Microvascular dysfunction and myocardial fibrosis impact on left ventricular myocardial deformation in hypertrophic cardiomyopathy: per segment analysis by magnetic resonance imaging

European Heart Journal - Cardiovascular Imaging(2022)

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摘要
Abstract Funding Acknowledgements Type of funding sources: None. Background Left ventricular hypertrophy (LVH) and microvascular dysfunction are hallmarks of hypertrophic cardiomyopathy (HCM). We hypothesized that microvascular dysfunction contributes to LV myocardial deformation impairment. Methods Prospective evaluation of adult patients with HCM (patients with "end-stage" HCM, prior septal reduction therapy or epicardial coronary artery disease were excluded). All underwent a cardiac magnetic resonance (CMR) protocol (1.5-T), from which the following parameters were analysed: maximal LV wall thickness (MLVWT), T1 and T2 mapping, extracellular volume, late gadolinium enhancement (LGE) and stress perfusion. Three-dimensional strain analysis was obtained by using feature-tracking from cine images. Results were stratified according to the 16 American Heart Association segments. Multivariate regression analyses for longitudinal, circumferential and radial strain were performed. Results A total of 1200 myocardial segments were analysed (Table 1) (75 patients, 63% male, age 54.6 ± 14.7 years) including 61% with asymmetric septal LVH, 29% with apical LVH, 8% with concentric LVH, 28% exhibiting LV outflow tract obstruction. The mean MLVWT was 20 ± 4.5mm. Higher values of longitudinal strain (lower deformation) were found in segments with MLVWT ≥15mm (β-estimate: 2.31, 95% CI 0.91-3.70, p < 0.001) and in patients with obstructive HCM (β-estimate: 2.44, 95% CI 1.15-3.72, p < 0.001]) (Table 2). No association was found between perfusion defects, LGE and longitudinal strain. Higher values of circumferential strain (lower deformation) were found in segments with MLVWT 12-14mm (β-estimate: 2.31, 95% CI 1.36-3.25, p < 0.001), MLVWT ≥15mm (β-estimate: 5.29, 95% CI 4.47-6.12, p < 0.001), with perfusion defects (β-estimate: 2.75, 95% CI 2.0-3.5, p < 0.001), with LGE (β-estimate: 2.49, 95% CI 1.77-3.22, p < 0.001) and in patients with obstructive HCM (β-estimate: 1.25, 95% CI 0.44-2.06, p = 0.003). Lower radial strain values were found in segments with MLVWT 12-14mm (β-estimate: -10.64, 95% CI -13.95 to -7.33, p < 0.001), with MLVWT ≥15mm (β-estimate: -20.67, 95% CI -23.36 to -17.97, p < 0.001), with perfusion defects (β-estimate: -10.60, 95% CI -13.08 to -8.13, p < 0.001), and with LGE (β-estimate: -10.49, 95% CI -12.86 to -8.11) (table 2). Diabetes, hypertension and BMI > 25 kg/m2 were also associated with impaired myocardial deformation. Male gender correlated with worse radial and circumferential strain values. No association was found between parametric mapping values and LV myocardial deformation. Conclusion In patients with HCM, three-dimensional speckle tracking parameters for LV systolic function were particularly impaired in segments with LVH, microvascular dysfunction or fibrosis. LVH was associated with abnormal longitudinal, circumferential and radial strain while perfusion defects and LGE correlated with impaired circumferential strain and radial strain. Abstract Table 1: Characteristics of AHA segments Abstract Table 2: Multivariate analysis
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关键词
ventricular myocardial deformation,myocardial fibrosis impact,microvascular dysfunction,magnetic resonance imaging
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