Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis.
Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis.
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DOI：
10.1016/j.jcmg.2016.10.007
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发表时间：
2017-11
期刊：
影响因子：
--
通讯作者：
Dweck MR
中科院分区：
文献类型：
--
作者：
Chin CWL;Everett RJ;Kwiecinski J;Vesey AT;Yeung E;Esson G;Jenkins W;Koo M;Mirsadraee S;White AC;Japp AG;Prasad SK;Semple S;Newby DE;Dweck MR
心脏磁共振（CMR）用于研究主动脉瓣狭窄患者的细胞外室和心肌纤维化，以及它们与左心室失代偿和死亡率的其他指标的关系。进行性心肌纤维化促使主动脉瓣狭窄患者从肥大转变为心力衰竭。弥漫性纤维化与细胞外容积扩张相关，可通过T1标测检测，而晚期钆增强（LGE）可检测替代性纤维化。在一项前瞻性观察性队列研究中，203例受试者（166例主动脉瓣狭窄[69岁; 69%为男性]; 37例健康志愿者[68岁; 65%为男性]）接受了综合表型表征和临床成像和生物标志物评价。在CMR上，我们量化了以体表面积（iECV）为指数的心肌细胞外总体积。对照组的iECV正常上限（22.5 ml/m2）用于定义细胞外室扩张。还确定了更换中壁LGE的区域。在2.9 ± 0.8年的随访期间确定全因死亡率。iECV与心肌活检的弥漫性组织学纤维化具有良好的相关性（r = 0.87; p < 0.001; n = 11），并且在主动脉瓣狭窄患者中增加（23.6 ± 7.2 ml/m2 vs.对照组16.1 ± 3.2 ml/m2; p < 0.001）。iECV与LGE一起用于将患者分为正常心肌（iECV <22.5 ml/m2; 51%的患者）、细胞外扩张（iECV ≥22.5 ml/m2; 22%）和替代性纤维化（存在中壁LGE，27%）。有证据表明心肌肥厚、心肌损伤、舒张功能障碍和纵向收缩功能障碍的增加与进行性左心室失代偿一致此外，这种分类具有预后价值，未校正的全因死亡率逐步增加。（分别为8例死亡/1,000患者-年vs. 36例死亡/1,000患者-年vs. 71例死亡/1,000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患者的心室失代偿。这在跟踪瓣膜疾病的心肌健康和优化瓣膜置换术的时机方面具有重大前景。(The心肌纤维化在主动脉瓣狭窄患者中的作用; NCT 01755936）
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/m2) 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/m2 vs. 16.1 ± 3.2 ml/m2 in control subjects; p < 0.001). iECV was used together with LGE to categorize patients with normal myocardium (iECV <22.5 ml/m2; 51% of patients), extracellular expansion (iECV ≥22.5 ml/m2; 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)
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影响因子：
37.8
作者：
RAKUSAN, K;FLANAGAN, MF;VANPRAAGH, R
通讯作者：
VANPRAAGH, R
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6.4
作者：
Maceira, A. M.;Prasad, S. K.;Pennell, D. J.
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Pennell, D. J.
影响因子：
39.3
作者：
Chin, Calvin W. L.;Shah, Anoop S. V.;Dweck, Marc R.
通讯作者：
Dweck, Marc R.