T1 mapping技术用于评估心尖肥厚型心肌病患者心肌钆沉积

目的 观察T1 mapping技术用于评估心尖肥厚型心肌病（AHCM）患者心肌钆沉积的可行性。方法 回顾性分析60例AHCM患者资料,根据是否接受含钆对比剂（GBCA）注射分为增强组和对照组各30例;基于2组心脏T1 mapping测量左心室基底部、中间部、心尖部心肌T1值及相应层面脾脏T1值,计算T1相对值（T1R）,比较组间及增强组内左心室不同部位心肌T1R,并对增强组T1R基于性别、年龄、体质量指数、心功能、高血压、高血脂、糖尿病、心尖厚度、射血分数、延迟强化、首次增强检查至末次复查间隔时间及GBCA总量进行进一步分析。结果 组间T1R_基底部、T1R_中间部、T1R_心尖部差异均无统计学意义（t=0.329、1.484、0.720,P均>0.05）。增强组内,左心室不同部位心肌T1R差异无统计学意义（F=0.765,P>0.05）,不同性别及有无高血压患者间心肌T1R差异均有统计学意义（P均<0.05）。结论 T1 mapping技术可用于评估AHCM患者心肌钆沉积。     

心肌纤维化心脏磁共振及在糖尿病心肌病的应用进展

糖尿病心肌病(diabetic cardiomyopathy, DbCM)早期采取干预措施,能够阻止甚至逆转DbCM改变,预防心脏结构的重塑并改善心脏舒张功能,因此,通过对心脏功能、心肌微循环灌注状态和心肌纤维化的检测评估,实现对DbCM精确诊断、危险分级及预后评估具有重要的临床意义。心脏磁共振(cardiac magnetic resonance, CMR)具有良好的软组织分辨率和多序列、多参数成像的优势,不仅可以准确评估心脏解剖结构和功能改变,还能够无创性观察心肌的组织学特征,对心肌纤维化的精确诊断及危险分级具有重要临床价值。本文就MR心肌延迟强化、T1 mapping、T2 mapping、扩散张量成像及T1ρ mapping技术在心肌纤维化临床应用的前沿进展予以综述,并展望未来该技术的发展应用。     

心肌T1 mapping和细胞外容积诊断陈旧心肌梗死

目的 探讨心脏磁共振(CMR)T1 mapping技术对陈旧心肌梗死心肌纤维化的诊断价值。方法 对31例陈旧心肌梗死患者行心脏T1 mapping MOLLI序列和延迟强化检查,以延迟强化为金标准,将心肌节段分为阳性及阴性组,测定心肌17个节段初始T1值和强化后T1值,计算强化后T1缩短值(△T1)和细胞外容积(ECV),比较两组间初始T1值、△T1值和心肌ECV值的差异并行ROC曲线分析。结果 陈旧心肌梗死患者中LGE阳性和阴性节段的平均初始T1值、强化后T1值、△T1值和ECV值差异均有统计学意义[(1521.77±150.49)ms vs(1258.02±72.52)ms, P<0.001,(404.64±66.39)ms vs(594.92±66.92)ms,P<0.001,(1117.12±179.55)ms vs (663.10±103.12)ms,P<0.001, (57.76±11.07)% vs (27.72±5.61)%, P<0.001)]。采用初始T1值、△T1值和ECV诊断心肌梗死的ROC曲线下面积分别为0.964、0.994和0.990,初始T1阈值为1341.15 ms时,敏感度为91.75%(189/206),特异度为91.97%(275/299);△T1值阈值为843.05 ms时,敏感度为97.09%(200/206),特异度为96.66%(289/299);ECV阈值为38.87%时,敏感度为98.06%(202/206),特异度为96.99%(290/299)。采用初始T1值和ECV值诊断心肌梗死的准确率、敏感度、特异度、阳性预测值、阴性预测值的差异均有统计学意义([QX(Y10]P[QX)]均<0.05),而△T1值与ECV值比较,差异均无统计学意义([QX(Y10]P[QX)]均>0.05)。结论 心脏T1 mapping技术可用于识别及定量评估陈旧心肌梗死纤维化,其中心肌初始T1值、△T1值和ECV值的准确性均较高,且ECV明显高于初始T1值。     

