In HCM patients, early diastolic slope of strain-volume loops negatively correlates with maximal wall thickness (ρ=-0.39, p=0.016), indicating hypertrophy affects diastolic function.
In patients with HCM, 3D strain-volume loop parameters during early diastole correlate with the magnitude of hypertrophy (wall thickness and mass) but not with myocardial fibrosis.
Absolute Event Rate: 0% vs 0%
Abstract Background Left ventricular (LV) longitudinal strain-volume loops (SVLs) combine temporal changes in global longitudinal strain (GLS) with LV volume across a cardiac cycle. SVLs have been previously examined in patients with bicuspid aortic valve, Duchenne muscular dystrophy and healthy individuals, providing insights into cardiac hemodynamics and underlying pathophysiological alterations. Purpose This study aimed to evaluate the association between SVL-derived quantitative metrics and phenotypic characteristics of hypertrophic cardiomyopathy (HCM), including maximal wall thickness (MWT), LV mass indexed to body surface area (LVMi) and presence or not of LGE. Methods Adult HCM patients underwent 3D-speckle tracking echocardiography and cardiac magnetic resonance with late gadolinium enhancement (LGE) on the same day. LV GLS and LV volume data were automatically exported to a spreadsheet. Cubic spline interpolation was applied to generate 300-points for each cardiac phase and construct the SVLs. Based on previous studies, the following SVL parameters were assessed: systolic slope of strain-volume relation (Sslope), slope during the first 5% of SV in systole (ESslope) and diastole (EDslope), slope during the last 5% of SV in diastole (LDslope), and the mean systolic-diastolic strain difference at any given volume (total, early diastolic, and late diastolic uncoupling) (Figure 1). Additionally, presence of fibrosis was defined by LGE (5 standard deviations compared to nulled myocardium) in CMR slices. Results A total of 39 HCM patients (mean age 50±15 years, 32 (82%) males) were included. LGE was present in 27 (69%) patients, while 16 (41%) had LV outflow tract obstruction (LVOTO30 mm Hg at rest). Mean LVMi was 78.6±14.6 g/m2 and median MWT 19 (16 - 21) mm (evaluated by 3D echocardiography). Among the SVL-derived parameters tested, the slope during the first 5% of SV in diastole (early diastolic slope – EDslope) showed a statistically significant correlation with MWT (ρ=-0.39, p=0.016) (Figure 2). The early diastolic uncoupling corresponding to the first 2/3 of SV in diastole also presented a positive correlation with LVMi (ρ=0.37, p=0.021). LGE presence was not correlated with SVL quantitative parameters. Conclusion SVLs is an innovative application of 3D deformation imaging, enlightening not only the systolic phase of cardiac cycle, but also the complicated inter-relation between longitudinal strain and volume changes during diastole. In a simplified manner, our data suggest that magnitude of hypertrophy and not fibrosis, affects myocardial deformation/relaxation during early diastolic phase, opening new perspectives and questions in the study of HCM diastology. The role of SVLs in HCM is yet to be examined in larger studies, necessitating also cross-validation with invasive-hemodynamic data.
Pagourelias et al. (Sat,) reported a other. In HCM patients, early diastolic slope of strain-volume loops negatively correlates with maximal wall thickness (ρ=-0.39, p=0.016), indicating hypertrophy affects diastolic function.