Interpretation of the central aortic pressure waveform in elderly patients with aortic stenosis.

The central aortic pressure waveform, while simple in form, is complex in its physiological interpretation. Although general agreement has been reached on the contour and mechanisms responsible for pressure waveforms in the ascending aorta of healthy humans, in recent years there has been increasing interest in the contour of the pressure wave in elderly patients with aortic valve stenosis (AS). As aortic valve leaflets succumb to fibrosis and calcification, they increase opposition to forward flow. This results in a protracted pressure rise and manifests as the classical finding of pulsus parvus et tardus. Equally, changes to arterial properties (including elasticity and geometry) and pulse wave velocity (PWV) with age, heart failure, or hypertension can cause profound changes to the contour. Increased accessibility of methods to measure the central aortic pressure waveform, as well as the rapid uptake of transcatheter aortic valve implantation technologies, has created a renewed focus on better understanding of characteristic perturbations to the waveform in elderly patients with AS. In this review, we investigate the evolution of our understanding of the central aortic pressure waveform in varying AS disease states to highlight the importance of the physiological and biological basis for alterations in this waveform.

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

The effect of arterial stiffening on elevated pulsatile left ventricular afterload patients with aortic stenosis (AS) is pronounced beyond systemic hypertension. Circulatory afterload pulsatile efficiency (CAPE) is a marker of vascular function, defined as the ratio of steady state energy consumption (SEC) to maintain systemic circulation and pulsatile energy consumption (PEC). Twenty patients aged 80 ± 7 years were assessed at baseline and a median of 60 days post transcatheter aortic valve replacement (TAVR), with pulsatile vascular load calculated using simultaneous radial applanation tonometry derived aortic pressure and cardiac magnetic resonance phase-contrast imaging derived ascending aortic flow. Eight out of 20 patients had a reduction in PEC post TAVR, and the reduction of PEC correlated strongly with the number of days post TAVR (R = 0.62, P < 0.01). Patients assessed within the 100 days of TAVR had a rise in their PEC when compared to baseline (0.19 ± 0.09 vs 0.14 ± 0.08 W, P = 0.04). Baseline PEC correlated moderately with baseline SEC (R = 0.49, P = 0.03), and a high baseline PEC was predictive of post TAVR PEC reduction (R = 0.54, P =0.01). Overall, no significant differences were found between baseline and post TAVR for systolic aortic pressure (131 ± 20 vs 131 ± 20 mmHg), systemic vascular resistance (1894 ± 493 vs 2015 ± 519 dynes.s/cm5), aortic valve ejection time (337 ± 22 vs 324 ± 34 ms) or aortic characteristic impedance (120 ± 48 vs 107 ± 41 dynes.s/cm5). Improved flow profiles after TAVR likely unmask the true vascular properties by altering ventriculo-valvulo-arterial coupling, leading to downstream vascular remodelling secondary to flow conditioning, and results in eventual improvement of pulsatile afterload as reflected by our proposed index of CAPE.

Ageing, Hypertension and Aortic Valve Stenosis: A Conscious Uncoupling.

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.

A novel method to assess valvulo-arterial load in patients with aortic valve stenosis.

INTRODUCTION: Ventricular function in elderly patients with aortic stenosis is impeded both by restricted aortic flow and arterial stiffening. A number of patients continue to have exertional intolerance after relief of aortic valvular obstruction due to unrecognized ventriculo-arterial coupling mismatch. HYPOTHESIS: Quantification of valvulo-arterial load (VAL), using a simultaneous applanation tonometry/cardiac magnetic resonance (CMR) technique, can accurately assess the relative contributions of aortic stiffness and valve gradient in older patients with aortic stenosis. METHODS: Elderly patients with aortic stenosis underwent a simultaneous applanation tonometry/CMR protocol. CMR provided left ventricular volume and aortic flow simultaneously with radial applanation tonometry pressure acquisition. Central aortic pressure was derived by transformation of the radial applanation tonometry waveform. VAL was determined as the relationship of derived aortic pressure to CMR aortic flow in frequency domain (central illustration). RESULTS: Twenty patients (age 80 ±â€Š9 years; 12 males; blood pressure 140/75 ±â€Š20 mmHg) with aortic stenosis on transthoracic echocardiogram (16 severe; mean gradient 45 ±â€Š16 mmHg; aortic valve area 0.8 ±â€Š0.2 cm2) were enrolled. Derived aortic pressure and flow waveforms correlated well with invasive data. Increased VAL was significantly associated with advanced age (P = 0.04) and raised SBP (P < 0.01), irrespective of aortic stenosis severity. CONCLUSION: Difficulties in the measurement and accuracy of ventriculo-arterial coupling means that it is not routinely measured in patients with aortic stenosis. We describe a new noninvasive index that provides an accurate assessment of valvular and arterial load on the left ventricle. VAL may help detect those at risk of ventriculo-arterial coupling mismatch and assist in selection of those most likely to benefit from an invasive procedure.