Myocardial T1 Research Articles

Technical note: Accuracy and precision of T2 and T2* with a gradient-echo spin-echo (GESE) sequence for cardiac imaging.

The use of a gradient echo spin echo (GESE) method to obtain rapid T2 and T2* estimation in the heart has been proposed. The effect of acquisition parameter settings on T2 and T2* bias and precision have not been investigated in depth. To understand factors impacting the quantification of T2 and T2* values with a gradient echo spin echo (GESE) method using echo planar imaging (EPI) readouts in a reduced field of view acquisition. The GESE method is implemented with a reduced field-of-view using an outer volume suppression (OVS) technique to minimize the time for multi-echo EPI readouts. The number of EPI readouts (images) for the GESE is optimized using Cramer-Rao Lower Bound (CRLB) and Monte Carlo simulations with a nonlinear least-square (NLLS) estimator. The SNR requirements were studied using the latter simulation method for a selected range of T2 and T2* values and T2/T2* ratios. Two healthy control subjects were imaged with the proposed GESE sequence and evaluated with the NLLS estimation method. In addition, the proposed OVS method was compared with a saturation bands OVS method in one subject. Clinical T2 and T2* mappings were used as the reference. The optimal number of EPI readouts is five and the performance is slightly better when the refocusing pulse is placed between the 2nd and 3rd readouts. The SNR requirement for achieving a target bias<1ms and standard deviation (SD)<5ms is more demanding when T2/T2* ratio increases. The minimum SNR requirement in the GESE acquisition should vary from 6 to 20 depending on specific myocardial T2 and T2* values at 3T. The T2 and T2* estimates using the proposed OVS method and the saturation bands OVS method are both similar to the reference. The GESE sequence with five EPI readouts is a feasible and efficient technique that can estimate T2 and T2* values in the septal myocardium within a heartbeat when the SNR requirement can be satisfied.

Hepatic t1 mapping: a new easily obtained biomarker for heart failure patients undergoing cardiac magnetic resonance

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Hepatic venous pressure overload and subsequent liver damage are frequent in patients with Chronic Heart Failure (CHF) but are difficult to quantify except in the late stages of disease. Myocardial T1 mapping is now commonly performed in patients undergoing cardiac magnetic resonance (CMR), with short axis images usually intercepting the liver, therefore allowing the opportunistic measurement of hepatic T1 values. Purpose The aim of this study was to quantify hepatic T1 values in HF patients undergoing CMR, and to assess its clinical and prognostic significance as a biomarker in this setting. Methods Consecutive patients with CHF (LVEF ≤ 50%) who underwent CMR at a single centre since Jan2019 were retrospectively identified. Those with known chronic liver disease, cardiac amyloidosis or suspected alcoholic cardiomyopathy were excluded. Native myocardial T1 mapping [MOLLI 5(3)3 sequence] basal short axis images were used to measure hepatic T1, with the region of interest drawn in the liver, avoiding organ vessels. A control group of subjects without known cardiovascular disease (n=57) was used to define the limits of normality for hepatic T1 values. The clinical significance of hepatic T1 values was assessed by its relationship with markers of right-sided CHF, and its prognostic value by the association with cardiovascular mortality. Results A total of 267 patients (mean age 62±15 years, 69% men, 38% with ischemic cardiomyopathy) were included. Median LVEF was 35% (IQR 26 – 44%) and median RVEF was 51% (IQR 40 – 59%). Overall, 46 patients (17%) had hepatic T1 values above 684 ms (the upper limit of normal for controls). Patients with elevated hepatic T1 had significantly higher RV volumes and lower RVEF (all p values &amp;lt;0.03). Hepatic T1 values were significantly higher in patients with RVEF&amp;lt;45% and in those with moderate or severe tricuspid regurgitation (Figure 1), and were also inversely correlated with RVEF (Spearman R −0.20, p&amp;lt;0.001). During a median follow-up period of 17 months (IQR 11–24), there were 11 cardiovascular deaths. Elevated hepatic T1 was associated with an increased risk of this endpoint (HR 3.04, 95%CI 1.02 – 9.11, p = 0.047). Conclusions Hepatic T1 values can be easily measured in standard myocardial T1 maps, are associated with markers of right-sided heart failure, and have prognostic value in patients with HF. Further studies are warranted to assess the potential clinical usefulness of this new biomarker.