磁共振T1 mapping成像评价肥厚型和扩张型心肌病弥漫性心肌纤维化

目的 探讨磁共振纵向弛豫时间定量(T1 mapping)成像评价肥厚型心肌病(HCM)和扩张型心肌病(DCM)心肌纤维化的价值,及心肌纤维化与左心室射血分数的关系。方法 收集经临床诊断证实的30例HCM患者(HCM组)、27例DCM患者(DCM)和符合纳入标准的33例患者(对照组)。对所有受检者均行心脏电影成像、对比增强前、后T1 mapping成像、延迟对比增强(LGE)成像。测量不同受检者增强前、后左心室平均T1值及心功能参数并进行统计学分析,分析心肌平均T1值与心功能指标的相关性。结果 HCM组22例(22/30,73.33%)患者存在延迟强化,DCM组15例(15/27,55.56%)患者存在延迟强化,对照组无延迟强化。比增强前,HCM组[(1294.79±85.22)ms]、DCM组[(1312.88±59.57)ms]左心室心肌T1值均较对照组[(1266.56±57.33)ms]显著增加(P均<0.05);对比增强后,HCM组[(491.31±121.59)ms]、DCM组[(466.77±126.34)ms]左心室心肌T1均值较对照组[(534.09±92.73)]显著减低(P均<0.05)。HCM患者左心室心肌增强前T1值与左心室射血分数呈负相关(r=-0.58,P<0.05),增强后T1值与其呈正相关(r=0.59,P<0.05);DCM患者左心室心肌增强前T1值与左心室射血分数呈负相关(r=-0.55,P<0.05),增强后T1值与其呈正相关(r=0.51,P<0.05)。结论 HCM和DCM患者心肌纤维化与心功能相关;T1 mapping成像有助于评价HCM和DCM患者心肌纤维化。     

T1 mapping技术用于心脏疾病危险分层及预后评估研究进展

近年心脏MR(CMR)技术快速发展,在心脏疾病中的应用越来越受到重视。T1 mapping成像技术可量化评价心肌组织T1弛豫时间,在评价心肌组织学特征和定量分析方面具有较大潜力,可为判断多种心脏疾病的预后提供有价值的信息。本文就T1 mapping技术在心脏疾病危险分层及预后评估中的研究进展进行综述。     

3.0T磁共振钆延迟强化技术评价小型猪慢性阻塞性肺病模型心肌纤维化的实验研究

目的利用3.0 T心脏磁共振(cardiovascular magnetic resonance,CMR)钆延迟强化(late gadolinium enhancement,LGE)技术评估巴马小型猪慢性阻塞性肺病(chronic obstructive pulmonary disease,COPD)模型左心室(lef...     

心脏磁共振延迟强化对心肌病心功能的诊断价值分析

目的:探讨心脏磁共振延迟强化对心肌病心功能的诊断价值.方法:选取2019年6月—2020年6月在泰州市人民医院收治的20例原发性扩张型心肌病患者,将其作为观察组,选择同期基础心律为窦性心律的20名健康体检者作为对照组.两组均进行心脏磁共振延迟强化检查,比较两组左心功能相关参数、心肌组织特征性追踪参数,观察心肌磁共振延迟...     

心脏MR延迟钆强化评估心肌淀粉样变性患者预后:Meta分析北大核心CSCD

目的采用Meta分析方法评价心脏MR(CMR)延迟钆强化(LGE)评估心肌淀粉样变(CA)患者预后的价值。方法检索PubMed、EMbase、Cochrane Library、中国生物医学文献数据库、中国知网及万方医学网自建库至2020年10月以CMR-LGE评价CA患者死亡风险的队列研究,依照纳入及排除标准筛选文献;合并纳入文献中的死亡风险比(HR),评价LGE阳性、LGE类型或位置、CA类型与CA患者死亡风险的关系,以STATA 15.0软件行Meta分析。结果共纳入14篇文献,均为英文文献,包括1490例患者,其中666例发生死亡事件。合并分析结果显示LGE阳性患者死亡风险增大,HR为1.46[95%CI(1.06,2.02),P<0.05];透壁性[HR=2.36,95%CI(1.79,3.12),P<0.05]及心内膜下LGE阳性[HR=3.83,95%CI(2.12,6.91),P<0.05]患者死亡风险增高;左心室[HR=2.82,95%CI(1.33,5.98),P<0.05]及右心室LGE阳性[HR=1.94,95%CI(1.12,3.35),P<0.05]患者死亡风险不同程度升高;轻链型淀粉样变性患者LGE阳性死亡风险增大,HR为1.94[95%CI(1.53,2.46),P<0.05]。结论CMR-LGE阳性与CA患者死亡风险增加密切相关,可作为预测CA患者预后的独立因素。     

