Ageing, Hypertension and Aortic Valve Stenosis: A Conscious Uncoupling

Abstract

Aortic valve stenosis (AS) is no longer considered to be a disease of fixed left ventricular (LV) afterload (due to an obstructive valve), but rather, functions as a series circuit with important contributions from both the valve and ageing vasculature. Patients with AS are frequently elderly, with hypertension and a markedly remodelled aorta. The arterial component is sizable, and yet, the contribution of ventricular afterload has been difficult to determine. Arterial stiffening increases the speed of propagation of the blood pressure wave along the central arteries (estimated as the pulse wave velocity), which results in an earlier return of reflected waves. The effect is to augment blood pressure in the proximal aorta during systole, increasing the central pulse pressure and, in turn, placing even greater afterload on the heart. Elevated global LV afterload is known to have adverse consequences on LV remodelling, function and survival in patients with AS. Consequently, there is renewed focus on methods to estimate the relative contributions of local versus global changes in arterial mechanics and valvular haemodynamics in patients with AS. We present a review on existing and upcoming methods to quantify valvulo-arterial impedance and thereby global LV load in patients with AS.

Perspective Chapter: Evolution of Techniques to Assess Vascular Impedance in Patients with Aortic Stenosis

“…Despite the accessibility of Z VA and its widespread use, the technique has limitations including: (i) the potential for underestimation of flow velocity due to misalignment of the Doppler signal with flow direction; (ii) the risk of underestimation of LV outflow tract diameter due to inadequate quality and/or positioning of the imaging plane; (iii) measurement variability related to manual tracing of flow velocity contours, and; (iv) the calculation of mean pressure from brachial cuff pressure rather than direct measurement of central aortic pressure [12]. Furthermore, Z VA is measured as the ratio of pressure to indexed volume (rather than pressure to flow) and may therefore be more accurately described as a resistance index rather than a true measure of vascular impedance (Figure 2).…”

“…where |Z in | = |P|÷|Q| is the modulus and θ = (βϕ) is the phase of the impedance [10,11]. Both the steady-state and pulsatile load contribute to the total hydraulic load of the systemic circulation [12].…”

Impairment of Anti-Aggregatory Responses to Nitric Oxide and Prostacyclin: Mechanisms and Clinical Implications in Cardiovascular Disease

“…Thus, AS is a clinical marker of NO resistance and of coronary risk. This is not particularly surprising given that NO also functions to retard the development of aortic valve calcification [68][69][70][71].…”

“…A number of recent studies have demonstrated that the aging process is closely associated with extensive inflammatory activation and this inflammation, in turn, contributes to age-related increases in incidence of many forms of cardiovascular and cerebrovascular disease [69,79].…”

Pulsatile energy consumption as a surrogate marker for vascular afterload improves with time post transcatheter aortic valve replacement in patients with aortic stenosis

“…The traditional view that AS is a fixed, valvular LV outflow obstruction has recently been challenged by the concept that LV afterload is a series circuit involving both the valve and the vasculature [ 5 ], with an emphasis on ventriculo-valvulo-arterial coupling. Quantification of the vascular load in AS is nebulous, as current methods of afterload assessment typically focus on the LV or the valve itself in isolation, and often underestimate the effect of the vascular load [ 6 ]. Separation of pulsatile and steady state arterial load is rarely performed in the assessment of vascular load, especially in the context of AS.…”