Key result
End-systolic wall stress strongly predicts reduced LVEF in severe aortic stenosis better than myocardial fibrosis.
Why the study?
The extent, pattern, and functional impact of myocardial fibrosis in severe aortic stenosis with afterload mismatch was poorly understood.
Does end-systolic wall stress or myocardial fibrosis better predict reduced ejection fraction in patients with severe high-gradient aortic stenosis?
Observational (n=58)
Does end-systolic wall stress or myocardial fibrosis better predict reduced ejection fraction in patients with severe high-gradient aortic stenosis?
In severe high-gradient aortic stenosis with reduced ejection fraction, high afterload (end-systolic wall stress) rather than myocardial fibrosis is the primary driver of systolic impairment.
End-systolic wall stress may predominate over fibrosis in reduced LVEF with severe AS; hypothesis-generating and requires prospective validation.
BACKGROUND: Afterload mismatch (AM) refers to high-gradient (mean gradient ≥40 mm Hg) severe aortic stenosis (AS) with reduced left ventricular ejection fraction (LVEF <50%) that is hypothesised to arise from mechanisms other than true contractile impairment. The extent, pattern and functional impact of myocardial fibrosis (MF), which is associated with systolic impairment, is poorly understood in the context of AM. METHODS: High-gradient severe AS patients with (n=25; low ejection fraction high-gradient, LEF-HG) and without (n=33; normal ejection fraction high-gradient (NEF-HG)) reduced LVEF underwent cardiovascular MRI. Using T1 mapping, extracellular volume (ECV) fraction and late gadolinium enhancement (LGE), the extent and pattern of MF was compared between the two groups. End-systolic wall stress (ESWS) as a measure of afterload was estimated, and its relationship with LVEF was compared with that of MF and LVEF. In the LEF-HG group, high ESWS with cavity dilation and significant hypertrophy were observed compared with the NEF-HG group. MF was present in both groups with a significantly higher burden in the LEF-HG group (T1 time 1061±22 vs 1041±33 ms, ECV 26%±3% vs 24%±3%, LGE mass 4.3 (1.7-9.3) vs 0.1 (0.06-3.39) g). The association between MF and LVEF was weak, while ESWS was strongly associated with LVEF (r -0.8, p<0.0001) and was the best predictor of LVEF in multivariate prediction analysis. CONCLUSIONS: MF was present in both groups with a higher burden in those with LEF-HG AS. High ESWS, that is, afterload, rather than MF, was the strongest predictor of LVEF. While MF may not directly impact systolic function in AM, it is still an important factor to account for in AS given its association with increased mortality.
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Rajah et al. (2025) conducted an observational in High-gradient severe aortic stenosis (n=58). Low ejection fraction high-gradient (LEF-HG) severe AS vs. Normal ejection fraction high-gradient (NEF-HG) severe AS was evaluated on Association between end-systolic wall stress (ESWS) and LVEF (r -0.8, p=<0.0001). End-systolic wall stress was strongly associated with LVEF (r -0.8, p<0.0001) and was the strongest predictor of reduced ejection fraction in severe aortic stenosis, rather than myocardial fibrosis.
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