012 Longitudinal cardiac magnetic resonance assessment of diffuse and replacement myocardial fibrosis in aortic stenosis. (3rd April 2017) - Everett, RJ
Abstract : Objective: To investigate whether cardiac magnetic resonance (CMR) can assess the progression and regression of myocardial fibrosis in patients with aortic stenosis (AS). Methods: Sixty-three patients with aortic stenosis were followed up for 2 years with serial CMR and echocardiography: 28 patients (63±13 years, 68% male, 50% asymptomatic severe AS) did not undergo intervention ( natural history cohort ) and 35 patients (67±8 years, 73% male, 83% symptomatic severe AS) underwent aortic valve replacement (AVR) within the first year ( AVR cohort ). Replacement and diffuse myocardial fibrosis were assessed using the late gadolinium enhancement (LGE) and T1 mapping techniques respectively. Annualised change was calculated for all measures. Results: In the natural history cohort, left ventricular mass index (LVMi) increased over time (6%±1%, p<0.0001) and was accompanied by a fall in longitudinal systolic function (−4%±2% p=0.03). The indexed extracellular volume (iECV, a measure of diffuse fibrosis) also increased over time (7%±2%, p<0.0001). However, no changes were observed in native T1, post-contrast T1 or extracellular volume (ECV) fraction on serial imaging. Mid-wall LGE was observed in nine patients (32%). Absolute LGE mass increased by 3.8±0.8g (p<0.0001) amongst all the patients with baseline mid-wall LGE. Four patients with mid-wall LGE at baseline developed new areas of LGE in different myocardial segments. No patients without pre-existing mid-wall LGE developed new LGE during follow up. The AVR cohort displayed a fall in LVMi following surgery (−15%±2%, p<0.0001) mirrored by a reduction in diffuse fibrosis (iECV, −9%±2%, p<0.0001). The ECV fraction however was observed to increase (5% [2, 11], p<0.0001), with no change in native T1. Mid-wall LGE was present in 9 patients (26%). No patient went on to develop new LGE nor did existing LGE resolve in any patient and LGE mass did not change. Longitudinal systolic function increased following AVR (16%±6%, p=0.01). Conclusion: Changes in diffuse fibrosis can be tracked using iECV and increase with time in patients with AS alongside LV mass and replacement fibrosis. Following AVR there is a fall in LV mass driven predominantly by regression of cellular hypertrophy with more gradual reduction in diffuse fibrosis burden but no change in replacement fibrosis. Mid-wall LGE is present on baseline scan (white arrow) and new areas are seen on 1 year scan (red arrows). Following AVR there is no change in mid-wall LGE (white arrows). Annualised change in imaging measures is presented below in the natural history (black) and AVR (red) groups.