP).
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We also investigated whether a reduced nocturnal BP fall might be in itself a marker of arterial stiffness. No significant association was found between the degree of nocturnal BP fall and aortic pulse wave velocity (r=–0.09, P=0.09 for systolic BP; r=–0.05, P=0.30 for diastolic BP). The corresponding age-adjusted partial correlations were +0.01 for systolic BP (P=0.90) and –0.01 for diastolic BP (P=0.91). When subjects were categorized into dippers and nondippers, the latter showed a greater aortic pulse wave velocity (9.9±2 m s–1 versus 9.1±2 m s–1; P=0.02), but this difference was no more significant after adjustment for age (age-adjusted values, 9.5±2 m s–1 versus 9.2±2 m s–1; P=0.30).
AASI and LV Mass Index
AASI was significantly higher in individuals with than in those without LV hypertrophy (0.35±0.16 versus 0.31±0.17; P=0.019). A direct bivariate relationship was found between AASI and LV mass index (r=0.17; P<0.001). However, the association between AASI and LV mass index did not survive multivariate analysis. Results of the multivariate predictors of LV mass index are reported in Table 3: body mass index, age, male sex, daytime systolic BP, and day-night systolic BP reduction, but not AASI, were independently related to LV mass index.
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AASI as a Measure of Aortic Stiffness
A significant, albeit weak, direct relation was found between AASI and aortic pulse wave velocity with bivariate analysis (r=0.28; P<0.001; Figure 4). The relationship between AASI and aortic pulse wave velocity, however, was no longer significant in a multivariate regression analysis model. In this model, only age, heart rate, mean arterial pressure, and the metabolic syndrome were independent predictors of aortic pulse wave velocity (Table 4).
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Discussion |
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Arterial stiffness is a strong predictor of cardiovascular complications in different clinical settings, including essential hypertension.22–24 However, measurement of arterial stiffness needs dedicated and rather expensive instrumentation, which is not generally available in daily clinical practice. A simple technique for estimating arterial stiffness without the use of special equipments or qualified observers would, thus, be welcome. Indeed, the proposal of an index derived from 24-hour ambulatory BP monitoring as an indirect measure of arterial stiffness, termed AASI,1,2 has recently received great interest and favor in the scientific community,25 despite the need for caution inherent to the use of a surrogate for more direct measures of arterial rigidity.26,27
Our study provides a novel and somewhat provocative contribution to the ongoing discussion in this setting by showing that AASI is only weakly related to a widely used index of aortic stiffness, such as pulse wave velocity, in a group of untreated hypertensive patients. Moreover, our data show that even such a weak relation is partially explained by the confounding effects of age, distending pressure, heart rate, and the degree of nocturnal BP fall. These data are at least in part not in line with those reported by Li et al,1 who found a significant bivariate direct relation between AASI and carotid-to-femoral pulse wave velocity in 166 Chinese normotensive subjects. Several possible explanations can be offered for the inconsistency between our findings and the findings by Li et al.1 First, our study was carried out in a larger population, which was less subjected to the risk of a sampling bias. Second, at variance from our study, Li et al1 examined a predominantly normotensive population, and their findings may not be easily applicable to hypertensive patients. It is worth mentioning that, in the Dublin Outcome Study, AASI was found to be a better predictor of cardiovascular mortality among normotensive than among hypertensive subjects, whereas pulse pressure was a superior prognostic marker in hypertensive patients.2 Third, and most importantly, no adjustment was allowed for potential confounding factors in the article by Li et al,1 whereas our data suggest that the link with commonly related variables explains to a significant extent the association between AASI and aortic stiffness. It must be acknowledged that it has not been proposed that AASI is precisely the same as any measure of arterial stiffness. Indeed, arterial stiffness varies nonlinearly with distending pressure. Unlike pulse wave velocity, which is determined as an estimate of arterial stiffness at a single point on the pressure-volume curve, AASI is determined over a range of BPs and could provide insight into the position of the pressure-volume curve and, therefore, into intrinsic wall stiffness.
Our data suggest a possible alternative explanation, other than differences in arterial rigidity, for the observed between-subject differences in AASI. For the first time, our study offers a clear demonstration that AASI values are closely related to another parameter, that is, to the extent of nocturnal BP decline. Indeed, in the subjects of our study, AASI was heavily influenced by the nocturnal fall in both systolic and diastolic BP, and hypertensive patients with a reduced nocturnal BP fall (nondippers) had significantly higher values of AASI.
It is well known that nocturnal declines in systolic and diastolic BP are fairly well correlated. As depicted in the representative patients of Figure 3 (left), dipper subjects appear to have a large number of nocturnal systolic and diastolic BP values much lower than the corresponding daytime values, which increases the regression coefficient of diastolic BP on systolic BP. In contrast, nondippers tend to have a narrower range of diastolic BP values throughout the 24 hours. As shown in our study, as a mathematical consequence, in nondipper subjects, the coefficient of regression B of diastolic over systolic BP over the 24 hours tends to decrease, and its reciprocal (AASI, or 1–B) tends to increase.
