T1 mapping in children and young adults with hypertrophic cardiomyopathy

To assess the global and segmental left ventricular (LV) native T1 and extracellular volume fraction (ECV) in children and young adults with hypertrophic cardiomyopathy (HCM) compared to a control cohort. The study population included 21 HCM patients (mean 14.1?±?4.6 years) and 21 controls (mean 15.7?±?1.5 years). Native modified Look-Locker inversion recovery sequence was performed before and after contrast injection in 3 short axis planes. Global and segmental LV native T1 and ECV were quantified and compared between HCM patients and controls. Mean native T1 in HCM patients and controls was 1020.4?±?41.2 and 965.6?±?30.2 ms respectively (p?<?0.0001). Hypertrophied myocardium had significantly higher native global T1 and global ECV compared to non-hypertrophied myocardium in HCM (p?<?0.0001,?=?0.14 and 0.048,?=?0.01 respectively). In a subset of patients, ECV was higher in LV segments with LGE compared to no LGE (p?<?0.0001). No significant correlation was identified between global native T1 and ECV and parameters of LV structure and function. Native T1 cut-off of 987 ms provided the highest sensitivity (95?%) and specificity (91?%) to separate HCM patients from controls. Global and segmental native T1 are elevated in HCM patients. LV segments with hypertrophy and/or LGE had higher ECV in a subset of HCM patients. LV native T1 and ECV do not correlate with parameters of LV structure and function. T1 in children and young adults may be used as a non-invasive tool to assess for HCM and related fibrosis.     

Subclinical myocardial inflammation and diffuse fibrosis are common in systemic sclerosis – a clinical study using myocardial T1-mapping and extracellular volume quantification

Background

Systemic sclerosis (SSc) is characterised by multi-organ tissue fibrosis including the myocardium. Diffuse myocardial fibrosis can be detected non-invasively by T1 and extracellular volume (ECV) quantification, while focal myocardial inflammation and fibrosis may be detected by T2-weighted and late gadolinium enhancement (LGE), respectively, using cardiovascular magnetic resonance (CMR). We hypothesised that multiparametric CMR can detect subclinical myocardial involvement in patients with SSc.

Methods

19 SSc patients (18 female, mean age 55 ± 10 years) and 20 controls (19 female, mean age 56 ± 8 years) without overt cardiovascular disease underwent CMR at 1.5T, including cine, tagging, T1-mapping, T2-weighted, LGE imaging and ECV quantification.

Results

Focal fibrosis on LGE was found in 10 SSc patients (53%) but none of controls. SSc patients also had areas of myocardial oedema on T2-weighted imaging (median 13 vs. 0% in controls). SSc patients had significantly higher native myocardial T1 values (1007 ± 29 vs. 958 ± 20 ms, p < 0.001), larger areas of myocardial involvement by native T1 >990 ms (median 52 vs. 3% in controls) and expansion of ECV (35.4 ± 4.8 vs. 27.6 ± 2.5%, p < 0.001), likely representing a combination of low-grade inflammation and diffuse myocardial fibrosis. Regardless of any regional fibrosis, native T1 and ECV were significantly elevated in SSc and correlated with disease activity and severity. Although biventricular size and global function were preserved, there was impairment in the peak systolic circumferential strain (-16.8 ± 1.6 vs. -18.6 ± 1.0, p < 0.001) and peak diastolic strain rate (83 ± 26 vs. 114 ± 16 s-1, p < 0.001) in SSc, which inversely correlated with diffuse myocardial fibrosis indices.

Conclusions

Cardiac involvement is common in SSc even in the absence of cardiac symptoms, and includes chronic myocardial inflammation as well as focal and diffuse myocardial fibrosis. Myocardial abnormalities detected on CMR were associated with impaired strain parameters, as well as disease activity and severity in SSc patients. CMR may be useful in future in the study of treatments aimed at preventing or reducing adverse myocardial processes in SSc.     

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.     

