Quantifying the speed of fluctuations in systolic blood pressure

Increased blood pressure variability (BPV), even in the absence of hypertension, has been identified as an important independent cardiovascular risk factor (CVRF). However, the role of the speed of changes in systolic blood pressure (SBP; vSBP) on cardiovascular risk needs to be investigated. The ob...

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Veröffentlicht in:Hypertension research 2013-12, Vol.36 (12), p.1039-1044
Hauptverfasser: van Gestel, Arnoldus J R, Camen, Giovanni, Clarenbach, Christian F, Sievi, Noriane, Rossi, Valentina A, Kohler, Malcolm
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Sprache:eng
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Zusammenfassung:Increased blood pressure variability (BPV), even in the absence of hypertension, has been identified as an important independent cardiovascular risk factor (CVRF). However, the role of the speed of changes in systolic blood pressure (SBP; vSBP) on cardiovascular risk needs to be investigated. The objective of this study was to investigate whether subjects with a high cardiovascular risk profile have an increased degree and speed of changes in SBP compared with subjects with low or no risk. Resting beat-to-beat blood pressure (BP) was recorded for 5 min. Standard BPV measures in both time and frequency domains were conducted. The s.d. of SBP (s.d.-SBP) values was used to quantify the degree of BPV. vSBP was assessed by calculating the slopes of oscillatory fluctuations in SBP for different interbeat intervals (IBI). Subjects were allocated to one of four groups according to the number of CVRFs (0, 1, 2, ≥ 3 CVRF). Of 122 subjects, 19.7% had 0 CVRF, 27.0% had 1, 32.0% had 2 and 21.3% had ≥ 3 CVRFs. There was an increase in vSBP across the four risk groups. The vSBP in patients without CVRF was 3.12 (1.09), 1 CVRF 3.23 (1.07), 2 CVRF 4.16 (2.26) and ≥ 3 CVRF 4.22 (1.66; P = 0.015). The s.d.-SBP was not significantly different between the cardiovascular risk groups. The speed of fluctuations in SBP rather than the degree of BPV is pronounced in patients with elevated cardiovascular risk. Increased speed of BP fluctuations may thus be a contributing mechanism to cardiovascular morbidity.
ISSN:0916-9636
1348-4214
DOI:10.1038/hr.2013.62