A different explanation could be suggested for the inverse link between nocturnal BP fall and AASI, that is, the former might be in itself a correlate of arterial stiffness.7 Of note, a lower heart rate at night might affect pulse wave velocity and, thus, wave reflection, which might contribute to maintain peripheral systolic BP levels during this period. However, the absence in our study of a significant relationship between nocturnal BP fall and aortic pulse wave velocity makes this hypothesis unlikely.
Our data, therefore, allow us to conclude that day-night BP changes should be taken into account when assessing AASI and even more so when investigating its clinical significance. Based on the results of our cross-sectional study, it is in fact reasonable to hypothesize that the prognostic impact of AASI might, at least in part, depend on its association with a diminished nocturnal systolic and especially diastolic BP fall. Such associations were not taken into account either in the article by Dolan et al2 or in the articles subsequently published on its issue.3,4
Clinical Perspectives
The results of the present study provide for the first time evidence that AASI is not only related to arterial stiffness but also to the degree of BP changes between day and night. Given that a reduced nocturnal BP fall is a significant determinant of LV hypertrophy28,29 and cardiovascular morbidity and mortality30–32 in several prospective studies, including the Dublin Outcome Study,32 it might be an important confounder in the relation between AASI and subsequent cardiovascular complications. The demonstration provided in our study that AASI values are majorly influenced by the degree of nocturnal BP fall, therefore, suggests that the latter parameter should always be considered when quantifying AASI and when assessing its clinical relevance.
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Acknowledgments |
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Disclosures
None.
Received October 8, 2006; first decision October 25, 2006; accepted February 28, 2007.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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- Li Y, Wang J-G, Dolan E, Gao P-J, Guo H-F, Nawrot T, Stanton AV, Zhu D-L, O’Brien E, Staessen JA. Ambulatory arterial stiffness index derived from 24-hour ambulatory blood pressure monitoring. Hypertension. 2006; 47: 359–364.
[Abstract/Free Full Text] - 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.
[Abstract/Free Full Text] - Leoncini G, Ratto E, Viazzi F, Vaccaro V, Parodi A, Falqui V, Conti N, Tomolillo C, Deferrari G, Pontremoli R. Increased ambulatory arterial stiffness index is associated with target organ damage in primary hypertension. Hypertension. 2006; 48: 397–403.
[Abstract/Free Full Text] - Ratto E, Leoncini G, Viazzi F, Vaccaro V, Falqui V, Parodi A, Conti N, Tomolillo C, Deferrari G, Pontremoli R. Ambulatory arterial stiffness index and renal abnormalities in primary hypertension. J Hypertens. 2006; 24: 2033–2038.[Medline] [Order article via Infotrieve]
- Imai Y, Aihara A, Ohkubo T, Nagai K, Tsuji I, Minami N, Satoh H, Hisamichi S. Factors that affect blood pressure variability. A community-based study in Ohasama, Japan. Am J Hypertens. 1997; 10: 1281–1289.[CrossRef][Medline] [Order article via Infotrieve]
- Bilo G, Giglio A, Styczkiewicz K, Caldara G, Kawecka-Jaszcz K, Mancia G, Parati G. How to improve the assessment of 24-h blood pressure variability. Blood Press Monit. 2005; 10: 321–323.[CrossRef][Medline] [Order article via Infotrieve]
- Lekakis JP, Zakopoulos NA, Protogerou AD, Papaioannou TG, Kotsis VT, Pitiriga VCh, Tsitsirikos MD, Stamatelopoulos KS, Papamichael CM, Mavrikakis ME. Arterial stiffness assessed by pulse wave analysis in essential hypertension: relation to 24-h blood pressure profile. Int J Cardiol. 2005; 102: 391–395.[CrossRef][Medline] [Order article via Infotrieve]
- Mancia G, Parati G, Di Rienzo M, Zanchetti A. Blood pressure variability. In: Zanchetti A, Mancia G, eds. Handbook of Hypertension, Vol. 17: Pathophysiology of Hypertension. Amsterdam, the Netherlands: Elsevier Science BV; 1997: 117–169.
- Anderson KM, Wilson PW, Odell PM, Kannel WB. An updated coronary risk profile: a statement for health professionals. Circulation. 1991; 83: 356–362.
[Free Full Text] - Schillaci G, Verdecchia P, Zampi I, Battistelli M, Bartoccini C, Porcellati C. Non-invasive ambulatory BP monitoring during the night: randomised comparison of different reading intervals. J Hum Hypertens. 1994; 8: 23–27.[Medline] [Order article via Infotrieve]
- Schillaci G, Verdecchia P, Borgioni C, Ciucci A, Gattobigio R, Sacchi N, Benemio G, Porcellati C. Predictors of diurnal blood pressure changes in 2042 subjects with essential hypertension. J Hypertens. 1996; 14: 1167–1173.[Medline] [Order article via Infotrieve]
- Verdecchia P, Schillaci G, Porcellati C. Dippers versus non-dippers. J Hypertens. 1991; 9 (suppl 8): S42–S44.[CrossRef]
- Schillaci G, Pirro M, Vaudo G, Mannarino MR, Savarese G, Pucci G, Franklin SS, Mannarino E. Metabolic syndrome is associated with aortic stiffness in untreated essential hypertension. Hypertension. 2005; 45: 1078–1082.
