Detection Of Myocardial Fibrosis Research Articles

Speckle-tracking echocardiography as screening tool for myocardial fibrosis and Iron overload in transfusion-dependent beta-thalassemia

BackgroundTransfusion-dependent beta thalassemia (TDT) is a genetic disorder characterized by low haemoglobin levels, often leading to myocardial iron overload (MIO) and myocardial fibrosis (MF). Cardiac Magnetic Resonance (CMR) represents the gold standard for MIO and MF assessment, although its limited availability and high costs pose challenges. Left Ventricular Global Longitudinal Strain (LV GLS) measured by Speckle Tracking Echocardiography (STE) could offer a valuable alternative. MethodsA monocentric diagnostic accuracy study was conducted to compare the performance of LV GLS with CMR using T2* for evaluating MIO and late gadolinium enhancement (LGE) for detecting MF. Between January 2022 and January 2023, 44 consecutive patients with TDT were enrolled. For each participant was performed LV GLS with STE, including CMR with T2* technique and LGE sequences. ResultsCMR identified MIO in 8 patients (18 %) and MF in 5 (11 %). LV GLS STE was normal in patients without MIO (−20.6 ± 3.1 %) or MF (−20.6 ± 2.8 %), significantly differing from those with MIO (−18.2 ± 2.1 %, p = 0.043) and MF (−16.4 ± 1.7 %, p = 0.002). ROC analysis indicated an optimal LV GLS STE cutoff of −19.8 % for MIO (AUC = 0.76, 95 % CI: 0.59–0.93, p = 0.054) with an overall diagnostic accuracy of 64 % and an optimal cutoff of −18.3 % for MF (AUC = 0.93, 95 % CI: 0.85–1.00, p = 0.009) with an accuracy of 86 %. ConclusionsThe findings of this pilot study indicate that LV GLS with STE, may be a cost-effective screening tool for the early detection of MIO and MF in TDT patients.

Role of magnetic resonance imaging in the detection of myocardial fibrosis in life-threatening ventricular arrhythmias

Sudden cardiac death (SCD) is a major medical, economic and social problem. Survival after SCD remains low. Its leading mechanism is fatal ventricular tachyarrhythmias. The only highly effective aid remains an implantable cardioverter defibrillator (ICD). According to modern concepts, myocardial fibrosis (MF) is the leading cause of life-threatening ventricular arrhythmias. Magnetic resonance imaging (MRI) has become the standard for non-invasive MF imaging and one of the leading methods for its quantification, which is why this method is recommended for determining indications for ICD implantation. MRI can show the scar location, which should be taken into account when placing the lead, and determine its size, which predicts the effectiveness of ICD implantation. Identification of MF in patients with life-threatening ventricular arrhythmias is an important area of research aimed at identifying the risk of SCD. Delayed contrast-enhanced MRI can be considered as a marker to improve SCD risk stratification.

A deep learning approach to predict myocardial fibrosis in early contrast-enhanced CCT images

Abstract Funding Acknowledgements Type of funding sources: None. Background Late gadolinium enhancement (LGE) derived from cardiac magnetic resonance (CMR) has become a method of choice for the evaluation of myocardial tissue composition and detection of myocardial fibrosis. Advances in cardiac computed tomography (CCT) imaging have led to its growing role as possible alternative to CMR, because of its wider availability and suitability for patients with contraindication. Purpose To develop a myocardial fibrosis detection method from early contrast-enhanced CCT (CE-CCT) imaging using a deep learning (DL) approach. Methods Fifty consecutive patients (age: 62±10 y, male 84%) with known left ventricular dysfunction were enrolled. All patients underwent both LGE-CMR and early and delayed CE-CCT. According to the LGE-CMR patterns, patients were classified as ischemic (n=15, 30%) or non-ischemic (n=35, 70%). Scar regions were manually traced on delayed CE-CCT using LGE-CMR as reference. On early CE-CCT images, segments were extracted according to American Heart Association (AHA) 16-segment model and labeled (scar/no scar) based on the delayed CE-CCT manual tracing. A DL model was developed for automatic segmental classification. Results Based on 44187 segments analyzed, 71% of accuracy (ischemic: 66%; non-ischemic: 74%) for detecting scar on early CE-CCT images was achieved (Picture 1). In a per-segment analysis of the 16-segment AHA model, an accuracy of 91% (ischemic: 87%; non-ischemic: 93%) was obtained from early CE-CCT compared to the LGE-CMR. Conclusions DL on early CE-CCT acquisition may allow the detection of myocardial fibrosis without additional contrast-agent administration or radiation exposure, thus reducing the user interaction and visual inspection with benefit in both efforts and time.