Association between left ventricular mechanics and diffuse myocardial fibrosis in patients with repaired Tetralogy of Fallot: a cross-sectional study

Background

Patients with repaired tetralogy of Fallot (TOF) have progressive, adverse biventricular remodeling, leading to abnormal contractile mechanics. Defining the mechanisms underlying this dysfunction, such as diffuse myocardial fibrosis, may provide insights into poor long-term outcomes. We hypothesized that left ventricular (LV) diffuse fibrosis is related to impaired LV mechanics.

Methods

Patients with TOF were evaluated with cardiac magnetic resonance in which modified Look-Locker (MOLLI) T1-mapping and spiral cine Displacement encoding (DENSE) sequences were acquired at three LV short-axis positions. Linear mixed modeling was used to define the association between regional LV mechanics from DENSE based on regional T1-derived diffuse fibrosis measures, such as extracellular volume fraction (ECV).

Results

Forty patients (26?±?11 years) were included. LV ECV was generally within normal range (0.24?±?0.05). For LV mechanics, peak circumferential strains (?15?±?3%) and dyssynchrony indices (16?±?8 ms) were moderately impaired, while peak radial strains (29?±?8%) were generally normal. After adjusting for patient age, sex, and regional LV differences, ECV was associated with log-adjusted LV dyssynchrony index (β?=?0.67) and peak LV radial strain (β?=??0.36), but not LV circumferential strain. Moreover, post-contrast T1 was associated with log-adjusted LV diastolic circumferential strain rate (β?=?0.37).

Conclusions

We observed several moderate associations between measures of fibrosis and impaired mechanics, particularly the LV dyssynchrony index and peak radial strain. Diffuse fibrosis may therefore be a causal factor in some ventricular dysfunction in TOF.

     

How do hypertrophic cardiomyopathy mutations affect myocardial function in carriers with normal wall thickness? Assessment with cardiovascular magnetic resonance

Background

Clinical data on myocardial function in HCM mutation carriers (carriers) is sparse but suggests that subtle functional abnormalities can be measured with tissue Doppler imaging before the development of overt hypertrophy. We aimed to confirm the presence of functional abnormalities using cardiovascular magnetic resonance (CMR), and to investigate if sensitive functional assessment could be employed to identify carriers.

Results

28 carriers and 28 controls were studied. Global left atrial (LA) and left ventricular (LV) dimensions, segmental peak systolic circumferential strain (SCS) and peak diastolic circumferential strain rate (DCSR), as well as the presence of late Gadolinium enhancement (LGE) were determined with CMR. Septal and lateral myocardial velocities were measured with echocardiographic tissue Doppler imaging. lv mass and volumes were comparable between groups. Maximal septal to lateral wall thickness ratio (SL ratio) was larger in carriers than in controls (1.3 ± 0.2 versus 1.1 ± 0.1, p < 0.001). Also, LA volumes were larger in carriers compared to controls (p < 0.05). Both peak SCS (p < 0.05) and peak DCSR (p < 0.01) were lower in carriers compared to controls, particularly in the basal lateral wall. Focal LGE was present in 2 carriers and not in controls. The combination of a SL ratio >1.2 and a peak DCSR <105%.s^-1 was present in 45% of carriers and in none of the controls, yielding a positive predictive value of 100%. Two carriers and 18 controls had a SL ratio < 1.2 and peak DCSR >105%.s^-1, yielding a negative predictive value of 90%. With multivariate analysis, HCM mutation carriership was an independent determinant of reduced peak SCS and peak DCSR.

Conclusions

HCM mutation carriership is an independent determinant of reduced peak SCS and peak DCSR when LV wall thickness is within normal limits, and is associated with increased LA volumes and SL ratio. Using SL ratio and peak DCSR has a high accuracy to identify carriers. However, since carriers also display structural abnormalities and focal LGE, we advocate to also evaluate morphology and presence of LGE when screening for carriers.     

Increased left ventricular torsion in hypertrophic cardiomyopathy mutation carriers with normal wall thickness

Background

Increased left ventricular (LV) torsion has been observed in patients with manifest familial hypertrophic cardiomyopathy (HCM), and is thought to be caused by subendocardial dysfunction. We hypothesize that increased LV torsion is already present in healthy mutation carriers with normal wall thickness.

