Key result
In severe aortic stenosis, global longitudinal strain worsened across groups with compensated vs decompensated hypertrophy and correlated with collagen volume.
Why the study?
Does global longitudinal systolic strain correlate with myocardial structural changes in patients with severe symptomatic aortic stenosis and preserved ejection fraction?
Observational (n=26)
Does global longitudinal systolic strain correlate with myocardial structural changes in patients with severe symptomatic aortic stenosis and preserved ejection fraction?
Answers are grounded in this paper and cite their sources.
In patients with severe symptomatic aortic stenosis and preserved ejection fraction, altered global longitudinal systolic strain correlates with increased collagen volume and elevated LVEDP, indicating early myocardial structural and contractile changes.
Background: In severe symptomatic aortic stenosis (SSAS) altered global longitudinal systolic strain (GLSS) would correlate with changes in myocardial histological architecture and could identify early contractile involvement in patients with preserved ejection fraction (PEF).Objective: The aim of this study was to analyze GLSS, collagen volume (CV), myocyte area (MyAr) and contractile involvement in patients with SSAS and PEF.Methods: Twenty six patients with SSAS and PEF (67±11 years old, 53% male) were included in the study. A preoperative hemodynamic study and an intraoperative endomyocardial biopsy were performed to determine CV and MyAr. Three groups of patients were identified: G1: compensated left ventricular hypertrophy (LVH) without coronary disease (n=8); G2: decompensated LVH without coronary disease (n=7) and G3: decompensated LVH with coronary disease (n=11). GLSS was normalized by stroke volume, meridional end-systolic wall stress (δ) and end-diastolic diameter (EDD).Results: No significant differences in stroke volume, δ and EDD were observed between groups G1, G2 and G3. Differences between groups were observed in: CV (%) (G1: 4.7 ± 1.2, G2: 8.4 ± 1.2, G3: 11.0 ± 3.0; p < 0.01), MyAr (mm2) (G1: 328.7 ± 66.2, G2: 376.7 ± 21.9, G3: 385.0 ± 13.0; p = 0.01), LVEDP (mm Hg) (G1: 13.1 ± 1.5, G2: 19.0 ± 3.8, G3: 23.6 ± 5.8; p < 0.01), +dP/dtmax (mm Hg/sec / LVEDP, mm Hg) (G1: 176.4 ± 45.5, G2: 89.6 ± 20.1, G3: 113.1 ± 43.7; p < 0.01), and SGLS (%) (G1: -17.9 ± 4.2, G2: -13.5 ± 2.5, G3: -13.6 ± 3; p = 0.021). SGLS correlated with CV and LVEDP and it evidenced a trend to correlate with a contractility index (+dP/dtmax mm Hg/s / LVEDP, mm Hg).Conclusions: Altered GLSS in patients with SSAS and PEF expresses myocardial structural changes related to increase in CV, which is associated with enhanced LVEDP and probable myocardial contractile failure.
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Hita et al. (2014) conducted an observational in Severe symptomatic aortic stenosis with preserved ejection fraction (n=26). Decompensated left ventricular hypertrophy (with or without coronary disease) vs. Compensated left ventricular hypertrophy without coronary disease was evaluated on Differences in collagen volume, myocyte area, LVEDP, +dP/dtmax, and global longitudinal strain between LVH groups (p=0.021). In severe aortic stenosis, global longitudinal strain worsened across groups with compensated vs decompensated hypertrophy and correlated with collagen volume.
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