The usefulness of magnetic resonance imaging for the prognostic evaluation of patients with heart failure [Version 1; Peer Review - In process

Introduction: the role of magnetic resonance imaging (MRI) in heart failure (HF) is much discussed, both in the etiological and prognostic evaluation of this disease. Therefore, a description of the usefulness of MRI would show us its role in the evaluation of prognosis in patients with HF of various etiologies. Aim: to describe the usefulness of MRI for the evaluation of prognosis in patients with HF of various etiologies. Methodology: a narrative literature review was carried out by means of a search in databases such as PubMed, Scopus, Elsevier and Springer (BMC). Results: cardiac magnetic resonance (CMR) is superior to echocardiography in assessing left ventricular volumes and function with better reproducibility, also when analyzing systolic abnormalities and characterizing viable myocardial tissue, as well as that with the presence of myocardial fibrosis. Precisely, the detection of myocardial fibrosis has a predictive value for adverse events in patients with HF. Conclusion: CMR is useful to identify previously undetected pathology and pathologies that are difficult to diagnose. Thus, its use is associated with better diagnostic performance and, therefore, a better predictor of adverse events in patients with HF

Comparison of 68Ga-FAPI imaging and cardiac magnetic resonance in detection of myocardial fibrosis in a patient with chronic thromboembolic pulmonary hypertension

Comparison of 68Ga-FAPI imaging and cardiac magnetic resonance in detection of myocardial fibrosis in a patient with chronic thromboembolic pulmonary hypertension

Detection of myocardial fibrosis: Where we stand.

Myocardial fibrosis, resulting from the disturbance of extracellular matrix homeostasis in response to different insults, is a common and important pathological remodeling process that is associated with adverse clinical outcomes, including arrhythmia, heart failure, or even sudden cardiac death. Over the past decades, multiple non-invasive detection methods have been developed. Laboratory biomarkers can aid in both detection and risk stratification by reflecting cellular and even molecular changes in fibrotic processes, yet more evidence that validates their detection accuracy is still warranted. Different non-invasive imaging techniques have been demonstrated to not only detect myocardial fibrosis but also provide information on prognosis and management. Cardiovascular magnetic resonance (CMR) is considered as the gold standard imaging technique to non-invasively identify and quantify myocardial fibrosis with its natural ability for tissue characterization. This review summarizes the current understanding of the non-invasive detection methods of myocardial fibrosis, with the focus on different techniques and clinical applications of CMR.

Molecular Approaches and Echocardiographic Deformation Imaging in Detecting Myocardial Fibrosis.

The pathological remodeling of myocardial tissue is the main cause of heart diseases. Several processes are involved in the onset of heart failure, and the comprehension of the mechanisms underlying the pathological phenotype deserves special attention to find novel procedures to identify the site of injury and develop novel strategies, as well as molecular druggable pathways, to counteract the high degree of morbidity associated with it. Myocardial fibrosis (MF) is recognized as a critical trigger for disruption of heart functionality due to the excessive accumulation of extracellular matrix proteins, in response to an injury. Its diagnosis remains focalized on invasive techniques, such as endomyocardial biopsy (EMB), or may be noninvasively detected by cardiac magnetic resonance imaging (CMRI). The detection of MF by non-canonical markers remains a challenge in clinical practice. During the last two decades, two-dimensional (2D) speckle tracking echocardiography (STE) has emerged as a new non-invasive imaging modality, able to detect myocardial tissue abnormalities without specifying the causes of the underlying histopathological changes. In this review, we highlighted the clinical utility of 2D-STE deformation imaging for tissue characterization, and its main technical limitations and criticisms. Moreover, we focalized on the importance of coupling 2D-STE examination with the molecular approaches in the clinical decision-making processes, in particular when the 2D-STE does not reflect myocardial dysfunction directly. We also attempted to examine the roles of epigenetic markers of MF and hypothesized microRNA-based mechanisms aiming to understand how they match with the clinical utility of echocardiographic deformation imaging for tissue characterization and MF assessment.

