Background
Valvuloarterial impedance ( Z va ) can estimate the global hemodynamic load on the left ventricle in patients with severe aortic stenosis better than the standard indexes, as shown in previous studies. In fact, Z va can estimate global left ventricular hemodynamic load as the sum of valvular and vascular loads. The aim of this study was to evaluate the acute improvement of left ventricular performance in patients with symptomatic aortic stenosis after transcatheter aortic valve implantation (TAVI) using Z va .
Methods
One hundred two consecutive patients who underwent TAVI were submitted to transthoracic echocardiography immediately before and after aortic valve implantation, together with invasive hemodynamic measurements.
Results
After TAVI, immediate reductions in the transaortic peak pressure gradient ( P < .0001) and mean pressure gradient ( P < .0001) and a concomitant increase in aortic valve area ( P < .0001) were seen on echocardiography. Left ventricular ejection fraction significantly increased immediately after TAVI in all patients (from 48.9 ± 10.3% to 52.1 ± 11.1%, P < .0001). Regarding global left ventricular hemodynamic load, acute and significant reductions in end-systolic meridional wall stress (from 82.7 ± 42.6 to 57.8 ± 30.1 kdyne · cm −2 , P < .0001) and in Z va (from 6.81 ± 2.51 to 5.38 ± 2.13 mm Hg · mL −1 · m −2 , P < .0001) were observed. Furthermore, patients who died at 6-month follow-up had higher baseline Z va values compared with those who were alive at 6-month follow-up (8.13 ± 3.08 vs 6.41 ± 2.12 mm Hg · mL −1 · m −2 , P < .004).
Conclusions
TAVI is characterized by an immediate enhancement of global left ventricular hemodynamic performance, as demonstrated by an acute Z va improvement, even in patients with low baseline ejection fractions.
Aortic stenosis (AS) remains the most common native valve disease, most often observed in elderly patients with comorbidities. The hemodynamic effects of AS on left ventricular (LV) function before and after aortic valve replacement (mainly the interaction between valvular load and arterial load) are so complex that the analysis of these physiopathologic aspects with standard indexes is totally inadequate. In particular, in these patients, the left ventricle often must face a double load: the valvular load caused by AS and the arterial load determined by a decrease in systemic arterial compliance (SAC) and/or an increase in systemic vascular resistance (SVR). In this regard, Hachicha et al. recently proposed a new index of global LV hemodynamic load, valvuloarterial impedance ( Z va ), that can quantify stenosis severity better than the standard indexes. In fact, Z va can estimate global LV hemodynamic load as the sum of valvular and vascular loads.
Recent studies have demonstrated that transcatheter aortic valve implantation (TAVI) offers a viable and “less invasive” option for the treatment of patients with critical AS at high risk with conventional surgery. This technique, in fact, can decrease elevated LV afterload in patients with AS, acutely reducing transaortic pressure gradients. However, a few studies have already shown changes in LV systolic function after TAVI. One study recently conducted by our group showed that TAVI is associated with an early significant reduction (normalization) of both ventricular-arterial coupling and LV work efficiency.
The main objective of this study was to analyze, in patients with symptomatic AS, the real incremental value of Z va in comparison with other conventional echocardiographic parameters, such as aortic gradient or aortic valve area (AVA), in the evaluation of TAVI efficacy and its prognostic stratification.
Methods
Patient Population
One-hundred two consecutive patients who were symptomatic for AS were treated with TAVI at the Cardiac Thoracic and Vascular Department of the University of Pisa between January 2009 and April 2011. Inclusion criteria for TAVI were (1) severe native AS with an area of <1 cm 2 or <0.6 cm 2 /m 2 and age 80 years or a logistic European System for Cardiac Operative Risk Evaluation score of 15% or age 65 years and at least one of the following complications: liver cirrhosis, pulmonary insufficiency (forced expiratory volume in 1 sec <1L), previous cardiac surgery, pulmonary hypertension (pulmonary artery systolic pressure of 60 mm Hg), porcelain aorta, recurrent pulmonary embolus, right ventricular insufficiency, thoracic burning sequelae with contraindication for open-chest surgery, history of mediastinum radiotherapy, severe connective tissue disease with contraindication for surgery, or cachexia (body mass index < 18 kg/m 2 ); (2) echocardiographic aortic valve annular diameter of 20 to 27 mm; and (3) ascending aortic diameter < 45 mm at the sinotubular junction.