Exploring the prognostic value of myocardial inflammation in Fabry cardiomyopathy

Abstract Funding Acknowledgements Type of funding sources: None. Background Cardiac involvement in Fabry Disease (FD) manifests as left ventricular hypertrophy (LVH) often complicated by myocardial fibrosis and/or inflammation. Indeed, glycosphingolipid storage does not explain the whole spectrum of FD pathophysiology. Lysosomal deposits of unmetabolized glycolipid substrates stimulate the activation of immunological pathways, taking to a chronic inflammatory process.1 In a subgroup of FD patients with late gadolinium enhancement (LGE), signs of myocardial inflammation can be detected by cardiac magnetic resonance (CMR) using T2-weighted (T2w) sequences and T2 mapping. T2 value in inferolateral wall (IL) has been described as the strongest predictor of increase in troponin level. 2 Aim The aims of the study were: 1) to compare CMR parameters in LVH and LGE positive FD patients with and without myocardial inflammation; 2) to verify if myocardial inflammation plays an incremental prognostic role in FD compared to LVH and LGE. Methods Among 190 consecutive FD patients referred for CMR, 47 patients with LVH and LGE were selected for this study. All patients underwent an extensive CMR protocol to provide a detailed evaluation of cardiac morphology and function, with multiparametric tissue characterization. Myocardial inflammation was detected by T2w and T2 mapping sequences. A comparison of CMR parameters between patients with and without inflammation was performed. A composite endpoint of cardiovascular (CV) events was used for survival analysis. Results No differences in age and Mainz Severity Score Index were found between LVH+/LGE+ FD patients with and without myocardial inflammation. Patients with inflammation showed significantly greater left ventricular mass index (LVMI) compared to patients without inflammation. Regarding tissue characterization, patients with myocardial inflammation had more extensive LGE and significantly higher ECV in IL wall. Native myocardial T1 was reduced in both groups without statistically significant difference. (Table 1) Myocardial inflammation always involved IL wall. During a median follow-up of 30 months, Kaplan-Meier curves showed similar event-free survival probability in patients with and without myocardial inflammation (Log-Rank p = 0,215, Figure 1). Conclusion In a population of LVH+/LGE+ FD patients, the presence of CMR signs of myocardial inflammation was associated with more severe LVH and more extensive LGE. However, the presence of myocardial inflammation did not showed an incremental prognostic value on CV outcomes on top of LVH and LGE. Larger studies are needed to verify this findings.

A deep learning approach for accurate and robust T1 estimation from cardiac magnetic resonance MOLLI sequences

Abstract Funding Acknowledgements Type of funding sources: None. Background T1 parametric maps of the myocardium are a recent development in cardiac Magnetic Resonance Imaging (MRI). They can be used to characterize the composition of the heart and identify alterations that can be indicative of a pathology. A common method of T1 estimation involves pixel-wise non-linear curve fitting from Modified Look-Locker Inversion Recovery (MOLLI) series [1]. Whilst relatively accurate, this method presents several drawbacks. Firstly, it assumes magnetization recovery to be a purely exponential process dependent on T1, thus neglecting other parameters such as T2 and B1 that can interfere in the process. Secondly, it does not consider that each acquisition during an inversion recovery experiment inverts the magnetization vector by a given angle and thus interferes with the recovery leading to the measurement of a shorter T1* rather than the actual T1 [2]. Additionally, since it considers each pixel individually, neglecting spatial information, it is sensitive to image quality [3]. Finally, since non-linear curve fitting is an iterative algorithm, it is computationally expensive and time-consuming. Methods To address these issues a convolutional neural network, DeepBLESS [4], and two spatially aware variants of it, were trained to predict T1, T2, and B1 with a dataset of MOLLI series simulated from experimental data. The simulation was performed using Bloch simulations and parameters extracted from a dataset composed of 27 single-slice MOLLI series acquired with the 5(3s)3 protocol using a b-SSFP readout at a main magnetic field strength of 3 Tesla. Thus, a dataset could be generated without relying on exponential fitting for ground truth generation. Results The exponential fitting of T1 was shown to consistently underestimate true T1 values by 138 +- 90 ms. In comparison, the spatially naïve DeepBLESS approach showed a mean absolute error of 14 +- 9 ms and the spatially aware DeepBLESS approach (Median-DeepBLESS) showed a mean absolute error of 13 +- 9 ms. As can be seen in Figure 1, Median-DeepBLESS also showed considerably more resilience to noise than exponential fitting and the spatially naïve version of DeepBLESS. Additionally, the deep learning approaches showcased promising results with regards to the estimation of T2 and B1 from MOLLI sequences (See Figure 2). Conclusions It was shown that the Deep Learning approaches eliminated the underestimation bias of exponential fitting with the spatially aware network Median-DeepBLESS being more robust to noise than both exponential fitting and the standard DeepBLESS network for myocardial T1 estimation. Relatively accurate estimation of T2 and B1 from MOLLI sequences was also accomplished through the Deep Learning approach, which may lead to simultaneous T1, T2, and B1 estimation in common clinical practice in the future.

