P6484Invasive and non-invasive characterisation of low gradient aortic stenosis
Authors: McConkey H Z R , Marber M , Lee J , Ellis H , Joseph J , Allen C , Rahman H , Patterson T , Scannell C , Pibarot P , Chiribiri A , Redwood S , Prendergast B D 
Published: October 2019

Abstract

Background
Low gradient severe aortic stenosis (LGAS) is associated with unfavourable outcomes when compared to high gradient aortic stenosis (HGAS), yet the contributing pathophysiology is poorly understood.

Methods
Symptomatic LGAS and HGAS patients undergoing trans-catheter aortic valve implantation (TAVI) underwent 3T stress perfusion cardiac magnetic resonance imaging (CMR) pre-(within 24 hours) and post-(4–6 months) TAVI. Left ventricular (LV) contractility and coronary flow/pressure were measured during hyperaemia and rapid pacing, immediately before and after TAVI, using a conductance LV catheter and dual-pressure and Doppler sensor–tipped guidewire in the mid-left anterior descending coronary artery.

Results
24 patients were recruited resulting in 19 suitable datasets (LGAS N=9, HGAS N=10, equally matched for comorbidities and B-natriuretic peptide level). LGAS patients had a smaller LV end diastolic volume index (p=0.035) and lower LV mass index (LVMI) (p=0.037). Pre-TAVI stress global endocardium-epicardium gradient was 0.88±0.09 and global myocardial perfusion reserve (MPR) 2.0±0.48 in 14 patients (6 LGAS and 8 HGAS patients, no difference between groups). Pre-TAVI, baseline coronary data demonstrated lower augmentation pressure (AP, p=0.035) and augmentation index (AIx, p=0.02) in the LGAS group. LGAS patients also exhibited a shorter ejection time (p=0.015), larger forward compression waves during rest, hyperaemia and rapid pacing, and smaller backward expansion waves (BEW) (p=0.001). Lower baseline end systolic pressure (p=0.004), inotropy (dP/dt+, p=0.045), lusitropy (dP/dt-, p=0.069), and stroke work (p=0.019) were observed in the LGAS group. Whilst LV size was smaller the LGAS group, rapid pacing induced a more significant drop in end systolic volume (p=0.045) and ejection fraction (p=0.015) in patients with HGAS. Post-TAVI, the hyperaemic BEW fell sharply (p<0.001), along with coronary VTI (p=0.02), and average pulse velocity (p=0.028), and AP and AIx remained lower (p=0.034 and p=0.031, respectively). The forward expansion wave was reduced in LGAS during rapid pacing. The HGAS group displayed a more profound drop in dP/dt+ (p=0.011) and dP/dt- p=0.014) at rest following intervention. Repeat CMR demonstrated statistically significant reduction in LV size and LVMI (p=0.012 and p<0.001, respectively) with significant increase in 3D global peak radial, circumferential and longitudinal strain (p=0.004, p=0.001 and p=0.018, respectively). Post-TAVI stress global endocardium-epicardium gradient was 0.88±0.13 and MPR 2.46±0.59 (improved from pre-TAVI, p=0.05). There was no difference in remodelling patterns or perfusion between the two groups.

Conclusion
This is the first study detailing the combined invasive and CMR pathophysiological changes in LGAS. Despite invasive parameters indicating a disease of less severe AS, the level of perfusion abnormality is disproportionate which may in part, relate to their adverse prognosis.

Acknowledgement/Funding
This research is funded by a Clinical Research Training Fellowship grant from the British Heart Foundation (FS/16/51/32365).