Delayed hyperenhancement in magnetic resonance imaging of left ventricular hypertrophy caused by aortic stenosis and hypertrophic cardiomyopathy: visualisation of focal fibrosis
Delayed hyperenhancement in magnetic resonance imaging of left ventricular hypertrophy caused by aortic stenosis and hypertrophic cardiomyopathy: visualisation of focal fibrosis
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DOI：
10.1136/hrt.2005.079392
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发表时间：
2006-10-01
期刊：
影响因子：
5.7
通讯作者：
Luchner, A.
中科院分区：
文献类型：
--
作者：
Debl, K.;Djavidani, B.;Luchner, A.
目的：目的：比较钆对比增强磁共振成像（MRI）对主动脉瓣狭窄（AS）和遗传性肥厚型心肌病（HCM）患者左室肥厚（LV）病灶纤维化程度和分布的影响。在1.5 T扫描仪（Sonata，Siemens Medical Solutions）上使用稳态进动快速成像（trueFISP）采集电影图像。钆对比增强MRI采用分段反转-恢复序列。结果：左室平均质量为238.6（SD 75.3）g的AS和205.4（SD 80.5）g的HCM（p = 0.17）。在27%的AS患者和73%的HCM患者中观察到高增强（p < 0.01）。在AS中，60%的患者最大舒张期室壁厚度>= 18 mm，而最大舒张期室壁厚度<18 mm的患者没有观察到增强（p < 0.05）。高强化患者比无高强化患者有更严重的AS（主动脉瓣面积0.80（0.09）cm（2）v0.99（0.3）cm（2），p < 0.05;最大跨瓣压差98（22）mm Hg v74（24）mm Hg，p 0.05）。在HCM中，前间隔区主要为高增强，高增强患者的舒张末期容积（125.4（36.9）ml vs 98.8（16.9）ml，p，0.05）和收缩末期容积（38.9（18.2）ml vs 25.2（1.7）ml，p，0.05）较高。高增强体积（占整个左室心肌的百分比）在AS中低于HCM（4.3（1.9）% v8.6（7.4）%，p < 0.05）。AS和HCM分别在4.5（3.1）和4.6（2.7）节段观察到高增强（p = 0.93），增强模式主要是斑片状多灶性focus.Conclusions：局灶性瘢痕形成可在AS和HCM引起的严重LV肥大中观察到，并与LV重塑的严重程度相关。然而，局灶性瘢痕形成在AS引起的适应性LV肥大中的发生率明显低于遗传决定的HCM。
Objective: To compare the extent and distribution of focal fibrosis by gadolinium contrast-enhanced magnetic resonance imaging (MRI; delayed hyperenhancement) in severe left ventricular (LV) hypertrophy in patients with pressure overload caused by aortic stenosis (AS) and with genetically determined hypertrophic cardiomyopathy (HCM).Methods: 44 patients with symptomatic valvular AS (n = 22) and HCM ( n = 22) were studied. Cine images were acquired with fast imaging with steady-state precession (trueFISP) on a 1.5 T scanner (Sonata, Siemens Medical Solutions). Gadolinium contrast-enhanced MRI was performed with a segmented inversion-recovery sequence. The location, extent and enhancement pattern of hyperenhanced myocardium was analysed in a 12-segment model.Results: Mean LV mass was 238.6 (SD 75.3) g in AS and 205.4 (SD 80.5) g in HCM (p = 0.17). Hyperenhancement was observed in 27% of patients with AS and in 73% of patients with HCM (p < 0.01). In AS, hyperenhancement was observed in 60% of patients with a maximum diastolic wall thickness >= 18 mm, whereas no patient with a maximum diastolic wall thickness, 18 mm had hyperenhancement (p < 0.05). Patients with hyperenhancement had more severe AS than patients without hyperenhancement (aortic valve area 0.80 (0.09) cm(2) v 0.99 (0.3) cm(2), p < 0.05; maximum gradient 98 (22) mm Hg v 74 (24) mm Hg, p, 0.05). In HCM, hyperenhancement was predominant in the anteroseptal regions and patients with hyperenhancement had higher end diastolic (125.4 (36.9) ml v 98.8 (16.9) ml, p, 0.05) and end systolic volumes (38.9 (18.2) ml v 25.2 (1.7) ml, p, 0.05). The volume of hyperenhancement ( percentage of total LV myocardium), where present, was lower in AS than in HCM (4.3 (1.9)% v 8.6 (7.4)%, p < 0.05). Hyperenhancement was observed in 4.5 (3.1) and 4.6 (2.7) segments in AS and HCM, respectively ( p = 0.93), and the enhancement pattern was mostly patchy with multiple foci.Conclusions: Focal scarring can be observed in severe LV hypertrophy caused by AS and HCM, and correlates with the severity of LV remodelling. However, focal scarring is significantly less prevalent in adaptive LV hypertrophy caused by AS than in genetically determined HCM.