#4572 EFFECTS OF EMPAGLIFLOZIN ON KIDNEY AND CARDIAC MRI MEASURES IN PATIENTS WITH CHRONIC KIDNEY DISEASE

Abstract Background and Aims EMPA-KIDNEY demonstrated empagliflozin reduced the risk of kidney disease progression or cardiovascular death in patients with CKD at risk of progression, but the mechanisms of benefit are uncertain. MRI was used to assess whether empagliflozin modified the structure and function of the kidneys and heart at around 18 months after randomization. Method Randomized participants from 8 sites in UK and Germany without a contraindication to MRI scanning, were eligible and invited to participate in this substudy. MRI scans were performed using a standardized protocol. Renal T1 mapping (MOLLI 5[3]3 scheme which measures fibrosis and inflammation) was computed by first segmenting MOLLI data using a U-net and then applying the masks to both kidneys. Cardiac MRI included cine steady-state free precession imaging to assess biventricular volumes, mass and function, and T1 mapping to assess myocardial inflammation and fibrosis. The primary outcome was kidney cortical T1 mapping measured by MOLLI. Secondary outcomes included LV ejection fraction, myocardial T1 MOLLI and LV mass index. Differences in MRI measurements between treatment groups were analysed using linear regression adjusted for baseline age, sex, eGFR, UACR and diabetes status. 172 participants were required to provide 90% power at 2p = 0.05 to detect a 50 ms difference in T1. Results 172 participants had an MRI scan around 18 months after randomization. 93 (54%) were allocated empagliflozin and 79 (46%) placebo. Mean (SD) age was 60 (15) years, 26% were female and 23% had diabetes. Mean eGFR was 37 (13) mL/min/1.73m2 and geometric mean (95% CI) UACR was 242 (182-322) mg/g (Table 1). Adjusted mean (SE) cortical T1 mapping by MOLLI was 1623 (10) ms in those allocated empagliflozin versus 1634 (11) ms in those allocated placebo, difference in means (95% CI) −11 (−41 to 18), P = 0.45 (Table 2). Medullary T1 MOLLI scores were similar. Empagliflozin had no significant effect on cardiac MRI measures: difference (95% CI) in LV ejection fraction 1% (−1 to 4); myocardial T1 MOLLI −3 ms (−16 to 10); LV mass index −3 g/m2 (−5 to 0) (Table 2). Conclusion Empagliflozin had no significant effect on MRI-based measures of fibrosis within the kidney cortex or myocardium in people with CKD at risk of progression. There was no effect of treatment on measures of cardiac structure or function. Further MRI measures will be available for presentation by the time of the ERA congress. Funding Boehringer Ingelheim, Eli Lilly and others; Clinicaltrials.gov:NCT03594110.

Characterizing the hypertensive cardiovascular phenotype in the UK Biobank.

To describe hypertension-related cardiovascular magnetic resonance (CMR) phenotypes in the UK Biobank considering variations across patient populations. We studied 39 095 (51.5% women, mean age: 63.9 ± 7.7 years, 38.6% hypertensive) participants with CMR data available. Hypertension status was ascertained through health record linkage. Associations between hypertension and CMR metrics were estimated using multivariable linear regression adjusting for major vascular risk factors. Stratified analyses were performed by sex, ethnicity, time since hypertension diagnosis, and blood pressure (BP) control. Results are standardized beta coefficients, 95% confidence intervals, and P-values corrected for multiple testing. Hypertension was associated with concentric left ventricular (LV) hypertrophy (increased LV mass, wall thickness, concentricity index), poorer LV function (lower global function index, worse global longitudinal strain), larger left atrial (LA) volumes, lower LA ejection fraction, and lower aortic distensibility. Hypertension was linked to significantly lower myocardial native T1 and increased LV ejection fraction. Women had greater hypertension-related reduction in aortic compliance than men. The degree of hypertension-related LV hypertrophy was greatest in Black ethnicities. Increasing time since diagnosis of hypertension was linked to adverse remodelling. Hypertension-related remodelling was substantially attenuated in hypertensives with good BP control. Hypertension was associated with concentric LV hypertrophy, reduced LV function, dilated poorer functioning LA, and reduced aortic compliance. Whilst the overall pattern of remodelling was consistent across populations, women had greater hypertension-related reduction in aortic compliance and Black ethnicities showed the greatest LV mass increase. Importantly, adverse cardiovascular remodelling was markedly attenuated in hypertensives with good BP control.

Longitudinal Changes in the Myocardial T1 Relaxation Time, Extracellular Volume Fraction, and Left Ventricular Function in Asymptomatic Men.

