Vascular stiffness and increased pulse pressure in the aging cardiovascular system

Abstract

Aging leads to a multitude of changes in the cardiovascular system, including systolic hypertension, increased central vascular stiffness, and increased pulse pressure. In this paper we will review the effects of age-associated increased vascular stiffness on systolic blood pressure, pulse pressure, augmentation index, and cardiac workload. Additionally we will describe pulse wave velocity as a method to measure vascular stiffness and review the impact of increased vascular stiffness as an index of vascular health and as a predictor of adverse cardiovascular outcomes. Furthermore, we will discuss the underlying mechanisms and how these may be modified in order to change the outcomes. A thorough understanding of these concepts is of paramount importance and has therapeutic implications for the increasingly elderly population.

Figure 1

This figures illustrates the composition of the arterial pressure waveform from a combination of a forward pressure wave created by ventricular contraction and a reflected wave. MAP: mean arterial pressure; SBP: systolic blood pressure (see [13]).

Figure 2

Schematic representation of pulse pressure amplification. Pressure tracings from the brachial artery and central aorta are shown, from a young individual with a highly compliant vasculature tree (left) and from an old one with stiff vessels (right). Despite similar brachial blood pressures, central blood pressures vary considerably. In young individuals, P₁ (which coincides with systolic blood pressures) marks the outward traveling blood pressure wave, while P₂ represents the arrival of the reflected pressure wave in diastole, augmenting diastolic blood pressure, and coronary filling. Pulse pressure augmentation in old, stiff vessels leads to a significant increase in P₂ as compared to P₁, as wave reflection occurs earlier and faster, leading to an augmentation in systolic blood pressure. Augmentation index is calculated as the difference between the second (P₂) and first (P₁) systolic peaks (delta P) as a percentage of pulse pressure (see [23]).

Figure 3

This figure shows pooled RR and 95% CI for aortic PWV and total CV events (a), CV mortality (b), and total mortality (c), according to baseline risk and disease state. Data are provided for high versus low aortic pulse wave velocity (PWV) (left column), increase in aortic PWV by 1 m/s (middle column), and increase in aortic PWV by 1 SD (right column) (see [46]).