[Abstract/Free Full Text] - Schillaci G, De Socio GV, Pirro M, Savarese G, Mannarino MR, Baldelli F, Stagni G, Mannarino E. Impact of treatment with protease inhibitors on aortic stiffness in adult patients with human immunodeficiency virus infection. Arterioscler Thromb Vasc Biol. 2005; 25: 2381–2385.
[Abstract/Free Full Text] - Pirro M, Schillaci G, Paltriccia R, Bagaglia F, Menecali C, Mannarino MR, Capanni M, Velardi A, Mannarino E. Increased ratio of CD31+/CD42- microparticles to endothelial progenitors as a novel marker of atherosclerosis in hypercholesterolemia. Arterioscler Thromb Vasc Biol. 2006; 26: 2530–2535.
[Abstract/Free Full Text] - Kelly R, Hayward C, Ganis J, Daley J, Avolio A, O’Rourke M. Noninvasive registration of the arterial pressure pulse waveform using high-fidelity applanation tonometry. J Vasc Med Biol. 1989; 1: 142–149.
- Pauca AL, O’Rourke MF, Kon ND. Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform. Hypertension. 2001; 38: 932–937.
[Abstract/Free Full Text] - Schillaci G, Verdecchia P, Porcellati C, Cuccurullo O, Cosco C, Perticone F. Continuous relation between left ventricular mass and cardiovascular risk in essential hypertension. Hypertension. 2000; 35: 580–586.
[Abstract/Free Full Text] - Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation. 1978; 58: 1072–1083.
[Abstract/Free Full Text] - Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986; 57: 450–458.[CrossRef][Medline] [Order article via Infotrieve]
- de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol. 1992; 20: 1251–1260.[Abstract]
- Blacher J, Safar ME, Guerin AP, Pannier B, Marchais SJ, London GM. Aortic pulse wave velocity index and mortality in end-stage renal disease. Kidney Int. 2003; 63: 1852–1860.[CrossRef][Medline] [Order article via Infotrieve]
- Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L, Ducimetiere P, Benetos A. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001; 37: 1236–1241.
[Abstract/Free Full Text] - Laurent S, Katsahian S, Fassot C, Tropeano AI, Gautier I, Laloux B, Boutouyrie P. Aortic stiffness is an independent predictor of fatal stroke in essential hypertension. Stroke. 2003; 34: 1203–1206.
[Abstract/Free Full Text] - O’Brien E. Ambulatory blood pressure measurement: a trove of hidden gems? Hypertension. 2006; 48: 364–365.
[Free Full Text] - Benetos A, Lacolley P. From 24h blood pressure measurements to arterial stiffness. A valid shortcut? Hypertension. 2006; 47: 327–328.
[Free Full Text] - Laurent S. Surrogate measures of arterial stiffness. Hypertension. 2006; 47: 325–326.
[Free Full Text] - Verdecchia P, Schillaci G, Guerrieri M, Gatteschi C, Benemio G, Boldrini F, Porcellati G. Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension. Circulation. 1990; 81: 528–536.
[Abstract/Free Full Text] - Grandi AM, Broggi R, Jessula A, Laurita E, Cassinerio E, Piperno F, Bertolini A, Guasti L, Venco A. Relation of extent of nocturnal blood pressure decrease to cardiovascular remodeling in never-treated patients with essential hypertension. Am J Cardiol. 2002; 89: 1193–1196.[CrossRef][Medline] [Order article via Infotrieve]
- Verdecchia P, Porcellati C, Schillaci G, Borgioni C, Ciucci A, Battistelli M, Guerrieri M, Gatteschi C, Zampi I, Santucci A, Santucci C, Reboldi G Ambulatory blood pressure: an independent predictor of prognosis in essential hypertension [published correction appears in Hypertension. 1995;25:462]. Hypertension. 1994; 24: 793–801.
[Abstract/Free Full Text] - Staessen JA, Thijs L, Fagard R, O’Brien ET, Clement D, de Leeuw PW, Mancia G, Nachev C, Palatini P, Parati G, Tuomilehto J, Webster J, for the Systolic Hypertension in Europe (Syst-Eur) Trial Investigators. Predicting cardiovascular risk using conventional vs ambulatory blood pressure in older patients with systolic hypertension. JAMA. 1999; 282: 539–546.
[Abstract/Free Full Text] - Dolan E, Stanton A, Thijs L, Hinedi K, Atkins N, McClory S, DeHond E, McCormack P, Staessen JA, O’Brien E. Superiority of ambulatory over clinic blood pressure measurement in predicting mortality. Hypertension. 2005; 46: 146–151.
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