(1) Background: Longitudinal changes in myocardial T1 relaxation time are unknown. We aimed to assess the longitudinal changes in the left ventricular (LV) myocardial T1 relaxation time and LV function. (2) Methods: Fifty asymptomatic men (mean age, 52.0 years) who underwent 1.5 T cardiac magnetic resonance imaging twice at an interval of 54 ± 21 months were included in this study. The LV myocardial T1 times and extracellular volume fractions (ECVFs) were calculated using the MOLLI technique (before and 15 min after gadolinium contrast injection). The 10-year Atherosclerotic Cardiovascular Disease (ASCVD) risk score was calculated. (3) Results: No significant differences in the following parameters were noted between the initial and follow-up assessments: LV ejection fraction (65.0 ± 6.7% vs. 63.6 ± 6.3%, p = 0.12), LV mass/end-diastolic volume ratio (0.82 ± 0.12 vs. 0.80 ± 0.14, p = 0.16), native T1 relaxation time (982 ± 36 vs. 977 ± 37 ms, p = 0.46), and ECVF (24.97 ± 2.38% vs. 25.02 ± 2.41%, p = 0.89). The following parameters decreased significantly from the initial assessment to follow-up: stroke volume (87.2 ± 13.7 mL vs. 82.6 ± 15.3 mL, p = 0.01), cardiac output (5.79 ± 1.17 vs. 5.50 ± 1.04 L/min, p = 0.01), and LV mass index (110.16 ± 22.38 vs. 104.32 ± 18.26 g/m2, p = 0.01). The 10-year ASCVD risk score also remained unchanged between the two timepoints (4.71 ± 0.19% vs. 5.16 ± 0.24%, p = 0.14). (4) Conclusion: Myocardial T1 values and ECVFs were stable over time in the same middle-aged men.

Motion-corrected model-based reconstruction for 2D myocardial T1 mapping.

To allow for T1 mapping of the myocardium within 2.3 s for a 2D slice utilizing cardiac motion-corrected, model-based image reconstruction. Golden radial data acquisition is continuously carried out for 2.3 s after an inversion pulse. In a first step, dynamic images are reconstructed which show both contrast changes due to T1 recovery and anatomical changes due to the heartbeat. An image registration algorithm with a signal model for T1 recovery is applied to estimate non-rigid cardiac motion. In a second step, estimated motion fields are applied during an iterative model-based T1 reconstruction. The approach was evaluated in numerical simulations, phantom experiments and in in-vivo scans in healthy volunteers. The accuracy of cardiac motion estimation was shown in numerical simulations with an average motion field error of 0.7 ± 0.6 mm for a motion amplitude of 5.1 mm. The accuracy of T1 estimation was demonstrated in phantom experiments, with no significant difference (p = 0.13) in T1 estimated by the proposed approach compared to an inversion-recovery reference method. In vivo, the proposed approach yielded 1.3 × 1.3 mm T1 maps with no significant difference (p = 0.77) in T1 and SDs in comparison to a cardiac-gated approach requiring 16 s scan time (i.e., seven times longer than the proposed approach). Cardiac motion correction improved the precision of T1 maps, shown by a 40% reduced SD. We have presented an approach that provides T1 maps of the myocardium in 2.3 s by utilizing both cardiac motion correction and model-based T1 reconstruction.

Rapidly reversible acute neurological, renal, and cardiac impairment during malignant hypertension

BackgroundMalignant hypertension is a model of the rapid changes that a high afterload and renin-angiotensin levels can induce on target organs such as the heart. We present a case of a young man affected by malignant hypertension with multi-organ involvement who showed quick remission after adequate antihypertensive treatment.Case summaryA 41-year-old jazz pianist with a family history of coronary artery disease presented to the emergency department for asthenia and epigastric pain, associated with right eye visual impairment. No neurological symptoms. An echocardiogram showed left ventricular hypertrophy with severe impairment of ejection fraction (22%) due to global hypokinesia. There was renal insufficiency (creatinine 2.51 mg/dl, eGFR 34 ml/min, HS Troponin T 127 pg/dl, NT pro-BNP 22,672 pg/ml, CRP 32 mg/L, sodium 129 mEq/L with normal kaliemia. The following day, anterior T wave inversion was observed in the electrocardiogram. At a cardiac magnetic resonance. Concentric hypertrophy of the left ventricle was observed with normal myocardial T1 mapping values (1100 ± 38 ms), ruling out Fabry’s disease. There was no obvious myocardial edema at T2 weighted. The viral panel for acute myocarditis resulted in negative. After the exclusion of all possible secondary causes, malignant essential hypertension was the final diagnosis, and additional tests confirmed multi-organ damage. An ophthalmological examination demonstrated hypertensive retinopathy with hemorrhages, cottony exudates, and macular lipid exudation, especially in the right eye. A brain MRI showed small areolas of T2 hyperintensity in the white matter of both cerebral hemispheres, suggestive of chronic microangiopathy, and left nuclear micro lacunar ischemia.The patient was treated with full-dose calcium channel blockers (amlodipine 10 mg), beta-blockers (bisoprolol 10 mg), alpha2 agonists (slow-release clonidine patch), selective a1 blocker (doxazosine 16 mg), and furosemide 50 mg. After the exclusion of renal stenosis and improvement of renal function, Ramipril was added up to a final dose of 10 mg daily. In parallel with the achievement of a satisfactory blood pressure control, visual impairment disappeared with a reduction of retinal ischemic exudates and hemorrhages at the ophthalmological follow-up assessment.At the time of discharge, an echocardiographic re-evaluation confirmed concentric hypertrophy of the left ventricle with markedly reduced wall thicknesses, with a partial recovery in left ventricular ejection function (EF 44%).Six months after discharge, the patient is in good general condition under optimal medical therapy (without furosemide) with normalized blood pressure values (130–140/80 mmHg). At 6 months from discharge, creatinine was only mildly increased (1.5 mg/dl, eGFR 59.5 ml/min) and NT-pro BNP nearly normalized (452 pg/ml).DiscussionMalignant hypertension is a cardiovascular emergency and requires immediate and careful intervention to lower blood pressure and reduce organ injury. It is an exclusion diagnosis that can be advanced once the causes of secondary hypertension have been excluded. Remission of organ injury is possible and might be rapid under adequate antihypertensive treatment, but patients require a close follow-up.

