(Hypertension. 2002;39:710.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
From Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie (R.S., M.B., L.B., G.G., G.M.), and Centro Studi di Patologia Cronico Degenerativa (M.F.), University of Milano-Bicocca, Ospedale S. Gerardo, Monza; Cattedra di Epidemiologia, Dipartimento di Statistica (G.C., R.F.), University of Milano-Bicocca and Istituto Auxologico Italiano (G.G., G.M.), Milan, Italy.
Correspondence to Prof Giuseppe Mancia, Clinica Medica, Ospedale S. Gerardo dei Tintori, Via Donizetti 106 20052, Monza (MI), Italy.
| Abstract |
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Key Words: blood pressure blood pressure monitoring, ambulatory blood pressure determination ventricular function, left
| Introduction |
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With the exception of the aforementioned study (performed on a Japanese population),6 no information has ever been collected on the possible clinical relevance of 24-hour BP variability in the general population. The present study has addressed this issue by measuring 24-hour BP variability in a large sample representative of the population of Monza, a town in the northeast outskirts of Milan. The measured values were correlated with left ventricular mass (LVM) as derived from echocardiographic measurements because, in the population, this value has been shown to have prognostic significance.7
| Methods |
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In each individual, calculation was made of 24-hour average systolic BP, diastolic BP, and HR average and standard deviation (taken as index of the corresponding variability), the overall 24-hour variability being taken as the corresponding standard deviation around the average.14 In addition, (1) each single systolic BP reading collected over the 24 hours (total: 72 recordings) was averaged for all individuals, (2) the Fast Fourier transform spectral analysis15 was applied to the overall circadian BP profile so obtained to identify the cyclic components that accounted for most (>95%) of the systolic BP standard deviation, (3) these components were thereafter tested for their ability to fit the systolic BP profile in each subject, and (4) the sum squared of the differences between the observed and the fitted profile was taken as reflecting in each individual the systolic BP variability unexplained by the cyclic components, accounting for nearly all the systolic BP variability in the population as a whole. This was termed the individual residual variability. A similar procedure was employed for diastolic BP and HR. The 24-hour average values, standard deviation, cyclic components of variability, and individual residual variability were examined for their relationship to LVMI by bivariate regression analysis, separately for systolic BP, diastolic BP, and HR. Linear regression models were used because they were found to represent the best fitting models. Data obtained in bivariate analysis always were checked by multivariate analysis after adjustment for age, gender, and 24-hour mean values.16 The last adjustment was made because 24-hour BP variability is related to the mean values.14,17 The regression coefficient (ß) and its 95% confidence interval was always taken as an index of association between variables. A P<0.05 was taken as the level of statistical significance. The symbol± always refers to the standard deviation of the group mean.
| Results |
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Figure 1 (left panels) shows the circadian systolic BP, diastolic BP, and HR profiles in the whole group of subjects, together with the profile obtained by considering, via spectral analysis, the cyclic components of BP and HR variability. In each instance the first 2 cyclic components were able to accurately reproduce the circadian variations, and thus they accounted for most of the overall variability phenomena, with little or no contribution of the other faster components (Figure 1, right panels). For systolic BP the contribution of the first and the second cyclic components were 77.4% and 19.5%, respectively. The corresponding contributions for diastolic BP were 80.5% and 15.9%, and for HR were 88.7% and 6.9%.
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Table 2 shows the results by fitting the spectral models that accounted for most of the variability phenomena in the group as a whole to individual subjects. It is clear that, at variance from the whole population, in the individual subjects the first 2 cyclic components accounted for a much lower fraction of the overall variability, and that, thus, on average the individual residual variability had a substantial magnitude (51.4% for systolic BP, 49.1% for diastolic BP, and 51.3% for HR).
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As shown in Table 3, in the whole group of subjects there was a significant positive association between LVMI and gender (on average LVMI was greater in males), age, and 24-hour systolic and diastolic BP averages and standard deviations (LVMI was progressively greater with increasing 24-hour values). LVMI did not correlate with the 2 cyclic components of systolic and diastolic BP variability, but it showed, however, a significant positive relationship with the individual residual variability. The correlations between LVMI and 24-hour systolic BP mean and residual variability are shown in Figure 2.
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Table 4 shows the relationship between LVMI and variability phenomena derived by multivariate analysis after LVMI adjustment is made for gender, age, and 24-hour average systolic and diastolic BP values. LVMI did not correlate with the 24-hour standard deviation and the 2 cyclic components of the systolic and diastolic BP variability, but it maintained a significant correlation with systolic and diastolic individual residual BP variability. In both bivariate and multivariate analyses, no association was found between LVMI and 24-hour mean standard deviation, cyclic variability components, and individual residual HR variability.
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| Discussion |
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In previous studies on hypertensive patients, alterations in cardiac structure (as well as other types of organ damage) have been reported to be related to overall 24-hour BP variability as quantified by the standard deviation around the mean of all 24-hour BP values.15 This has not been the case with the present study, in which there was no relationship between LVMI, 24-hour BP standard deviation, and the first 2 cyclic components that explained most of the variability value in the population as a whole. Instead, LVMI was related to what we called the individual residual BP variability, ie, the respectable fraction (about 50%) of 24-hour BP variations that could not be explained by the above cyclic components in individual subjects. This suggests that this residual variability is by no means just "noise." On the contrary, it may represent the tendency for BP to vary in a rather "erratic" fashion that may influence the structure of the heart (and possibly that of the other organs as well) across the heterogeneous characteristics typical of the population. We can speculate that this "erratic" variability is the first to play such a role and that only when BP or LVM values become elevated is this complemented by the participation of the 2 large cyclic variability components and, thus, by the overall BP variability. Because these components reflected, respectively, the regularly occurring day and night BP difference and postprandial hypotension, their later contribution may reflect the intervention of disturbances in BP regulation and homeostasis.
Three additional points deserve to be mentioned. (1) In our study LVMI was similarly related to systolic and diastolic 24-hour BP means, thereby failing to provide any additional population evidence of the clinical superiority of the former over the latter value.21 (2) Because no relationship was found between LVMI and 24-hour HR mean and variability, there was no population evidence of the clinical importance of HR values.22 (3) Our results are in favor of the importance of performing spectral analysis of ambulatory BP monitoring data, despite the limitation represented by their rarefied sampling rate typical of this procedure. By identifying noncyclic components of 24-hour BP, this approach may contribute to the understanding of the BP phenomena involved in the origin and progression of organ damage.
Received September 23, 2001; first decision November 21, 2001; accepted December 13, 2001.
| References |
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13. Devereux RB, Reicheck N. Echocardiographic determination of left ventricular mass in man. Circulation. 1977; 55: 613618.
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22. Palatini P, Julius S. Heart rate and the cardiovascular risk. J Hypertens. 1997; 15: 317.[CrossRef][Medline] [Order article via Infotrieve]
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