Methods

Seventeen carriers with an LV wall thickness <10 mm, and seventeen age and gender matched controls had cardiovascular magnetic resonance (CMR) cine imaging and tissue tagging. LV volumes and mass were calculated from the cine images. LV torsion, torsion rate, endocardial circumferential strain and torsion-to-endocardial-circumferential-shortening (TECS) ratio, which reflects the transmural distribution in contractile function, were determined using tissue tagging.

Results

LV volumes, mass and circumferential strain were comparable between groups, whereas LV ejection fraction, torsion and TECS-ratio were increased in carriers compared to controls (63 ± 3% vs. 60 ± 3%, p = 0.04, 10.1 ± 2.5° vs. 7.7 ± 1.2°, p = 0.001, and 0.52 ± 0.14°/% vs. 0.42 ± 0.10°/%, p = 0.02, respectively).

Conclusions

Carriers with normal wall thickness display increased LV torsion and TECS-ratio with respect to controls, which might be due to subendocardial myocardial dysfunction. As similar abnormalities are observed in patients with manifest HCM, the changes in healthy carriers may be target for clinical intervention to delay or prevent the onset of hypertrophy.     

速度向量成像技术评价肥厚型心肌病左心室扭转功能

目的应用超声心动图速度向量成像技术对肥厚型心肌病患者心脏扭转运动进行初步分析,探讨肥厚型心肌病患者在左心室射血分数(LVEF)正常时心脏局部和整体扭转功能是否有改变。方法肥厚型心肌病患者和健康体检者各30名。常规测量有关左心功能参数:LVEF、舒张末期容积(EDV)、收缩末期容积(ESV)、每搏量(SV)、二尖瓣口E、A峰值血流速度等。速度向量成像模式下在系列胸骨旁短轴观图像上测量收缩期心内膜下和心外膜下心肌的最大旋转角度、峰值旋转速率、圆周应变(CS)、圆周应变率(CSR)、舒张期和等容舒张期峰值解旋转速率。结果肥厚型心肌病组EDV、ESV、SV明显减低,A峰增高(P0.01);心内膜下心肌左心室扭转角度和扭矩增高,解扭转率减低(P0.05);心外膜下心肌的基底部峰值旋转速率、峰值解旋转速率减低(P0.05);心外膜下心肌的CS、CSR明显减低(P0.05)。结论肥厚型心肌病患者心脏整体扭转角度和速度较正常人增高,局部心肌圆周方向形变能力下降,以心外膜下心肌下降更为明显。     

应变率成像评价肥厚型心肌病患者左心室局部功能和室壁运动同步性

目的 评价应变率成像技术在定量检测肥厚型心肌病(HCM)患者左心室局部心肌功能及室壁运动同步性中的价值.方法 HCM患者21例,根据室间隔及左室壁厚度分为3组:①非肥厚组(NH),室壁厚度≤11 mm,101节段;②轻度肥厚组(MH),11mm＜室壁厚度≤15 mm,86节段;③重度肥厚组,室壁厚度＞15mm,65节段.对照组18例,216节段.获取各受试者心尖四腔观、左室长轴及两腔观组织速度图像存盘供脱机分析.测量收缩期峰值应变率(SRs)、舒张早期峰值应变率(SRe)、舒张晚期峰值应变率(SRa),计算SRe/SRa;测量收缩期应变率达峰时间(TssR),并计算收缩期应变率达峰时间变异(CVTSSR);测量舒张早期应变率达峰时间(TESR),并计算舒张早期应变率达峰时间变异(CVTESR).结果 与对照组室壁节段比较,HCM组NH、MH、SH亚组SRs、SRe、SRe/SRa均显著降低,且三个亚组间SRe依次降低,即NH＞MH＞SH,NH与MH组间SRe/SRa差异无统计学意义,与NH、MH组比较,SH组SRe/SRa显著减低;与对照组比较,MH、SH组SRa显著降低,而NH组较对照组差异无统计学意义,且NH＞MH＞SH;与对照组比较,HCM组CVTSSR及CVTESR显著增大.结论 HCM患者无论有无室壁肥厚,其左室局部收缩舒张功能均受损;HCM患者左室心肌运动存在不同步现象,应变率成像技术能准确、定量评价其左室局部心肌功能及其左室心肌运动不同步.     