Endogenous assessment of late gadolinium enhancement grey zone in patients with non-ischaemic cardiomyopathy with T1ρ and native T1 mapping.

This study aims to validate and compare the feasibility of T1ρ and native longitudinal relaxation time (T1) mapping in detection of myocardial fibrosis in patients with non-ischaemic cardiomyopathy, focusing on the performance of both methods in identifying late gadolinium enhancement (LGE) grey zone. Twenty-seven hypertrophic cardiomyopathy (HCM) patients, 16 idiopathic dilated cardiomyopathy (DCM) patients, and 18 healthy controls were prospectively enrolled for native T1 and T1ρ mapping imaging and then all the patients underwent enhancement scan for LGE extent and extracellular volume (ECV) values. In LGE positive patients, the LGE areas were divided into LGE core (6 SDs above remote myocardium) and grey zone (2-6 SDs above remote myocardium) according to the signal intensity of LGE. Both HCM and DCM patients showed significantly higher native T1 values and T1ρ values than controls no matter the presence of LGE (all P < 0.01). There were significant differences in native T1 and T1ρ values among four different types of myocardia (LGE core, grey zone, remote area and control, P < 0.0001). However, the T1ρ values of grey zone were significantly higher than control (P < 0.01), while the native T1 values were not (P = 0.089). T1ρ values were significantly associated with both native T1 values (r = 0.54, P < 0.001) and ECV values (r = 0.54, P < 0.001). T1ρ mapping is a feasible method to detect myocardial fibrosis in patients with non-ischaemic cardiomyopathy no matter the presence of LGE. Compared with native T1, T1ρ may serve as a better discriminator in the identification of LGE grey zone.

Detection of myocardial fibrosis by speckle-tracking echocardiography: from prediction to clinical applications.

Myocardial fibrosis (MF) represents the underlying pathologic condition of many cardiac disease, leading to cardiac dysfunction and heart failure (HF). Biopsy studies have shown the presence of MF in patients with decompensating HF despite apparently normal cardiac function. In fact, basic indices of left ventricular (LV) function, such as LV ejection fraction (EF), fail to recognize subtle LV dysfunction caused by MF. Cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) is currently recognized as the gold standard imaging investigation for the detection of focal and diffuse cardiac chambers MF; however, its use is limited by its availability and the use of contrast agents, while echocardiography remains the first level cardiac imaging technique due to its low cost, portability and high accessibility. Advanced echocardiographic techniques, above all speckle-tracking echocardiography (STE), have demonstrated reliability for early detection of structural myocardial abnormalities and for the prediction of prognosis in acute and chronic HF. Myocardial strain of both ventricles and also left atrium has been shown to correlate with the degree of MF, providing useful prognostic information in several diseases, such as HF, cardiomyopathies and valvular heart disease. This paper aims to provide an overview of the pathophysiology of MF and the clinical application of STE for the prediction of left and right heart chambers MF in HF patients.

Abstract 12682: Markers of Microbial Translocation Biomarkers in People Living With HIV Infection and Their Relationship With Myocardial Function and Fibrosis: Myocardial and Coronary Abnormalities in HIV Infection (MACHIN) Study

Background: Microbial translocation (MT) is suggested to play a role in increases risk of myocardial fibrosis (MF) and LV dysfunction in people living with HIV infection (PLWH). We investigated the association of biomarkers of MT with myocardial disease in MACHIN study. Methods: Biomarkers of MT (soluble CD14 (sCD14), FABP, SGP130, and BDG) were measured in serum samples of 92 participants (54 PLWH and 38 HIV- controls, mean age 47±14 years, 28% female). Myocardial structure and function were assessed using CMR. In addition, our protocol included detection of overt MF using delayed-enhancement images as well as diffuse MF using extracellular volume (ECV)-measured by T1 mapping. Results: FABP levels were significantly higher in PLWH compared to controls (percentage of people in higher tertile 17% vs 47%, respectively, OR: 4.4, 95% CI: 1.4-13.5, p: 0.01) and this association was significant after adjustment for age and race. Higher values of FABP were significantly correlated with presence and extent of MF. Participants with higher tertile of FABP had a significantly higher odds of presence of MF (ECV above median) compared to controls (OR: 5.9, 95% CI: 1.3, 27.0, p: 0.02) after adjustment for HIV status, age, gender, and race. Furthermore, participants with high FABP also had higher extent of MF (calculated ECV values) compared to controls (adjusted regression coefficient 6.7%, p&lt;0.01). Importantly, while HIV infection was significantly associated with presence and extent of MF, these associations were not significant when FABP was added to the models, suggesting that FABP may explain the relationship between HIV infection and MF. PLWH had significantly higher levels of sCD14 compared to controls (p &lt;0.05), even after adjustment for age, gender, and race (p-value: 0.04). However, serum levels of sCD14 was not associated with LV and RV systolic function, LV mass, MF, or delayed-enhancement on cardiac MRI. SGP130 and BDG were not significantly associated with MF. Conclusion: Increased levels of biomarkers of microbial translocation is observed in virologically-suppressed PLWH and may explain the increased risk of MF in these patients.

