Spath Nicholas B, Gomez Miquel, Everett Russell J, Semple Scott, Chin Calvin W L, White Audrey C, Japp Alan G, Newby David E, Dweck Marc R
BHF/University Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, 47 Little France Crescent, Edinburgh EH16 4SB, Scotland (N.B.S., R.J.E., S.S., A.C.W., A.G.J., D.E.N., M.R.D.); Hospital del Mar Medical Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain (M.G.); Department of Cardiovascular Science, National Heart Center, Singapore (C.W.L.C.); and Department of Cardiology, Royal Infirmary of Edinburgh, Edinburgh, Scotland (A.G.J., D.E.N., M.R.D.).
Radiol Cardiothorac Imaging. 2019 Oct 31;1(4):e190027. doi: 10.1148/ryct.2019190027. eCollection 2019 Oct.
To use global longitudinal strain (GLS) as a marker of left ventricular decompensation in aortic stenosis and to investigate the relationship of GLS measured with cardiac MRI with markers of myocardial fibrosis, symptom development, remodeling, and clinical outcomes.
Patients with aortic stenosis and healthy control subjects were assessed. GLS was assessed by using cardiac MRI feature tracking, diffuse fibrosis by T1 mapping, and replacement fibrosis using late gadolinium enhancement. Follow-up was prospective for the primary endpoint of all-cause mortality.
GLS was reduced in aortic stenosis ( = 159) compared with control subjects ( = 41) (-17.6% ± 3.1 [standard deviation] vs -18.9% ± 2.6, = .02). GLS demonstrated weak associations with aortic stenosis severity (V; = 0.24, = .0005) but showed moderate correlation with T1 mapping measures of myocardial fibrosis (eg, indexed extracellular volume [iECV]; = 0.43, < .0001). Moreover, GLS was reduced in patients with midwall fibrosis compared with control subjects ( < .001), although values were similar to those of patients with myocardial infarction ( = .25). In adjusted analyses, GLS was associated with total myocardial fibrosis burden (iECV) and ejection fraction (both < .001). GLS offered poor discrimination between disease states, inability to distinguish between control subjects and patients (area under the curve [AUC], 0.60), presence or absence of fibrosis (AUC, 0.63), or symptomatic severity (left ventricular decompensation AUC, 0.64). At follow-up (median, 1466 days), 21 patients died. GLS did not independently predict clinical outcomes.
GLS correlates with established markers of myocardial fibrosis. However, widespread utility of single GLS measurements may be limited by overlap between disease states and its inability to predict clinical outcomes beyond current established markers.© RSNA, 2019
将整体纵向应变（GLS）用作主动脉瓣狭窄时左心室失代偿的标志物，并研究心脏磁共振成像测量的GLS与心肌纤维化、症状发展、重塑及临床结局标志物之间的关系。
对主动脉瓣狭窄患者和健康对照者进行评估。采用心脏磁共振成像特征追踪评估GLS，通过T1映射评估弥漫性纤维化，使用延迟钆增强评估替代性纤维化。对全因死亡率这一主要终点进行前瞻性随访。
与对照者（n = 41）相比，主动脉瓣狭窄患者（n = 159）的GLS降低（-17.6% ± 3.1[标准差]对-18.9% ± 2.6，P = .02）。GLS与主动脉瓣狭窄严重程度（Vmax；r = 0.24，P = .0005）呈弱相关性，但与心肌纤维化的T1映射测量值（如指数化细胞外容积[iECV]；r = 0.43，P < .0001）呈中度相关。此外，与对照者相比，中层心肌纤维化患者的GLS降低（P < .001），尽管其值与心肌梗死患者相似（P = .25）。在多因素分析中，GLS与心肌纤维化总负担（iECV）和射血分数均相关（均P < .001）。GLS对疾病状态的鉴别能力较差，无法区分对照者与患者（曲线下面积[AUC]，0.60）、有无纤维化（AUC，0.63）或症状严重程度（左心室失代偿AUC，0.64）。随访（中位时间，1466天）时，21例患者死亡。GLS不能独立预测临床结局。
GLS与已确立的心肌纤维化标志物相关。然而，单次GLS测量的广泛应用可能受到疾病状态重叠及其无法预测现有标志物以外临床结局的限制。©RSNA，2019