心脏磁共振T1 mapping和组织追踪技术在左心室肥厚相关疾病中的鉴别诊断价值

目的 使用心脏磁共振(cardiac magnetic resonance, CMR)T1 mapping及组织追踪(tissue tracking, TT)技术鉴别心肌淀粉样变性(cardiac amyloidosis, CA)、肥厚型心肌病(hypertrophic cardiomyopathy, HCM)及高血压性心脏病(hypertensive heart disease, HHD)等左室肥厚相关疾病。材料与方法 回顾性分析HCM、CA和HHD各20例(三组合称病例组)相关临床和CMR资料,纳入25名健康志愿者作为健康对照(healthy control, HC)组。使用单因素方差分析及Kruskal-Wallis检验比较四组间心肌初始T1值、整体和各节段心肌的纵向应变(longitudinal strain, LS)、周向应变(circumferential strain, CS)、径向应变(radial strain, RS),相对心尖应变(relative apical sparing of strain, RAS)等定量参数。结果 CA组的初始T1值[(1473.05±...     

Frequency and distribution of late gadolinium enhancement in magnetic resonance imaging of patients with apical hypertrophic cardiomyopathy and patients with asymmetrical hypertrophic cardiomyopathy: a comparative study

Our aim was to compare the frequency and distribution of late gadolinium enhancement (LGE) on contrast MRI between hypertrophic cardiomyopathy (HCM) patients with apical hypertrophic cardiomyopathy (APH) and those with asymmetrical septal hypertrophy (ASH). We studied 66 patients with HCM (50 men and 16 women; average age: 58.8 ± 29.8 years) who had undergone MRI. All the MRI examinations were performed using a 1.5 T system. LGE images were acquired using the inversion recovery segmented spoiled-gradient echo and phase-sensitive inversion recovery methods. We evaluated 17 segments of the left ventricle as defined by the American Heart Association criteria for LGE determination. LGE was detected at the junction of the right ventricle and the interventricular septum in 25 (73.5%) of the 34 HCM patients with ASH and in the apex of the heart in 13 (40.6%) of the 32 patients with APH. LGE-positive areas were more widely distributed in the case of the ASH group than in the case of the APH group. The distribution of LGE was clearly different between the two groups (Fisher’s exact probability test, P = 0.0068). The number of LGE-positive cases and LGE-positive segments were significantly higher in the ASH group than in the APH group and there was a significant difference in the distribution of the LGE-positive areas between the two groups. LGE was mainly detected in the hypertrophied areas of the myocardium.     

Late gadolinium enhancement cardiovascular magnetic resonance in genotyped hypertrophic cardiomyopathy with normal phenotype

A 35 year-old asymptomatic Caucasian female with a family history of hypertrophic cardiomyopathy (HCM) was referred for cardiologic evaluation. The electrocardiogram and transthoracic echocardiogram were normal. Cardiovascular magnetic resonance (CMR) was performed for further assessment of myocardial function and presence of myocardial scar. CMR showed normal left ventricular systolic size, measurements and function. However, there was extensive, diffuse late gadolinium enhancement (LGE) throughout the left ventricle. This finding was consistent with extensive myocardial scarring and was highly suggestive of advanced, non-ischemic cardiomyopathy. Genotyping showed a heterozygous mis-sense mutation (275G>A) in the cardiac troponin T (TNNT2) gene, which is causally associated with HCM. There have been no previous reports of such extensive, atypical pattern of myocardial scarring despite an otherwise structurally and functionally normal left ventricle in an asymptomatic individual with HCM. This finding has important implications for phenotype screening in HCM.     