Histopathologic Validation of Stress T1 Mapping in Myocardial Ischemia: Another Step toward Clinical Translation?

Histopathologic Validation of Stress T1 Mapping in Myocardial Ischemia: Another Step toward Clinical Translation?

Detection of Early Diffuse Myocardial Fibrosis and Inflammation in Chagas Cardiomyopathy with T1 Mapping and Extracellular Volume

Purpose To evaluate myocardial T1 mapping and extracellular volume (ECV) parameters in different stages of Chagas cardiomyopathy and determine whether they are predictive of disease severity and prognosis. Materials and Methods Prospectively enrolled participants (July 2013 to September 2016) underwent cine and late gadolinium enhancement (LGE) cardiac MRI and T1 mapping with a precontrast (native) or postcontrast modified Look-Locker sequence. The native T1 and ECV values were measured among subgroups that were based on disease severity (indeterminate, Chagas cardiomyopathy with preserved ejection fraction [CCpEF], Chagas cardiomyopathy with midrange ejection fraction [CCmrEF], and Chagas cardiomyopathy with reduced ejection fraction [CCrEF]). Cox proportional hazards regression and the Akaike information criterion were used to determine predictors of major cardiovascular events (cardioverter defibrillator implant, heart transplant, or death). Results In 107 participants (90 participants with Chagas disease [mean age ± SD, 55 years ± 11; 49 men] and 17 age- and sex-matched control participants), the left ventricular (LV) ejection fraction and the extent of focal and diffuse or interstitial fibrosis were correlated with disease severity. Participants with CCmrEF and participants with CCrEF showed significantly higher global native T1 and ECV values than participants in the indeterminate, CCpEF, and control groups (T1: 1072 msec ± 34 and 1073 msec ± 63 vs 1010 msec ± 41, 1005 msec ± 69, and 999 msec ± 46; ECV: 35.5% ± 3.6 and 35.0% ± 5.4 vs 25.3% ± 3.5, 28.2% ± 4.9, and 25.2% ± 2.2; both P < .001). Remote (LGE-negative areas) native T1 and ECV values were also higher (T1: 1056 msec ± 32 and 1071 msec ± 55 vs 1008 msec ± 41, 989 msec ± 96, and 999 msec ± 46; ECV: 30.2% ± 4.7 and 30.8% ± 7.4 vs 25.1% ± 3.5, 25.1% ± 3.7, and 25.0% ± 2.2; both P < .001). Abnormal remote ECV values (>30%) occurred in 12% of participants in the indeterminate group, which increased with disease severity. Nineteen combined outcomes were observed (median follow-up time: 43 months), and a remote native T1 value greater than 1100 msec was independently predictive of combined outcomes (hazard ratio, 12 [95% CI: 4.1, 34.2]; P < .001). Conclusion Myocardial native T1 and ECV values were correlated with Chagas disease severity and may serve as markers of myocardial involvement in Chagas cardiomyopathy that precede LGE and LV dysfunction. Keywords: MRI, Cardiac, Heart, Imaging Sequences, Chagas Cardiomyopathy Supplemental material is available for this article. © RSNA, 2023

Pilot study to establish the myocardium native T1 mapping reference values in 1.5 Tesla cardiac magnetic resonance of healthy Malaysians

BackgroundCardiac magnetic resonance (CMR) is a powerful and robust imaging modality with the capability for tissue characterisation by quantifying the intrinsic magnetic properties of tissues. The current international consensus recommendation is to determine the local normal T1 mapping value. Recent advancement suggests pooled data or benchmarking of CMR mapping reference values. We present the adult myocardial native T1 mapping value of a common MR acquisition in healthy Malaysians who are predominantly brown skin Asians.MethodsThis is a prospective, cross-sectional study in a single centre. CMR was performed on a 1.5 T MR using 5(3s)3 MOLLI sequence with motion correction, TE = 1.31 ms, TR = 2.78 ms. The analysis of the mid-septal T1 value was done using third-party software (CVi42) and the OsiriX software by two blinded cardiac radiologists.ResultsA total of 51 eligible adults were recruited of which 1 was excluded due to incidental finding of moderate mitral regurgitation. The mean age was 30 years ± 7.0, the majority (64%) was female, the median heart rate was 72 ± 20 bpm and mean the BSA was 1.6 ± 0.1 m2. The ethnicity distribution is Malay 76%, Indian 12%, Chinese 8% and Sabahan 4%. The normal range for mid-septum myocardial T1 using CVi42 was 1012 ± 33 ms and using OsiriX was 1018 ± 37 ms. There is no correlation observed against gender, ethnicity and heart rate. The moderate correlation observed with age is not gender specified. The interobserver reliability was good (coefficient 0.813).ConclusionsFor T1 mapping to be applied clinically, it is imperative to determine the local normal value as recommended by international consensus. The first-ever database on native T1 mapping for 1.5 T CMR reference value for Malaysians who are predominantly brown skin Asians is provided in this pilot study.

Quantitative myocardial T2 mapping adds value to Japanese circulation society diagnostic criteria for active cardiac sarcoidosis.

Noninvasive identification of active myocardial inflammation in patients with cardiac sarcoidosis plays a key role in management but remains elusive. T2 mapping is a proposed solution, but the added value of quantitative myocardial T2 mapping for active cardiac sarcoidosis is unknown. Retrospective cohort analysis of 56 sequential patients with biopsy-confirmed extracardiac sarcoidosis who underwent cardiac MRI for myocardial T2 mapping. The presence or absence of active myocardial inflammation in patients with CS was defined using a modified Japanese circulation society criteria within one month of MRI. Myocardial T2 values were obtained for the 16 standard American Heart Association left ventricular segments. The best model was selected using logistic regression. Receiver operating characteristic curves and dominance analysis were used to evaluate the diagnostic performance and variable importance. Of the 56 sarcoidosis patients included, 14 met criteria for active myocardial inflammation. Mean basal T2 value was the best performing model for the diagnosis of active myocardial inflammation in CS patients (pR2 = 0.493, AUC = 0.918, 95% CI 0.835-1). Mean basal T2 value > 50.8ms was the most accurate threshold (accuracy = 0.911). Mean basal T2 value + JCS criteria was significantly more accurate than JCS criteria alone (AUC = 0.981 vs. 0.887, p = 0.017). Quantitative regional T2 values are independent predictors of active myocardial inflammation in CS and may add additional discriminatory capability to JCS criteria for active disease.

Automatic uncertainty-based quality controlled T1 mapping and ECV analysis from native and post-contrast cardiac T1 mapping images using Bayesian vision transformer.

Deep learning-based methods for cardiac MR segmentation have achieved state-of-the-art results. However, these methods can generate incorrect segmentation results which can lead to wrong clinical decisions in the downstream tasks. Automatic and accurate analysis of downstream tasks, such as myocardial tissue characterization, is highly dependent on the quality of the segmentation results. Therefore, it is of paramount importance to use quality control methods to detect the failed segmentations before further analysis. In this work, we propose a fully automatic uncertainty-based quality control framework for T1 mapping and extracellular volume (ECV) analysis. The framework consists of three parts. The first one focuses on segmentation of cardiac structures from a native and post-contrast T1 mapping dataset (n=295) using a Bayesian Swin transformer-based U-Net. In the second part, we propose a novel uncertainty-based quality control (QC) to detect inaccurate segmentation results. The QC method utilizes image-level uncertainty features as input to a random forest-based classifier/regressor to determine the quality of the segmentation outputs. The experimental results from four different types of segmentation results show that the proposed QC method achieves a mean area under the ROC curve (AUC) of 0.927 on binary classification and a mean absolute error (MAE) of 0.021 on Dice score regression, significantly outperforming other state-of-the-art uncertainty based QC methods. The performance gap is notably higher in predicting the segmentation quality from poor-performing models which shows the robustness of our method in detecting failed segmentations. After the inaccurate segmentation results are detected and rejected by the QC method, in the third part, T1 mapping and ECV values are computed automatically to characterize the myocardial tissues of healthy and cardiac pathological cases. The native myocardial T1 and ECV values computed from automatic and manual segmentations show an excellent agreement yielding Pearson coefficients of 0.990 and 0.975 (on the combined validation and test sets), respectively. From the results, we observe that the automatically computed myocardial T1 and ECV values have the ability to characterize myocardial tissues of healthy and cardiac diseases like myocardial infarction, amyloidosis, Tako-Tsubo syndrome, dilated cardiomyopathy, and hypertrophic cardiomyopathy.

Cardiovascular Magnetic Resonance in Survivors of Critical Illness: Cardiac Abnormalities Are Associated With Acute Kidney Injury.

Background The objective of this study was to investigate cardiac abnormalities in intensive care unit (ICU) survivors of critical illness and to determine whether temporary acute kidney injury (AKI) is associated with more pronounced findings on cardiovascular magnetic resonance. Methods and Results There were 2175 patients treated in the ICU (from 2015 until 2021) due to critical illness who were screened for study eligibility. Post-ICU patients without known cardiac disease were prospectively recruited from March 2021 to May 2022. Participants underwent cardiovascular magnetic resonance including assessment of cardiac function, myocardial edema, late gadolinium enhancement, and mapping including extracellular volume fraction. Student t test, Mann-Whitney U test, and χ2 tests were used. There were 48 ICU survivors (46±15 years of age, 28 men, 29 with AKI and continuous kidney replacement therapy, and 19 without AKI) and 20 healthy controls who were included. ICU survivors had elevated markers of myocardial fibrosis (T1: 995±31 ms versus 957±21 ms, P<0.001; extracellular volume fraction: 24.9±2.5% versus 22.8±1.2%, P<0.001; late gadolinium enhancement: 1% [0%-3%] versus 0% [0%-0%], P<0.001), more frequent focal late gadolinium enhancement lesions (21% versus 0%, P=0.03), and an impaired left ventricular function (eg, ejection fraction: 57±6% versus 60±5%, P=0.03; systolic longitudinal strain: 20.3±3.7% versus 23.1±3.5%, P=0.004) compared with healthy controls. ICU survivors with AKI had higher myocardial T1 (1002±33 ms versus 983±21 ms; P=0.046) and extracellular volume fraction values (25.6±2.6% versus 23.9±1.9%; P=0.02) compared with participants without AKI. Conclusions ICU survivors of critical illness without previously diagnosed cardiac disease had distinct abnormalities on cardiovascular magnetic resonance including signs of myocardial fibrosis and systolic dysfunction. Findings were more abnormal in participants who experienced AKI with necessity of continuous kidney replacement therapy during their ICU stay. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT05034588.

Cardiac magnetic resonance in Fabry disease.

Fabry disease (FD) is a rare X-linked inherited lysosomal storage disorder caused by deficient a-galactosidase A activity that leads to an accumulation of glycolipids, mainly globotriaosylceramide (Gb3) and globotriaosylsphingosine, in affected tissues, including the heart. Cardiovascular involvement usually manifests as left ventricular hypertrophy (LVH), myocardial fibrosis, heart failure, and arrhythmias, which limit the quality of life and represent the most common causes of death. Following the introduction of enzyme replacement therapy, early diagnosis and treatment have become essential in slowing down the disease progression and preventing major cardiac complications. Recent advances in the understanding of FD pathophysiology suggest that in addition to Gb3 accumulation, other mechanisms contribute to the development of cardiac damage. FD cardiomyopathy is characterized by an earlier stage of glycosphingolipid accumulation and a later one of hypertrophy. Morphological and functional aspects are not specific in the echocardiographic evaluation of Anderson-Fabry disease. Cardiac magnetic resonance with tissue characterization capability is an accurate technique for the differential diagnosis of LVH. Progress in imaging techniques has improved the diagnosis and staging of FD-related cardiac disease: a decreased myocardial T1 value is specific of FD. Late gadolinium enhancement is typical of the later stage of cardiac involvement but as in other cardiomyopathy is also valuable to predict the outcome and cardiac response to therapy.

Chronic troponin elevation assessed by myocardial T1 mapping in patients with stable coronary artery disease.

Cardiac troponin detected with sensitive assays can be chronically elevated, in the absence of unstable coronary syndromes. In patients with chronic coronary artery disease, clinically silent ischemic episodes may cause chronic troponin release. T1 mapping is a cardiovascular magnetic resonance technique useful in quantitative cardiac tissue characterization. We selected patients with anatomically and functionally normal hearts to investigate associations between chronic troponin release and myocardial tissue characteristics assessed by T1 mapping. We investigated the relationship between cardiac troponin I concentrations and cardiovascular magnetic resonance T1 mapping parameters in patients with stable coronary artery disease enrolled in MASS V study before elective revascularization. Participants had no previous myocardial infarction, negative late gadolinium enhancement, normal left ventricular function, chamber dimensions and wall thickness. A total of 56 patients were analyzed in troponin tertiles: nativeT1 and extracellular volume (ECV) values (expressed as means ± standard deviations) increased across tertiles: nativeT1 (1006 ± 27 ms vs 1016 ± 27 ms vs 1034 ± 37 ms, ptrend = 0.006) and ECV (22 ± 3% vs 23 ± 1.9% vs 25 ± 3%, ptrend = 0.007). Cardiac troponin I concentrations correlated with native T1(R = 0.33, P = .012) and ECV (R = 0.3, P = .025), and were independently associated with nativeT1 (P = .049) and ventricular mass index (P = .041) in multivariable analysis. In patients with chronic coronary artery disease and structurally normal hearts, troponin I concentrations correlated with T1 mapping parameters, suggesting that diffuse edema or fibrosis scattered in normal myocardium might be associated with chronic troponin release.

Genetics of myocardial interstitial fibrosis in the human heart and association with disease.

Myocardial interstitial fibrosis is associated with cardiovascular disease and adverse prognosis. Here, to investigate the biological pathways that underlie fibrosis in the human heart, we developed a machine learning model to measure native myocardial T1 time, a marker of myocardial fibrosis, in 41,505 UK Biobank participants who underwent cardiac magnetic resonance imaging. Greater T1 time was associated with diabetes mellitus, renal disease, aortic stenosis, cardiomyopathy, heart failure, atrial fibrillation, conduction disease and rheumatoid arthritis. Genome-wide association analysis identified 11 independent loci associated with T1 time. The identified loci implicated genes involved in glucose transport (SLC2A12), iron homeostasis (HFE, TMPRSS6), tissue repair (ADAMTSL1, VEGFC), oxidative stress (SOD2), cardiac hypertrophy (MYH7B) and calcium signaling (CAMK2D). Using a transforming growth factor β1-mediated cardiac fibroblast activation assay, we found that 9 of the 11 loci consisted of genes that exhibited temporal changes in expression or open chromatin conformation supporting their biological relevance to myofibroblast cell state acquisition. By harnessing machine learning to perform large-scale quantification of myocardial interstitial fibrosis using cardiac imaging, we validate associations between cardiac fibrosis and disease, and identify new biologically relevant pathways underlying fibrosis.

Myocardial tissue characterization by segmental T2 mapping in thalassaemia major: detecting inflammation beyond iron.

We measured myocardial T2 values by a segmental approach in thalassaemia major (TM) patients, comparing such values against T2* values for the detection of myocardial iron overload (MIO), evaluating their potential in detecting subclinical inflammation, and correlating with clinical status. One-hundred and sixty-six patients (102 females, 38.29 ± 11.49years) enrolled in the Extension-Myocardial Iron Overload in Thalassemia Network underwent magnetic resonance imaging for the assessment of hepatic, pancreatic, and cardiac iron overload (T2* technique), of biventricular function (cine images), and of replacement myocardial fibrosis [late gadolinium enhancement (LGE)]. T2 and T2* values were quantified in all 16 myocardial segments, and the global value was the mean of all segments. Global heart T2 values were significantly higher in TM than in a cohort of 80 healthy subjects. T2 and T2* values were significantly correlated. Out of the 25 patients with a decreased global heart T2* value, 11 (44.0%) had reduced T2 values. No patient with a normal T2* value had a decreased T2 value.Eleven (6.6%) patients had a decreased global heart T2 value, 74 (44.6%) a normal global heart T2 value, and 81 (48.8%) an increased global heart T2 value. Biventricular function was comparable amongst the three groups, whilst LGE was significantly more frequent in patients with reduced vs. increased global heart T2 value. Compared with the other two groups, patients with reduced T2 values had significantly higher hepatic and pancreatic iron deposition. In TM, T2 mapping does not offer any advantage in terms of sensitivity for MIO assessment but detects subclinical myocardial inflammation.

The relationship between epicardial adipose tissue thickness and arrhythmias in patients with hypertension: a 3.0T cardiac magnetic resonance study.

To investigate the relationship between epicardial adipose tissue (EAT) thickness using cardiac magnetic resonance imaging (CMR) and arrhythmias in hypertensive patients. Fifty-four hypertensive patients with arrhythmias (HTN [arrhythmias+]), 79 hypertensive patients without arrhythmias (HTN [arrhythmias-]), and 39 normal controls were retrospectively enrolled. EAT thickness was measured on cine images. Analysis of covariance with Bonferroni's post hoc correction, Pearson or Spearman analysis, receiver operating characteristic curve, and intraclass correlation coefficient analysis were performed. All hypertensive patients had impaired left ventricular (LV) and left atrial (LA) myocardial deformation, and HTN (arrhythmias+) patients displayed higher LV myocardial native T1, LA volume index, and increased EAT thickness than HTN (arrhythmias-) patients and normotensive controls. The presence of LV late gadolinium enhancement (LGE) was higher in hypertensive patients with arrhythmias than in those without arrhythmias. EAT thickness metrics significantly correlated with age, systolic blood pressure, body mass index, triglycerides and high-density lipoprotein levels, LV mass index and native T1 (all p < 0.05). EAT thickness parameters were able to differentiate hypertensive patients with arrhythmias from those without arrhythmias and normal controls, and the right ventricular free wall had the highest diagnostic performance. An accumulation of EAT thickness could further induce cardiac remodeling, promote myocardial fibrosis, and exaggerate function in hypertensive patients with arrhythmias. CMR-derived EAT thickness metrics could be a useful imaging marker for differentiating hypertensive patients with arrhythmias, which might be a potential target for the prevention of cardiac remodeling and arrhythmias.