The role of left ventricular deformation in the assessment of microvascular obstruction and intramyocardial haemorrhage

In the setting of acute ST-elevation myocardial infarction (STEMI), it remains unclear which strain parameter most strongly correlates with microvascular obstruction (MVO) or intramyocardial haemorrhage (IMH). We aimed to investigate the association of MVO, IMH and convalescent left ventricular (LV) remodelling with strain parameters measured with cardiovascular magnetic resonance (CMR). Forty-three patients with reperfused STEMI and 10 age and gender matched healthy controls underwent CMR within 3-days and at 3-months following reperfused STEMI. Cine, T2-weighted, T2*-imaging and late gadolinium enhancement (LGE) imaging were performed. Infarct size, MVO and IMH were quantified. Peak global longitudinal strain (GLS), global radial strain (GRS), global circumferential strain (GCS) and their strain rates were derived by feature tracking analysis of LV short-axis, 4-chamber and 2-chamber cines. All 43 patients and ten controls completed the baseline scan and 34 patients completed 3-month scans. In multivariate regression, GLS demonstrated the strongest association with MVO or IMH (beta?=?0.53, p?<?0.001). The optimal cut-off value for GLS was ?13.7% for the detection of MVO or IMH (sensitivity 76% and specificity 77.8%). At follow up, 17% (n?=?6) of patients had adverse LV remodeling (defined as an absolute increase of LV end-diastolic/end-systolic volumes >20%). Baseline GLS also demonstrated the strongest diagnostic performance in predicting adverse LV remodelling (AUC?=?0.79; 95% CI 0.60–0.98; p?=?0.03). Post-reperfused STEMI, baseline GLS was most closely associated with the presence of MVO or IMH. Baseline GLS was more strongly associated with adverse LV remodelling than other CMR parameters.     

Electrocardiography based prediction of hypertrophy pattern and fibrosis amount in hypertrophic cardiomyopathy: comparative study with cardiac magnetic resonance imaging

Although, cardiac magnetic resonance imaging (CMR) is a gold standard for risk stratification of hypertrophic cardiomyopathy (HCM), is limited in some situations. We sought to evaluate the predictive power of quantitative electrocardiography in assessing hypertrophy pattern and fibrosis in HCM. Eighty-eight patients with HCM were studied. Voltage of R–S–T waves, number of fragmented QRS (fQRS) complexes, and T wave morphology were measured by 12-lead electrocardiography. Sixteen segmental thickness, late gadolinium enhancement (LGE), native T1, extracellular volume fraction (ECV), and T2, left ventricular (LV) mass and %LGE were measured by CMR. Patterns of LV hypertrophy were classified as pure apical, mixed, or asymmetrical septal hypertrophy. Positive and negative predictive values of biphasic T wave for pure apical type were 70.4 and 63.9%, and the predictive values of precordial negative T wave sums \(>\)?12.5 mm were 69.2 and 79.6%. Precordial S waves, especially Cornell voltage index, were significantly correlated to LV mass index and maximal thickness (p?\(<\hspace{0.17em}\)0.001). The number of fQRS leads was significantly correlated to %LGE, average ECV, and T2 (all p?\(<\hspace{0.17em}\)0.001). More than one lead with fQRS could predict \(>\hspace{0.17em}\)5% of LGE mass with 58% sensitivity and 63% specificity (p?=?0.049, area under the curve?=?0.627). However, degree of correlation between maximal thickness and precordial S was poor in cases with fQRS more two leads. T wave morphology and precordial S helps discriminate hypertrophy pattern and maximal hypertrophy, however, in cases with more than two leads of concomitant fQRS, CMR defines fibrosis amount and hypertrophy more accurately.     

应变率成像评价肥厚型心肌病左心室局部功能

目的探讨应变成像技术评价肥厚型心肌病患者左心室功能的价值。方法对17例肥厚型心肌病患者和42例健康志愿者行心脏超声检查,获取标准心尖四腔、二腔和长轴观以及胸骨旁短轴观,脱机分析测量纵向峰值收缩速度、应变、应变率,径向应变、应变率,周向应变、应变率。结果肥厚型心肌病组纵向峰值收缩速度S峰和舒张早期速度E峰明显低于正常对照组,且从基底段至心尖段的纵向速度（S峰、E峰、A峰）存在递减趋势。肥厚型心肌病组的舒张早期纵向应变率和周向应变率也明显低于对照组。结论应变成像技术能够定量评价左室功能。肥厚型心肌病患者虽然左室射血分数在正常范围内,但其局部心肌已经存在收缩和舒张功能异常。     

Left ventricular energy loss and wall shear stress assessed by vector flow mapping in patients with hypertrophic cardiomyopathy

The aim of this study was to assess left ventricular (LV) summation of energy loss (EL-SUM), average energy loss (EL-AVE) and wall shear stress (WSS) using vector flow mapping (VFM) in patients with hypertrophic cardiomyopathy (HCM). Forty HCM patients, and 40 controls were evaluated by transthoracic echocardiography. Conventional echocardiographic parameters, summation and average of energy loss (EL-total, EL-base, EL-mid and EL-apex), and WSS in each segment were calculated at different phases. Compared with controls, conventional diastolic measurements were impaired in HCM patients. HCM patients also showed increased EL-SUM-total and EL-AVE-total at the peak of LV rapid ejection period as well as decreased EL-SUM-total and EL-AVE-total at the end of early diastole. In controls, EL-SUM and EL-AVE showed a gradual decrease from the basal segment to the apex, this regularity was not observed in HCM patients. Compared with controls, HCM patients showed increased WSS at the peak of the LV rapid ejection period and the atrial contraction period as well as decreased WSS at the end of early diastole (all p?<?0.05). WSS was increased slightly at the peak of the LV rapid filling period in HCM patients (p?=?0.055). EL and WSS values derived from VFM are novel flow dynamic parameters that can effectively evaluate systolic and diastolic hemodynamic function in HCM patients.     

磁共振特征性追踪技术对肥厚型心肌病心肌应变的初步研究

目的采用心脏磁共振特征性追踪(cardiovascular magnetic resonance feature tracking,CMR-FT)技术对肥厚型心肌病患者的心功能及心肌节段应变进行分析,探讨CMR-FT对肥厚性心肌病患者早期运动异常检测的可行性。材料与方法对17例肥厚型心肌病患者及14名健康志愿者进行3.0 T SSFP电影序列扫描,使用CVI软件检测心功能,并对48个肥厚的心肌节段及健康志愿者中42个正常心肌节段进行特征性追踪(feature tracking,FT)后处理。结果肥厚型心肌病患者与健康志愿者左心功能参数(左心室舒张末期容积、左心室收缩末期容积及左心室射血分数)的差异无统计学意义(P均0.05),肥厚的心肌节段的圆周应变、长轴应变及峰值收缩期圆周应变、峰值收缩期长轴应变均低于正常的心肌节段[(-5.26±2.70)%vs(-11.68±2.06)%,(-7.92±5.07)%vs(-13.93±3.89)%,(-10.44±5.46)%vs(-18.43±2.99)%,(-12.29±8.17)%vs(-20.26±2.93)%,P均0.05]。结论对于心功能正常的肥厚性心肌病患者,CMR-FT技术能够早期检测出肥厚患者肥厚心肌节段应变的变化,提示心肌应变量的改变能够比左心室功能参数更早地发现心肌收缩功能异常。     

应用超声二维应变成像技术评估肥厚型心肌病患者左心室心肌收缩的不同步性

目的 应用超声二维应变成像技术评估肥厚型心肌病(HCM)患者左心室心肌收缩的不同步性.方法 21例肥厚型心肌病患者、21例高血压病患者及21例正常人,分别记录并存储二尖瓣环、乳头肌及心尖部水平左心室短轴二维图像;获取其径向应变和圆周应变曲线.分别测量每个节段从心电图R波到峰值径向应变之间的时间(Trs)和从心电图R波到峰值圆周应变之间的时间(Tcs);并且分别计算每个患者18个节段Trs的标准差(Trs-18SD)和18个节段Tcs的标准差(Tcs-18SD).将HCM组患者所有心肌节段分为肥厚节段与非肥厚节段心肌,比较两组间Trs和Tcs的差异.结果 HCM组患者Trs-18SD明显高于HHD组患者及正常对照组[HCM组: (83±18)ms, HHD组: (52±15)ms, 对照组: (46±9)ms, P<0.001],而高血压组与正常对照组之间无明显差异.HCM组患者Tcs-18SD明显高于HHD组患者及正常对照组[HCM组:(84±18)ms, HHD组:(48±10)ms,对照组:(46±10)ms,P<0.001],而高血压组与正常对照组之间无明显差异.肥厚节段心肌Trs明显低于非肥厚节段心肌(341±42 vs 388±40,P<0.05);而肥厚节段心肌Tcs虽然低于非肥厚节段心肌,但其差异无统计学意义.结论 肥厚型心肌病患者左心室收缩存在不同步性,超声二维应变成像技术为评估左心室收缩不同步性提供了无创性新方法.     

CMR findings in patients with hypertrophic cardiomyopathy and atrial fibrillation

Objectives

We sought to evaluate the relation between atrial fibrillation (AF) and the extent of myocardial scarring together with left ventricular (LV) and atrial parameters assessed by late gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM).

Background

AF is the most common arrhythmia in HCM. Myocardial scarring is also identified frequently in HCM. However, the impact of myocardial scarring assessed by LGE CMR on the presence of AF has not been evaluated yet.

Methods

87 HCM patients underwent LGE CMR, echocardiography and regular ECG recordings. LV function, volumes, myocardial thickness, left atrial (LA) volume and the extent of LGE, were assessed using CMR and correlated to AF. Additionally, the presence of diastolic dysfunction and mitral regurgitation were obtained by echocardiography and also correlated to AF.

Results

Episodes of AF were documented in 37 patients (42%). Indexed LV volumes and mass were comparable between HCM patients with and without AF. However, indexed LA volume was significantly higher in HCM patients with AF than in HCM patients without AF (68 ± 24 ml·m^-2 versus 46 ± 18 ml·m^-2, p = 0.0002, respectively). The mean extent of LGE was higher in HCM patients with AF than those without AF (12.4 ± 14.5% versus 6.0 ± 8.6%, p = 0.02). When adjusting for age, gender and LV mass, LGE and indexed LA volume significantly correlated to AF (r = 0.34, p = 0.02 and r = 0.42, p < 0.001 respectively). By echocardiographic examination, LV diastolic dysfunction was evident in 35 (40%) patients. Mitral regurgitation greater than II was observed in 12 patients (14%). Multivariate analysis demonstrated that LA volume and presence of diastolic dysfunction were the only independent determinant of AF in HCM patients (p = 0.006, p = 0.01 respectively). Receiver operating characteristic curve analysis indicated good predictive performance of LA volume and LGE (AUC = 0.74 and 0.64 respectively) with respect to AF.

Conclusion

HCM patients with AF display significantly more LGE than HCM patients without AF. However, the extent of LGE is inferior to the LA size for predicting AF prevalence. LA dilation is the strongest determinant of AF in HCM patients, and is related to the extent of LGE in the LV, irrespective of LV mass.     

Reproducibility of peak filling and peak emptying rate determined by cardiovascular magnetic resonance imaging for assessment of biventricular systolic and diastolic dysfunction in patients with pulmonary arterial hypertension

