Postural blood pressure changes and arterial stiffness: a vicious circle?

Abstract

C urrently, the diagnosis and treatment of hypertension is based mainly on average blood pressure (BP) values over a period of time. However, BP is dynamic and varies over time, often depending on physical activity, such as increasing BP during exercise and a decrease in BP during sleep. As such, BP is not fully captured by its mean value of a series of measurements. Moreover, excessive BP variability has been shown to be detrimental to vascular health, as it has been associated with markers of (sub)clinical organ damage, such as (micro)albuminuria [1] and increased arterial stiffness [2], as well as cardiovascular events and mortality [3]. Importantly, these associations were independent of high mean BP, indicating that increased BP variability does harm beyond an elevated mean BP. Interestingly, researchers have defined various forms of harmful BP variability: variability over a series of BP readings, that is increased short-term (beat-to-beat or over 24 h) to long-term (over days, weeks, years) BP variability, or specific patterns in a 24-h BP profile, such as nocturnal nondipping, increased morning BP surge or orthostatic hypertension and hypotension [4]. Excessive BP changes during postural changes may be especially important, as most individuals change from a supine or sitting position to a standing position over 40 times a day [5]. In this issue of the Journal of Hypertension, Nolde et al. [6] provide an interesting insight into the association between postural BP changes and arterial stiffness. They studied a cohort of 200 patients referred to a tertiary hypertension clinic and evaluated the association between orthostatic hypertension and hypotension, and arterial stiffening. The authors measured BP in a sitting position and after 1 min standing upright, and considered change in BP of more than 10mmHg as compared with the seated BP to be abnormal: orthostatic hypertension was defined as a BP increase of 10mmHg and orthostatic hypotension was defined as a BP decrease of 10mmHg after standing. Arterial stiffness was measured using carotid-to-femoral pulse wave velocity (cfPWV). They found that the association between postural BP changes and cfPWV followed a Ushaped curve: both orthostatic hypertension and hypotension were associated with greater arterial stiffness, independent of important confounders, such as age, type 2 diabetes and mean 24-h BP. In unadjusted analyses, cfPWV was 1.4 and 1.1 m/s higher in the orthostatic hypertension and hypotension group, respectively, as compared to those with stable BP after 1min standing upright. Such high cfPWV values are quite impressive, as these high degrees of arterial stiffness are equivalent to approximately 10–15 years of vascular ageing [7]. At first sight, this U-shaped association between postural BP changes and arterial stiffening may perhaps seem somewhat surprising. However, it becomes more understandable when looking at the order of sequences of what comes first: orthostatic hypertension/hypotension or arterial stiffening? With regard to orthostatic hypertension, one may on the one hand hypothesize that a sudden surge in BP may cause arterial stiffening by putting greater mechanical stress on the arterial wall, which in turn deteriorates its elastin components. If these BP surges occur more often, it may be even more damaging to the vessel wall than a high mean BP. In fact, this concept has been revisited multiple times and has been named ‘stress fatigue theory’ in earlier studies [8,9], and is derived from the field of mechanical engineering: ‘high cycle fatigue’. Examples are found readily in everyday life: bending a paperclip very often breaks much easier than when only applying constant stress. Actual structural ruptures due to cyclic stress do not occur often in arterial walls, as their structural properties will change into stiffer arteries that can withstand the cyclic stress via an increased extracellular matrix deposition and enhanced vascular smooth cell proliferation [10]. On the other hand, reverse causality is also plausible: arterial stiffening may cause orthostatic hypertension due to the decreased buffering capacity of the large arteries, which will increase pulse pressure [11] and may lead to a BP overshoot in combination with the compensatory heart rate increase whilst standing up. Moreover, as these mechanisms seem equally biologically plausible, it is entirely feasible that both are Journal of Hypertension 2021, 39:1311–1313 Department of Internal Medicine, Zuyderland Medical Centre, Sittard/Heerlen, The Netherlands