TABLE 4.
EP phenotype |
|||||
Non-EPs | EPs | P | |||
0 h | 0–2 h | 0 h | 0–2 h | ||
RHI | 2.78 ± 0.14 | 0.40 ± 0.23 | 2.71 ± 0.17 | −0.09 ± 0.23 | 0.16 |
Diastolic BP, mm Hg | 80 ± 2 | 1 ± 2 | 78 ± 2 | 0 ± 2 | 0.76 |
Systolic BP, mm Hg | 134 ± 3 | 1 ± 2 | 125 ± 4 | 1 ± 2 | 0.94 |
CO, L/min | 4.60 ± 0.25 | −0.17 ± 0.17 | 3.93 ± 0.27 | 0.03 ± 0.17 | 0.44 |
AI, % | 24 ± 1 | 0 ± 1 | 24 ± 1 | −1 ± 1 | 0.19 |
cfPWV, m/s | 9.8 ± 0.3 | 0.1 ± 0.2 | 10.2 ± 0.4 | −0.5 ± 0.2 | 0.13 |
Baseline values are means ± SEMs; values for 0–2 h are adjusted means ± SEMs, with age used as a covariate. n = 14/group. Differences in study endpoints between interventions were analyzed by using general linear model (univariate analysis). AI, augmentation index; BP, blood pressure; cfPWV, carotid-femoral pulse-wave velocity; CMC, carboxy-methyl cellulose; CO, cardiac output; EP, equol producer; RHI, reactive hyperemia index.