BHF/Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom; Department of Cardiovascular Science, National Heart Center, Singapore.
BHF/Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom.
JACC Cardiovasc Imaging. 2017 Nov;10(11):1320-1333. doi: 10.1016/j.jcmg.2016.10.007. Epub 2016 Dec 21.
Cardiac magnetic resonance (CMR) was used to investigate the extracellular compartment and myocardial fibrosis in patients with aortic stenosis, as well as their association with other measures of left ventricular decompensation and mortality.
Progressive myocardial fibrosis drives the transition from hypertrophy to heart failure in aortic stenosis. Diffuse fibrosis is associated with extracellular volume expansion that is detectable by T1 mapping, whereas late gadolinium enhancement (LGE) detects replacement fibrosis.
In a prospective observational cohort study, 203 subjects (166 with aortic stenosis [69 years; 69% male]; 37 healthy volunteers [68 years; 65% male]) underwent comprehensive phenotypic characterization with clinical imaging and biomarker evaluation. On CMR, we quantified the total extracellular volume of the myocardium indexed to body surface area (iECV). The iECV upper limit of normal from the control group (22.5 ml/m) was used to define extracellular compartment expansion. Areas of replacement mid-wall LGE were also identified. All-cause mortality was determined during 2.9 ± 0.8 years of follow up.
iECV demonstrated a good correlation with diffuse histological fibrosis on myocardial biopsies (r = 0.87; p < 0.001; n = 11) and was increased in patients with aortic stenosis (23.6 ± 7.2 ml/m vs. 16.1 ± 3.2 ml/m in control subjects; p < 0.001). iECV was used together with LGE to categorize patients with normal myocardium (iECV <22.5 ml/m; 51% of patients), extracellular expansion (iECV ≥22.5 ml/m; 22%), and replacement fibrosis (presence of mid-wall LGE, 27%). There was evidence of increasing hypertrophy, myocardial injury, diastolic dysfunction, and longitudinal systolic dysfunction consistent with progressive left ventricular decompensation (all p < 0.05) across these groups. Moreover, this categorization was of prognostic value with stepwise increases in unadjusted all-cause mortality (8 deaths/1,000 patient-years vs. 36 deaths/1,000 patient-years vs. 71 deaths/1,000 patient-years, respectively; p = 0.009).
CMR detects ventricular decompensation in aortic stenosis through the identification of myocardial extracellular expansion and replacement fibrosis. This holds major promise in tracking myocardial health in valve disease and for optimizing the timing of valve replacement. (The Role of Myocardial Fibrosis in Patients With Aortic Stenosis; NCT01755936).
心脏磁共振（CMR）用于研究主动脉瓣狭窄患者的细胞外间隙和心肌纤维化，以及它们与左心室失代偿和死亡率的其他衡量标准的关系。
进行性心肌纤维化推动了主动脉瓣狭窄从心肌肥厚向心力衰竭的转变。弥漫性纤维化与细胞外容积扩张有关，可通过 T1 映射检测到，而晚期钆增强（LGE）则可检测到替代纤维化。
在一项前瞻性观察队列研究中，203 名受试者（166 名主动脉瓣狭窄患者[69 岁；69%为男性]；37 名健康志愿者[68 岁；65%为男性]）接受了临床影像学和生物标志物评估的全面表型特征描述。在 CMR 上，我们量化了心肌细胞外体积与体表面积的比值（iECV）。对照组的 iECV 上限（22.5ml/m）用于定义细胞外间隙扩张。还确定了中层壁 LGE 的替代区域。在 2.9±0.8 年的随访期间，确定了全因死亡率。
iECV 与心肌活检的弥漫性组织纤维化具有良好的相关性（r=0.87；p<0.001；n=11），且在主动脉瓣狭窄患者中增加（23.6±7.2ml/m与对照组 16.1±3.2ml/m相比；p<0.001）。iECV 与 LGE 一起用于对具有正常心肌的患者进行分类（iECV<22.5ml/m；51%的患者）、细胞外扩张（iECV≥22.5ml/m；22%）和替代纤维化（中层壁 LGE 存在，27%）。证据表明，随着左心室失代偿的进行，存在逐渐增加的心肌肥厚、心肌损伤、舒张功能障碍和纵向收缩功能障碍（所有 p<0.05）。此外，这种分类具有预后价值，未经调整的全因死亡率逐渐增加（分别为每 1000 患者年 8 例死亡/1000 患者年、36 例死亡/1000 患者年和 71 例死亡/1000 患者年；p=0.009）。
CMR 通过识别心肌细胞外扩张和替代纤维化来检测主动脉瓣狭窄中的心室失代偿。这在瓣膜疾病中跟踪心肌健康和优化瓣膜置换时机方面具有重要意义。（主动脉瓣狭窄患者的心肌纤维化作用；NCT01755936）。
