Myocardial extracellular volume pre and post aortic valve replacement in severe aortic stenosis

Introduction

Histological studies show that myocardial fibrosis accompanies cellular hypertrophy in severe aortic stenosis (AS). Following aortic valve replacement (AVR), left ventricular hypertrophy regresses by 20%-30% by one year (1) and both cellular hypertrophy and fibrosis may regress as early as 6 months post AVR (2, 3). With T1 mapping, CMR can measure diffuse fibrosis by quantifying extracellular volume fraction (ECV) which reflects the fraction of the myocardium occupied by the extracellular matrix and is an independent predictor of mortality and outcome in patients with severe AS (4). Previous methods of measuring T1 and quantifying ECV in patients with severe AS have used Modified Look-Locker Inversion recovery (MOLLI) sequences and have shown a significant reduction in both cell volume and extracellular matrix volume 12 months post AVR(5). We aimed to investigate the changes in ECV seen pre and post AVR, using multiparametric SAturation-recovery single-SHot Acquisition (mSASHA) which has higher accuracy and precision due to its reduced sensitivity to T2 (6). This is particularly important as the T2 of blood changes markedly after contrast administration (7).

Methods

16 patients with severe AS referred for AVR were recruited after consent. Mean age was 66 ± 6 years with 56% male. Patients were scanned before (visit 1) and after AVR (visit 2). T1 measurements were made on a 3 T Siemens system using mSASHA before contrast and at 10 minutes post gadobutrol injection (0.15 mmol/kg) as per recommendations by SCMR for calculation of ECV (8) . Derived indexed cell volume and derived indexed matrix volume were calculated from the product of left ventricular mass index ´ [1-ECV] and ECV, respectively as previously described.(5)

Results

Visit 2 data were acquired 167 ± 44 days post AVR. There was significant reduction in left ventricular hypertrophy, left ventricular end-diastolic volume and left ventricular mass (table 1, figure 1). Post AVR there was a significant reduction in derived indexed cell volume and, while there was a significant increase in ECV, there was no significant change in derived indexed matrix volume (table 2, figure 2).

Conclusion

For the first time using mSASHA, we have shown that in patients with severe AS, less than 6 months post AVR, there is a significant reduction in cell volume (derived indexed cell volume decreases) with no significant change in matrix volume (derived indexed matrix volume remains stable). Further studies will need to be undertaken to determine if matrix volume decreases at 12 months using mSASHA.

Conflict of Interest

No