Comparison of quantitative imaging parameters using cardiovascular magnetic resonance between cardiac amyloidosis and hypertrophic cardiomyopathy: inversion time scout versus T1 mapping

To compare inversion time (TI) parameters, native T1, and extracellular volume (ECV) on cardiac magnetic resonance (CMR) imaging between patients with cardiac amyloidosis (CA) or hypertrophic cardiomyopathy (HCMP). Forty six patients with biopsy-confirmed CA and 30 patients with HCMP who underwent CMR were included. T1 and TI values were measured in the septum and cavity of the left ventricle on T1 mapping and TI scout images. TI values were selected at nulling point for each myocardium and blood pool. Native T1, ECV, and TI interval values were significantly different between the CA (1170.5?±?86.4 ms, 56.7?±?12.2, ? 11.5?±?28.4 ms) and HCMP (1059.5?±?63.4 ms, 28.5?±?5.8, 66.2?±?25.4 ms) (all p?<?0.001). The diagnostic performance of the TI interval (area under the ROC curve, 0.975) was not inferior to that of the ECV (0.980, p?=?0.776), and it was superior to that of the native T1 (0.845, p?=?0.004). The diagnostic performance of TI interval was comparable to that of ECV for differential diagnosis between CA and HCMP. TI interval showed the feasibility as quantitative CMR parameter when T1 mapping images are not available.     

Assessment of myocardial delayed enhancement with cardiac computed tomography in cardiomyopathies: a prospective comparison with delayed enhancement cardiac magnetic resonance imaging

To evaluate the feasibility of cardiac CT for the evaluation of myocardial delayed enhancement (MDE) in the assessment of patients with cardiomyopathy, compared to cardiac MRI. A total of 37 patients (mean age 54.9?±?15.7 years, 24 men) who underwent cardiac MRI to evaluate cardiomyopathy were enrolled. Dual-energy ECG-gated cardiac CT was acquired 12 min after contrast injection. Two observers evaluated cardiac MRI and cardiac CT at different kV settings (100, 120 and 140 kV) independently for MDE pattern-classification (patchy, transmural, subendocardial, epicardial and mesocardial), differentiation between ischemic and non-ischemic cardiomyopathy and MDE quantification (percentage MDE). Kappa statics and the intraclass correlation coefficient were used for statistical analysis. Among different kV settings, 100-kV CT showed excellent agreements compared to cardiac MRI for MDE detection (κ?=?0.886 and 0.873, respectively), MDE pattern-classification (κ?=?0.888 and 0.881, respectively) and differentiation between ischemic and non-ischemic cardiomyopathy (κ?=?1.000 and 0.893, respectively) for both Observer 1 and Observer 2. The Bland–Altman plot between MRI and 100-kV CT for the percentage MDE showed a very small bias (?0.15%) with 95% limits of agreement of ?7.02 and 6.72. Cardiac CT using 100 kV might be an alternative method to cardiac MRI in the assessment of cardiomyopathy, particularly in patients with contraindications to cardiac MRI.     

Absence of late gadolinium enhancement on cardiac magnetic resonance imaging in ventricular fibrillation and nonischemic cardiomyopathy

Introduction

Cardiac magnetic resonance (CMR)‐identified late gadolinium enhancement (LGE), representing regional fibrosis, is often used to predict ventricular arrhythmia risk in nonischemic cardiomyopathy (NICM). However, LGE is more closely correlated with sustained monomorphic ventricular tachycardia (SMVT) than ventricular fibrillation (VF). We characterized CMR findings of ventricular LGE in VF survivors.

Methods

We examined consecutively resuscitated VF survivors undergoing contrast‐enhanced 1.5T CMR between 9/2007 and 7/2016. We excluded coronary artery disease, hypertrophic cardiomyopathy, amyloid, sarcoid, arrhythmogenic right ventricular cardiomyopathy, and channelopathy. Preexisting implantable cardioverter‐defibrillator (ICD) was a CMR contraindication. VF patients were divided into three groups: (1) NICM, (2) left ventricular (LV) dilatation with normal LV ejection fraction (LVEF), and (3) normal LV size and LVEF. Two groups of NICM patients with and without SMVT were examined for comparison.

Results

We analyzed 87 VF patients, and found that LGE was seen in 8/22 (36%) with NICM (LVEF 38 ± 11%, LV end‐diastolic volume index [LVEDVI] 134 ± 68 mL/BSA), 11/40 (28%) with LV dilatation and normal LVEF (LVEDVI 103 ± 17 mL/BSA), 4/25 (16%) with normal LV size and LVEF. Incidence of LGE in NICM patients without prior ventricular tachycardia/VF (LVEF 36 ± 12%, LVEDVI 141 ± 46 mL/body surface area [BSA]) was 117/277 and was not lower than those with VF and NICM (42% vs 36%; P = 0.59). By contrast, 22/37 NICM patients with SMVT (LVEF 42 ± 11%, LVEDVI 123 ± 48 mL/BSA) were LGE‐positive (59% NICM‐SMVT vs 36% NICM‐VF; P = 0.04).

