Progression of hypertrophy and myocardial fibrosis in aortic stenosis: a multicenter cardiac magnetic resonance study

Everett, Russell J.; Tastet, Lionel; Clavel, Marie-Annick; Chin, Calvin W.L.; Capoulade, Romain; Vassiliou, Vassilios S.; Kwiecinski, Jacek; Gómez Pérez, Miguel Angel; van Beek, Edwin J.R.; White, Audrey C.; Prasad, Sanjay K.; Larose, Eric; Tuck, Christopher; Semple, Scott; Newby, David E.; Pibarot, Philippe; Dweck, Marc R.

doi:http://dx.doi.org/10.1161/CIRCIMAGING.117.007451

Progression of hypertrophy and myocardial fibrosis in aortic stenosis: a multicenter cardiac magnetic resonance study

Citation

Everett RJ, Tastet L, Clavel MA, Chin CWL, Capoulade R, Vassiliou VS et al. Progression of hypertrophy and myocardial fibrosis in aortic stenosis: a multicenter cardiac magnetic resonance study. Circ Cardiovasc Imaging. 2018 Jun;11(6):e007451. DOI: 10.1161/CIRCIMAGING.117.007451

Abstract

BACKGROUND: Aortic stenosis is accompanied by progressive left ventricular hypertrophy and fibrosis. We investigated the natural history of these processes in asymptomatic patients and their potential reversal post-aortic valve replacement (AVR). METHODS: Asymptomatic and symptomatic patients with aortic stenosis underwent repeat echocardiography and magnetic resonance imaging. Changes in peak aortic-jet velocity, left ventricular mass index, diffuse fibrosis (indexed extracellular volume), and replacement fibrosis (late gadolinium enhancement [LGE]) were quantified. RESULTS: In 61 asymptomatic patients (43% mild, 34% moderate, and 23% severe aortic stenosis), significant increases in peak aortic-jet velocity, left ventricular mass index, indexed extracellular volume, and LGE mass were observed after 2.1±0.7 years, with the most rapid progression observed in patients with most severe stenosis. Patients with baseline midwall LGE (n=16 [26%]; LGE mass, 2.5 g [0.8-4.8 g]) demonstrated particularly rapid increases in scar burden (78% [50%-158%] increase in LGE mass per year). In 38 symptomatic patients (age, 66±8 years; 76% men) who underwent AVR, there was a 19% (11%-25%) reduction in left ventricular mass index (P<0.0001) and an 11% (4%-16%) reduction in indexed extracellular volume (P=0.003) 0.9±0.3 years after surgery. By contrast midwall LGE (n=10 [26%]; mass, 3.3 g [2.6-8.0 g]) did not change post-AVR (n=10; 3.5 g [2.1-8.0 g]; P=0.23), with no evidence of regression even out to 2 years. CONCLUSIONS: In patients with aortic stenosis, cellular hypertrophy and diffuse fibrosis progress in a rapid and balanced manner but are reversible after AVR. Once established, midwall LGE also accumulates rapidly but is irreversible post valve replacement. Given its adverse long-term prognosis, prompt AVR when midwall LGE is first identified may improve clinical outcomes.