Bedside Renal Doppler Ultrasonography and Acute Kidney Injury after TAVR.

Acute kidney injury (AKI) following transcatheter aortic valve replacement (TAVR) is associated with a dismal prognosis. Elevated renal resistive index (RRI), through renal Doppler ultrasound (RDU) evaluation, has been associated with AKI development and increased systemic arterial stiffness. Our pilot study aimed to investigate the performance of Doppler based RRI to predict AKI and outcomes in TAVR patients. From May 2018 to May 2019, 100 patients with severe aortic stenosis were prospectively enrolled for TAVR and concomitant RDU evaluation at our institution (Nouvel Hôpital Civil, Strasbourg University, France). AKI by serum Creatinine (sCr-AKI) was defined according to the VARC-2 definition and AKI by serum Cystatin C (sCyC-AKI) was defined as an sCyC increase of greater than 15% with baseline value. Concomitant RRI measurements as well as renal and systemic hemodynamic parameters were recorded before, one day, and three days after TAVR. It was found that 10% of patients presented with AKIsCr and AKIsCyC. The whole cohort showed higher baseline RRI values (0.76 ± 0.7) compared to normal known and accepted values. AKIsCyC had significant higher post-procedural RRI one day (Day 1) after TAVR (0.83 ± 0.1 vs. 0.77 ± 0.6, CI 95%, p = 0.005). AUC for AKIsCyC was 0.766 and a RRI cut-off value of ≥ 0.795 had the most optimal sensitivity/specificity (80/62%) combination. By univariate Cox analysis, Mehran Risk Score, higher baseline right atrial pressure at baseline > 0.8 RRI values one day after TAVR (HR 6.5 (95% CI 1.3-32.9; p = 0.021) but not RRI at baseline were significant predictors of AKIsCyC. Importantly, no significant impact of baseline biological parameters, renal or systemic parameters could be demonstrated. Doppler-based RRI can be helpful for the non-invasive assessment of AKI development after TAVR.

1), aortic stenosis (AS) patients face 3 major resistors: R1 the total pulmonary resistance made up of left ventricular (LV) filling pressure plus pulmonary vascular resistance that governs LV filling; R2, the resistance offered by the aortic valve; and R3, the systemic vascular resistance (SVR).
Following this principle, if resistance drops without a concomitant increase in output, pressure must also fall. In severe AS, R2 (valve resistance) substantially exceeds R3 (SVR) and TAVR allows an instant and unique reduction of the trans-aortic gradient, normalization of the aortic valve area. R2 drops to normal values (transprosthetic gradient assumed to be 5 to10mmHg).
As such, a fall in R2 caused by TAVR may increase LVEF and cardiac output in particular in low-flow low-gradient AS. However Ohm's model applied to aortic stenosis is too restrictive and doesn't integrate the dynamic interaction between the heart and the systemic circulation known as the ventriculo-arterial coupling concept.

The ventriculo-arterial coupling
The dynamic interaction between the heart and the systemic circulation allows the cardiovascular system to provide adequate cardiac output and arterial pressures to ensure adequate organ perfusion. The interplay between cardiac function and arterial system, which in turn affects ventricular performance, is known as the ventriculo-arterial coupling and is affected in AS. Because left ventricular stroke volume depends on myocardial contractility and loading conditions (preload and afterload) both myocardial, valvular, and arterial dysfunction can lead to ventriculo-arterial decoupling with resulting decrease in stroke volume, cardiac output, and organ perfusion including kidneys.
Addressing the post TAVR AKI question, both systemic and local renal modulation of the arterial system compliance and resistance with respect to left ventricular systolic performance is of paramount importance to address potential cardio-renal interaction The interdependence between the heart and the kidneys in TAVR has been a topic of extensive research but no study to our knowledge was specifically designed to tackle the question whether hemodynamic cardio-renal parameters could predict and influence AKI development.
In this study, we sought to provide extensive data investigating the potential link between cardiac function and output, renal function in a TAVR population with careful cardiac, renal and hemodynamic profiling.

Echocardiography protocol and hemodynamic parameters
Concomitant echocardiography was performed after RDU measurements 12 hours prior, 24 hours and 72 hours after TAVR procedure. The following echocardiographic and clinical variables were collected from each patient: heart rate; systolic, diastolic, and mean blood

Valvulo-arterial impedance
Common indices used for the evaluation of AS severity (aortic valve area, mean transvalvular pressure gradient, peak aortic jet velocity) focus on the extent of aortic valve disease. However, the ventricle in patients with AS face increased afterload from the valve but also from the arterial system. Reduced systemic aortic compliance increases the afterload and contributes to a reduced left ventricular function (1). Valvulo-arterial impedance incorporates both arterial impedance and valve severity. Valvulo-arterial impedance has been linked in several studies to worse outcome in medically (2)(3) and in TAVR managed aortic stenosis patients (4-8). Valvulo-arterial impedance is calculated by dividing the estimated left ventricular systolic pressure (systolic arterial pressure + mean transvalvular gradient) by the stroke volume indexed for the body surface area.

Others systemic vascular indices
Others vascular indices where calculated: -Total arterial load was measured as indexed arterial elastance ([0.9×systolic blood pressure]/ stroke volume index) (9)(10) -Pulsatile arterial load was measured by pulse pressure Pulse pressure = Systolic blood pressure -Diastolic blood pressure.
The resistive component of arterial load was evaluated by the systemic vascular resistance.The pulsatile load, which is related to the stiffness of the conduit vessels, was appreciated by pulse pressure and systemic arterial compliance

Renal vascular indices: Rational
Mean arterial pressure represents the renal preload while renal afterload is considered to be mostly driven by central venous pressure and intraabdominal pressure. While Renal blood flow can be assessed by RDU according to the following formula : [Renal blood flow (mL/min) = time-averaged flow velocity (cm/s) × cross-sectional area mm2 × 60 (s)]; such measurement is known to be difficult to measure with high intra and interobserver variability. An alternative is to consider that renal blood flow represents 20% of the cardiac output. According to these definitions, local renal hemodynamic criteria can be calculated as follow: