P62 Estimation of Wave Intensity in Humans Using only Pressure Waveforms and Reservoir Analysis

Background: Measurement of wave intensity (WI) requires simultaneous or quasi-simultaneous measurement of pressure and flow limiting its use. Previous work in dogs [1] and humans [2] has shown that the excess pressure waveforms calculated using reservoir analysis correspond closely with aortic flow...

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Bibliographic Details
Main Authors: Alun Hughes, Kim Parker, Nish Chaturvedi, Chloe Park
Format: Article
Language:English
Published: BMC 2020-02-01
Series:Artery Research
Online Access:https://www.atlantis-press.com/article/125934532/view
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Summary:Background: Measurement of wave intensity (WI) requires simultaneous or quasi-simultaneous measurement of pressure and flow limiting its use. Previous work in dogs [1] and humans [2] has shown that the excess pressure waveforms calculated using reservoir analysis correspond closely with aortic flow waveforms. This offers a potential method to estimate WI using only pressure waveforms (pWI). We investigated the feasibility of this approach and agreement with established methods. Methods: 262 participants (68.3 (SD = 5.5); 74% male) without aortic stenosis or heart failure were recruited from a UK-based longitudinal study, Southall and Brent Revisited. Central pressure waveforms, aortic flow velocity and carotid WI were measured using tonometry (Sphygmocor, AtCor), echocardiography (iE33, Philips) and ultrasonography (SSD-5500, Aloka) respectively. Reservoir analysis was performed as previously described [2] and excess pressure waveforms were calibrated to flow velocity assuming a peak velocity of 1 m/s. Method agreement was assessed as mean difference (MD), limits of agreement (LOA) and concordance coefficient (CC). Results: Analysis failed in 9 individuals; results for those with analysable data are shown in Table 1. Aortic pWI was higher than aortic WI but showed good concordance (logW1: MD(LOA) = −0.41(−0.73, −0.09) CC = 0.7; logW2: MD(LOA) = −0.41 (−0.73, −0.09); CC = 0.7). Agreement of pWI with carotid WI showed no bias and concordance was fair to poor (logW1: MD (LOA) = −0.16 (−1.30, 0.99) CC = 0.3; logW2: MD (LOA) = −0.02 (−1.23, 1.2); CC = 0.1). Table 1Results Variables N Median/(%) p25 p75 Age, y 207 67.9 63.6 71.9 BMI, kg/m2 207 26.6 24.1 30.1 Systolic BP, mmHg 207 139 126 148 Diastolic BP, mmHg 207 76 70 82 Heart rate, bpm 207 66 59 74.5 Male sex, % 150 72.5 Ethnicity   European 88 (42.5%)   South Asian 75 (36.2%)   African Caribbean 44 (21.3%) Current smoker 18 (8.8%) Diabetes 65 (31.4%) Hypertension 130 (62.8%) Aorta   W1, mmHg.m.s−3 207 7103 5041 9910   W2, mmHg.m.s−3 207 1637 1147 2518   pW1, mmHg.m.s−3 207 10,526 7677 14,336   pW2, mmHg.m.s−3 207 2491 1779 3560   time W1 to W2, s 207 0.25 0.23 0.27   Peak velocity, m/s 207 1.34 1.2 1.46 Carotid artery   W1, mmHg.m.s-3 207 8714 6550 12,883   W2, mmHg.m.s-3 207 2327 1471 3227   time W1 to W2, s 207 0.29 0.27 0.31   Peak velocity, m/s 207 1.10 0.92 1.30 BMI, body mass index; BP, blood pressure; p25, 25th centile; p75, 75th centile; pW1, peak intensity of initial forward compression wave (W1) estimated using pressure only; pW2, peak intensity of initial forward compression wave (W2) estimated using pressure only; W1, peak intensity of initial forward compression wave (W1) calculated using aortic velocity; W2, peak intensity of initial forward compression wave (W2) calculated using aortic velocity. Conclusion: Estimation of aortic WI from pressure waveforms using reservoir analysis is feasible.
ISSN:1876-4401