All patients gave written informed consent for the procedure. Hemodynamic parameters and transthoracic echocardiography were performed immediately before and after the procedure.
Some of the data presented in this report were already included in one of our previous publications. In this study, we focused on arterial ventricular coupling variation analysis, not on Z va analysis. Furthermore, we did not analyze the predictability of these new parameters.
Ventricular and Systemic Arterial Hemodynamic Parameters
During the procedure, aortic catheterization was carried out simultaneously with LV catheterization immediately before and after aortic valve implantation, together with Doppler echocardiographic measurement. Catheter position for aortic pressure measurement was located 2 to 3 cm distal from the valve apparatus, while for LV pressure measurement, the catheter was positioned in the left ventricle. Systolic aortic pressure (SAP), diastolic aortic pressure, peak systolic LV pressure, and LV end-systolic pressure were calculated on pressure tracings. Furthermore, peak-to-peak and mean systolic transaortic pressures were calculated.
Stroke volume (SV) was measured using echocardiography in the LV outflow tract (LVOT) and was indexed to body surface area (SVi). Arterial pulse pressure (PP) was calculated as the difference between systolic and diastolic arterial pressures. The ratio between SVi and PP was used as an indirect measure of total SAC (SAC = SVi/PP).
SVR was estimated using the following formula: SVR = (80 × mean arterial pressure)/cardiac output, where mean arterial pressure is defined as diastolic pressure plus one third of PP.
Doppler Echocardiographic Data
All patients were examined using two-dimensional Doppler echocardiography with a Philips iE33 ultrasound system (Philips Medical Systems, Andover, MA) immediately (within 10–15 min) before and after TAVI (in the hemodynamic room).
LV Geometry
Measures of LV end-diastolic diameter, LV end-systolic diameter, end-diastolic ventricular septal thickness, end-systolic ventricular septal thickness, end-diastolic LV posterior wall thickness, and end-systolic LV posterior wall thickness were calculated using M-mode echocardiography. LV mass was calculated using the corrected formula of the American Society of Echocardiography and was indexed to body surface area and height 2.7 . LV end-diastolic volume and end-systolic volume were calculated from the apical two-chamber and four-chamber views using a modified Simpson’s method.
LV Systolic Function
LV ejection fraction was calculated as (end-diastolic volume − end-systolic volume)/end-diastolic volume × 100. The LVOT was measured in mid-systole from the parasternal long-axis view according to standard criteria. SV was calculated as the product of LVOT area and the LVOT pulsed Doppler velocity-time integral. LV cardiac output was calculated as the product of heart rate and SV and was indexed to body surface area.
LV Diastolic Function
Diastolic function was assessed by measuring peak velocities of the E wave (early diastole), the A wave (late diastole), the deceleration time of the E wave, and the Ea wave (average of early diastolic lateral and septal mitral annular velocities). The ratio between peak early mitral inflow velocity (E) and peak early diastolic myocardial velocity (Ea) was calculated (E/Ea).
Global LV Hemodynamic Load
As a measure of global LV load, we calculated Z va as (SAP + mean transvalvular pressure gradient)/SVi. Hence, Z va represents the valvular and arterial factors opposing ventricular ejection by absorbing the mechanical energy developed by the left ventricle. Therefore, global LV afterload in patients with AS by end-systolic meridional wall stress was estimated as follows:
end – systolic meridional wall stress = 1.35 ( LV end – systolic pressure ) ( LV end – systolic diameter ) 4 h ( 1 + h / LV end – systolic diameter ) ,
Assessment of AS and Bioprosthetic Valve
Transaortic peak velocity was measured using continuous-wave Doppler echocardiography from an apical view, and pressure gradient was calculated using the simplified Bernoulli equation. AVA was determined using the continuity equation method using the velocity-time integral ratio across the valve area in the LVOT obtained using pulsed-wave Doppler and was indexed for body surface area (AVAi). The energy loss index (ELI) was calculated as follows
ELI = [ AVA× ( Aa/Aa − AVA ) / body Surface area ] ,
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