Right ventricular (RV) and left ventricular (LV) diastolic stiffness may be independent contributors to disease progression in pulmonary arterial hypertension (PAH). The aims of this study are to assess reproducibility of peak emptying rate (PER) and early diastolic peak filling rate (PFR) for both the RV and the LV in PAH and study their relationship to stroke volume (SV). Triple weekly repetition of 20 (totalling 60) cardiovascular magnetic resonance (CMR) scans, were done on 10 patients with PAH and 10 healthy controls. RV and LV volumes were measured over the full cardiac cycle. PER and PFR were calculated as the first derivative of the time–volume relationship in both the RV and the LV and indexed to body surface area. Reproducibility and the relation to SV were studied in a mixed model. PFR was lower in PAH in both the RV (PAH?=?170 mL/m²/s, controls?=?236 mL/m²/s [p?<?0.01]) and in the LV (PAH?=?209 mL/m²/s, controls?=?311 mL/m²/s [p?<?0.01]). PERs were not significantly different between patients and controls. Reproducibility of PER and PFR was high. A trial targeting normalization of PFR requires a total sample size of <?20. PER and PFR in both ventricles were strongly associated with stroke volume (all four: p?<?0.01). Biventricular diastolic dysfunctions are strongly associated with stroke volume, and CMR can quantify them with high reproducibility, enabling small sample sizes for trials of therapies targeting diastolic dysfunction to increase survival.     

The interplay between renin-angiotensin system activation,abnormal myocardial deformation and neurohumoral activation in hypertensive heart disease: a speckle tracking echocardiography study

Angiotensin converting enzyme (ACE) promotes cardiac fibrosis. LV myocardial deformation and torsion are markers of subclinical myocardial dysfunction. We investigated the association of serum ACE levels with LV deformation markers in untreated hypertensives. In 120 untreated patients (age: 53.5?±?11.2 years) with essential hypertension and 60 healthy controls, we measured (a) LV longitudinal, circumferential and radial strain (S), peak torsion and the percentage changes between peak twisting and untwisting at the end of early diastolic filling (%dpTw-Utw_EDF) using speckle tracking echocardiography and (b) serum levels of ACE and NTproBNP. Compared to controls, patients had decreased longitudinal strain (?19.1?±?2.9 vs. ?21.7?±?1.8%), increased peak twisting (19.1?±?4.6 vs.14.0?±?3.7 deg) but decreased %dpTw-Utw_EDF (78?±?8 vs. 86?±?8%) and higher serum ACE levels (27.6?±?8.0 vs 20.9?±?7.1 U/ml) (p?<?0.05 for all comparisons). Increasing serum ACE levels were related to impaired radial strain and longitudinal systolic SR (b?=??0.41 and b?=?0.31 respectively, p?<?0.01), as well as to reduced %dpTw-Utw_EDF (b?=??0.37, p?<?0.05). Furthermore, increasing serum ACE levels were related to increasing NTproBNP levels (b?=?0.41, p?<?0.01). In multivariate analysis, the above relations of serum ACE levels and LV function parameters remained significant after adjustment for other confounding factors (p?<?0.01). The close link between serum ACE levels and impaired LV deformation suggests that activation of renin-angiotensin system is involved in the impairment of LV function resulting in elevated LV filling pressures causing the concomitant elevation of BNP levels in untreated hypertensive patients.     

Incremental value of cardiac deformation analysis in acute myocarditis: a cardiovascular magnetic resonance imaging study

The aim of this study was to assess cardiac deformation patterns in myocarditis applying feature tracking imaging (FTI) to cardiovascular magnetic resonance (CMR) images. Thirty-six patients (31 males) with acute myocarditis and 36 age- and gender-matched healthy volunteers were studied. CMR examinations were performed in a 1.5 T MR-scanner including late gadolinium enhancement (LGE). FTI was applied to standard cine images of long and short axis views. Global peak circumferential, longitudinal and radial systolic strains as well as long axis strain (LAS) were measured. Patients showed significantly impaired global peak circumferential (?24.4?±?4.2?% vs. ?28.8?±?3.8?%, p?<?0.0001), longitudinal (?17.6?±?4.4?% vs. ?23.8?±?3.1?%, p?<?0.0001) and radial (26.1?±?5.4?% vs. 37.9?±?7.6?%, p?<?0.0001) systolic strains. Even patients with a preserved ejection fraction (pEF, ≥55?%) had significantly reduced longitudinal (?20.0?±?4.8?% vs. ?23.8?±?3.1?%, p?<?0.01) and radial (27.7?±?5.5?% vs. 37.9?±?7.6?%, p?<?0.0001) strains. The extent of LGE in patients did not correlate to their respective strains. Regarding the differentiation between patients and controls, the addition of global peak systolic strains to ejection fraction led to a significant improvement of the logistic regression model (χ² 48.7 vs. 71.5; p?<?0.001) resulting in a high AUC of 0.98. Applying previously published reference values, 75?% or 31?% of patients with pEF showed at least one strain value or a LAS, which fell below the limit of 1 or respectively 2 standard deviations from the reference mean value. Cardiac strains measured by CMR–FTI are significantly impaired in patients with acute myocarditis even in those with pEF. Therefore, strain assessment may improve the diagnostic accuracy of CMR for myocarditis.     