Conclusion

Most VF survivors with a diagnosis of NICM did not have LGE on CMR and would not have met primary prevention ICD criteria based on LVEF. Absence of LGE may not portend a benign prognosis in NICM. Novel strategies for determining SCD risk in this cohort are required.

     

In-vivo T1 cardiovascular magnetic resonance study of diffuse myocardial fibrosis in hypertrophic cardiomyopathy

Background

In hypertrophic cardiomyopathy (HCM), autopsy studies revealed both increased focal and diffuse deposition of collagen fibers. Late gadolinium enhancement imaging (LGE) detects focal fibrosis, but is unable to depict interstitial fibrosis. We hypothesized that with T1 mapping, which is employed to determine the myocardial extracellular volume fraction (ECV), can detect diffuse interstitial fibrosis in HCM patients.

Methods

T1 mapping with a modified Look-Locker Inversion Recovery (MOLLI) pulse sequence was used to calculate ECV in manifest HCM (n = 16) patients and in healthy controls (n = 14). ECV was determined in areas where focal fibrosis was excluded with LGE.

Results

The total group of HCM patients showed no significant changes in mean ECV values with respect to controls (0.26 ± 0.03 vs 0.26 ± 0.02, p = 0.83). Besides, ECV in LGE positive HCM patients was comparable with LGE negative HCM patients (0.27 ± 0.03 vs 0.25 ± 0.03, p = 0.12).

Conclusions

This study showed that HCM patients have a similar ECV (e.g. interstitial fibrosis) in myocardium without LGE as healthy controls. Therefore, the additional clinical value of T1 mapping in HCM seems limited, but future larger studies are needed to establish the clinical and prognostic potential of this new technique within HCM.     

Quantitative diffusion-weighted magnetic resonance imaging in the assessment of myocardial fibrosis in hypertrophic cardiomyopathy compared with T1 mapping

To identify myocardial fibrosis in hypertrophic cardiomyopathy (HCM) subjects using quantitative cardiac diffusion-weighted imaging (DWI) and to compare its performance with native T1 mapping and extracellular volume (ECV). Thirty-eight HCM subjects (mean age, 53?±?9 years) and 14 normal controls (mean age, 51?±?8 years) underwent cardiac magnetic resonance imaging (CMRI) on a 3.0T magnetic resonance (MR) machine with DWI, T1 mapping and late gadolinium enhancement (LGE) imaging as the reference standard. The mean apparent diffusion coefficient (ADC), native T1 value and ECV were determined for each subject. Overall, the HCM subjects exhibited an increased native T1 value (1241.04?±?78.50 ms), ECV (0.31?±?0.03) and ADC (2.36?±?0.34 s/mm²) compared with the normal controls (1114.60?±?37.99 ms, 0.24?±?0.04, and 1.62?±?0.38 s/mm², respectively) (p?<?0.05). DWI differentiated healthy and fibrotic myocardia with an area under the curve (AUC) of 0.93, while the AUCs of the native T1 values (0.93), (p?>?0.05) and ECV (0.94), (p?>?0.05) exhibited an equal differentiation ability. Both HCM LGE+ and HCM LGE? subjects had an increased native T1 value, ECV and ADC compared to the normal controls (p?<?0.05). HCM LGE+ subjects exhibited an increased ECV (0.31?±?0.04) and ADC (2.43?±?0.36 s/mm²) compared to HCM LGE? subjects (p?<?0.05). HCM LGE+ and HCM LGE? subjects had similar native T1 values (1250?±?76.36 ms vs. 1213.98?±?92.30 ms, respectively) (p?>?0.05). ADC values were linearly associated with increased ECV (R²?=?0.36) and native T1 values (R²?=?0.40) among all subjects. DWI is a feasible alternative to native T1 mapping and ECV for the identification of myocardial fibrosis in patients with HCM. DWI and ECV can quantitatively characterize the extent of fibrosis in HCM LGE+ and HCM LGE? patients.