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Mean ambulatory pulse pressure (PP) is a potent predictor of cardiovascular and all-cause mortality. Objectives. Investigating prognostic significance of elastic and non-elastic PP components Methods. Using a generalized nonlinear pressure–volume relationship in arteries (Fig. 1), PP can be split into an elastic component (PPel) with constant (diastolic) arterial stiffness and a non-elastic component (PPnel) that reflects arterial stiffening during the systole. We determined PPnel, PPel and the ratio WIF=PPnel/PPel (‘Widening Factor’) from 24-hour ambulatory BP measurements (ABPM) using a model. Standardized hazard ratios (HR) were estimated with Cox proportional hazards regression adjusted to age, gender, body mass index, mean arterial pressure, heart period (HP), systolic- and heart rate-dipping and diabetes and medication status. Assuming an exponential P-V relationship, the model provides the expression WIF=[(K-1)/ln(K)]-1, where K=SD(SBP)/SD(DBP) (SD=standard deviation) and PPel=PP/(1+WIF) Results. ABPM records of 2,105 individuals followed for 5 years for all-cause mortality were analyzed (age 56 ± 16, 55% women, 60% on medication and 9% diabetes, 115 died). Predictive power was demonstrated for patients with slower-than-median pulse rate (HP>0.87 s, n = 78): Mean(95%CI) HR of PPnel and WIF were 1.46(1.13–1.90) and 1.64(1.16–2.33) (P ≤ 0.005), respectively, and 1.59(1.21–2.1) and 1.83(1.27–2.63) (P = 0.001) for its subpopulation of older-than-median-age (>58 y, n = 73). The corresponding HR for PP was 1.34(1.03–1.75) (P = 0.03) and 1.53(1.15–2.03) (P = 0.004), respectively. PPel did not display predictive power. Fig. 2 shows that WIF varied strongly with age Conclusion. The 24-hour non-elastic PP component and the Widening Factor, which reflects arterial stiffening during the systole, are novel predictors for mortality, especially in elderly patients with slower pulse.

The increase of arterial volume during the systole (‘pulse volume’) is essential for buffering the pulsatile ventricular output. Objectives: Deriving some mechanical properties of arteries by assuming pulse volume homeostasis. Methods: A model that includes a generalized nonlinear relationship between arterial pressure P and volume V (see figure below). Results: If the pulse volume ΔV is constant, then for a given diastolic volume VD and pressure D the systolic volume VD+ΔV and pressure S are uniquely determined. For this reason, an infinitesimal increase of the diastolic pressure by dD would result in an increase of the systolic pressure by dS with the same volume change dV for both pressures. Since the systolic and diastolic stiffness is defined by G(S)=dS/dV and G(D)=dD/dV, respectively, we find that dS/dD=G(S)/G(D) (Eq.1). As D and ΔV determine S uniquely, dS/dD is a function of D and ΔV only. However, if dS/dD is independent of D and ΔV is constant, then K=dS/dD is a constant (Eq.2) equal to the relative increase of arterial stiffness during the systole. The only solution of Eq.2 is the well-documented linear relationship between the systolic and diastolic pressures with slope K and constant A, i.e., S=A+KD (Eq.3). The solution of Eq.3, rewritten as P(V+ΔV)=A+KP(V), is the observed exponential pressure-volume relationship in arteries that is also expressed by the demonstrated linear dependence of arterial stiffness on pressure. s: Arterial stiffening at elevated pressures may reflect an arterial design principle that aims at preserving the arterial buffering function via pulse volume homeostasis.