Diffuse myocardial fibrosis in hypertrophic cardiomyopathy can be identified by cardiovascular magnetic resonance,and is associated with left ventricular diastolic dysfunction

Background

The presence of myocardial fibrosis is associated with worse clinical outcomes in hypertrophic cardiomyopathy (HCM). Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) sequences can detect regional, but not diffuse myocardial fibrosis. Post-contrast T₁ mapping is an emerging CMR technique that may enable the non-invasive evaluation of diffuse myocardial fibrosis in HCM. The purpose of this study was to non-invasively detect and quantify diffuse myocardial fibrosis in HCM with CMR and examine its relationship to diastolic performance.

Methods

We performed CMR on 76 patients - 51 with asymmetric septal hypertrophy due to HCM and 25 healthy controls. Left ventricular (LV) morphology, function and distribution of regional myocardial fibrosis were evaluated with cine imaging and LGE. A CMR T₁ mapping sequence determined the post-contrast myocardial T₁ time as an index of diffuse myocardial fibrosis. Diastolic function was assessed by transthoracic echocardiography.

Results

Regional myocardial fibrosis was observed in 84% of the HCM group. Post-contrast myocardial T₁ time was significantly shorter in patients with HCM compared to controls, consistent with diffuse myocardial fibrosis (498 ± 80 ms vs. 561 ± 47 ms, p < 0.001). In HCM patients, post-contrast myocardial T₁ time correlated with mean E/e’ (r = −0.48, p < 0.001).

Conclusions

Patients with HCM have shorter post-contrast myocardial T₁ times, consistent with diffuse myocardial fibrosis, which correlate with estimated LV filling pressure, suggesting a mechanistic link between diffuse myocardial fibrosis and abnormal diastolic function in HCM.     

Gestational changes in left ventricular myocardial contractile function: new insights from two-dimensional speckle tracking echocardiography

The goal of this study was to evaluate the impact of pregnancy and labor on left ventricular (LV) myocardial mechanics using speckle tracking echocardiography (STE). Pregnancy is characterized by profound hormonal and hemodynamic alterations that directly or indirectly influence cardiac structure and function. However, the impact of these changes on left ventricular (LV) myocardial contractile function has not been fully elucidated. In this prospective, longitudinal study, 35 pregnant women underwent serial clinical and echocardiographic evaluation during each trimester and at labor. Two dimensional STE was performed to measure global LV longitudinal, circumferential and radial strain (GLS, GCS and GRS, respectively). Similar data obtained from 20 nulliparous, age-matched women were used as control. All strain values during pregnancy were adjusted for age and hemodynamic parameters. There was a progressive increase in heart rate, systolic and diastolic blood pressure, cardiac output and LV stroke-work during pregnancy. LV end-diastolic and end-systolic volumes also increased progressively but LV ejection fraction remained unaltered, except for slight reduction during the second trimester. Compared to the controls, GLS and GCS were reduced in the first trimester itself (GLS ?22.39?±?5.43?% vs. ?18.66?±?0.64?%, P 0.0002; GCS ?20.84?±?3.20 vs. ?17.88?±?0.09, P?<?0.001) and remained so throughout the pregnancy and labor. In contrast, GRS showed an increase during pregnancy which peaked during the second trimester (24.18?±?0.39?% vs. 18.06?±?8.14?% in controls, P?<?0.001). Alterations in loading conditions during pregnancy are associated with counterbalancing changes in the myocardial mechanics. LV longitudinal and circumferential strain are reduced whereas radial strain is increased. These counterbalancing changes serve to maintain overall LV ejection performance within a normal range and enable the maternal heart to meet the hemodynamic demands of pregnancy and labor.