Association Between Arterial Stiffness, High Blood Pressure, and Hypertensive Phenotypes: Insights from the PAMELA Study

Abstract

Hypertension is a clinical condition associated with structural alterations in small, medium, and large arteries, also affecting target organs due to the mechanical effects of high blood pressure and shear stress. However, these vascular changes are also influenced by various inflammatory and neurohumoral mediators originating from the endothelium, the renin-angiotensin-aldosterone system, the neuroadrenergic system, and the perivascular fat. Specifically, chronic hypertension leads to vascular stretching, which triggers complex signaling pathways that promote vascular remodeling. The endothelium plays a crucial role in this process, as its function is impaired in hypertensive patients, leading to reduced nitric oxide-mediated vasodilation, increased vascular tone, and a proinflammatory and prothrombotic state. Along with structural changes, hypertension also triggers dynamic alterations in arterial distensibility and arterial wall properties, leading to increased arterial stiffness, which is strongly linked to cardiovascular outcomes and associated disability, as well as subsequent rehabilitation needs. Several non-invasive and highly reproducible methods are currently used to assess arterial stiffness, one of which is the cardio-ankle vascular index (CAVI). This article examines the association between arterial stiffness and high blood pressure, with a particular focus on the results of the Pressioni Arteriose Monitorate e Loro Associazioni (PAMELA) study. This study analyzes the determinants of arterial stiffness in the general population, the different hypertensive phenotypes affecting diurnal and nocturnal blood pressure profiles, and the impact of blood pressure control through antihypertensive treatment on arterial stiffness.

Keywords: arterial stiffness; cardiovascular disability; chronic disease; endothelial function; exercise; hypertension; inflammation; lifestyle risk reduction; outcome; rehabilitation.

Figure 1

Mean ± standard errors in mean (SEM) values of cardio-ankle vascular index (CAVI) in the PAMELA population subdivided according to gender (left panel) and age (right panel). F: females, M: males. Numbers in parentheses refer to the subjects studied in each group. The figure was originally created using data from [9].

Figure 2

Mean ± standard error (SEM) values of cardio-ankle vascular index (CAVI) in the different normotensive and hypertensive phenotypes investigated in the PAMELA study. Numbers in parentheses refer to the subjects studied in each group. NT: normotensive subjects, age 65.4 ± 2.7 years, males 52.1%; WCH: white coat hypertensives, age: 64.3 ± 3.3 years, males 55.2%; MH: masked hypertensives, age: 62.3 ± 3.2 years, males 51.6%; SH: isolated systolic elderly hypertensives, age 68.4 ± 2.8 years, males 56.4%; Nocturnal HT: nocturnal hypertensives, age 66.1 ± 2.4 years, males 55.3%. The figure was originally created using data from [9].

Figure 3

Mean ± standard errors in mean (SEM) values of cardio-ankle vascular index (CAVI)) in hypertensive patients displaying blood pressure values controlled or uncontrolled by antihypertensive drug treatment and in resistant hypertensives. Numbers in parentheses refer to the subjects studied in each group. The figure was originally created using data from [15].