ABSTRACT
The assessment of spontaneous variability of blood pressure and heart rate is based on specific physiological hypotheses about dynamic features, for example, the baroreflex modulation of heart rate over time in daily life. Usually, arterial baroreflex control of heart rate is explored without delays between blood pressure and heart rate data points, within a narrow range of values, excluding the analysis of saturation regions or low-threshold changes. In this work, we examine the dynamic interactions between systolic blood pressure (SBP) and interbeat interval (IBI), in 15-min length time series and for the first time using the analysis of diagonals derived from a cross-recurrence plots in healthy persons and end-stage renal disease (ESRD) patients. We found that ESRD patients have stronger intermittent dynamical interactions between IBI and SBP, but they lose most of the dynamical interactions. Although healthy subjects exhibit a continuously changing order of precedence between IBI and SBP at different lags, ESRD patients preserve this changing order of precedence only for lags >0 beats.NEW & NOTEWORTHY This study is the first to compare the time-variant pattern of systolic blood pressure (SBP) and interbeat interval (IBI) coupling between ESRD patients and healthy volunteers through the analysis of diagonal in cross-recurrence plots, and in the face of an orthostatic challenge. Our results demonstrated alternant interactions on the order of precedence (IBI â SBP or SBPâ IBI) at different time delays. This pattern is different in resting position and during active standing for the two groups studied, and interestingly, some association patterns are lost in ESRD patients. These patterns of alternant interactions on the order of precedence could be related to autonomic neural activities and cardiovascular synchronization at different scales both in time and space. This could reflect physiological adaptive flexibility of cardiovascular regulation. Losing some association patterns in ESRD may be the result of chronic adjustments of many physiological mechanisms (including chronic sympathetic hyperactivity), which could increase cardiovascular vulnerability to hemodynamic challenges.