Diagnostic value of microRNA-27 and -339 in heart transplant recipients with myocardial fibrosis

Myocardial fibrosis plays a key role in the pathogenesis of heart failure. A family of small non-coding signaling molecules, microRNAs (miRNAs), has been identified as promising profibrogenic biomarkers capable of signaling a possible risk of adverse events after heart transplantation.Objective: to identify and evaluate the diagnostic significance of miRNAs, as well as comprehensive miRNA-based tests in heart recipients with graft myocardial fibrosis.Materials and Methods. The study included 83 heart recipients aged 16 to 64 (48.4 ± 13.1) years. The expression levels of five microRNAs (miR-27, -101, -142, -339, -424) in venous blood plasma were measured by quantitative real-time polymerase chain reaction; galectin-3 serum levels were determined by enzyme immunoassay.Results. Morphological signs of graft myocardial fibrosis were verified in 48 recipients. The miR-27 and miR-339 expression levels were significantly higher in heart recipients with myocardial fibrosis than in those without myocardial fibrosis (p = 0.018 and p = 0.043, respectively). Diagnostically significant threshold levels of miR-27 and miR-339 for detection of myocardial fibrosis in heart transplant recipients were determined (–4.33 and –5.24 units, respectively). The relative risk of detecting graft myocardial fibrosis in recipients with miR-27 expression value above the threshold level was RR = 1.5 ± 0.157 [95% CI 1.104-2.039], p = 0.009; for miR-339, RR = 1.31 ± 0.130 [95% CI 1.018-1.692], p = 0.036. When miR-27 expression levels and galectin-3 serum levels simultaneously exceeded their estimated thresholds, the risk of transplanted heart myocardial fibrosis increased to RR = 2.7 ± 0.456 [95% CI 1.090-6.524], p = 0.032; when miR-339 and galectin-3 simultaneously exceeded threshold values, the risk was RR = 2.0 ± 0.316 [95% CI 1.076-3.717], p = 0.028).Conclusion. The miR-27 and miR-339 expression levels are associated with the presence of fibrotic changes in the graft myocardium. The combination of molecular-genetic and proteomic biomarkers in one test improves the diagnostic characteristics of these expressions with respect to post-transplant complications in heart recipients.

Fast myocardial T1\u03c1 mapping in mice using k-space weighted image contrast and a Bloch simulation-optimized radial sampling pattern

PurposeT1ρ dispersion quantification can potentially be used as a cardiac magnetic resonance index for sensitive detection of myocardial fibrosis without the need of contrast agents. However, dispersion quantification is still a major challenge, because T1ρ mapping for different spin lock amplitudes is a very time consuming process. This study aims to develop a fast and accurate T1ρ mapping sequence, which paves the way to cardiac T1ρ dispersion quantification within the limited measurement time of an in vivo study in small animals.MethodsA radial spin lock sequence was developed using a Bloch simulation-optimized sampling pattern and a view-sharing method for image reconstruction. For validation, phantom measurements with a conventional sampling pattern and a gold standard sequence were compared to examine T1ρ quantification accuracy. The in vivo validation of T1ρ mapping was performed in N = 10 mice and in a reproduction study in a single animal, in which ten maps were acquired in direct succession. Finally, the feasibility of myocardial dispersion quantification was tested in one animal.ResultsThe Bloch simulation-based sampling shows considerably higher image quality as well as improved T1ρ quantification accuracy (+ 56%) and precision (+ 49%) compared to conventional sampling. Compared to the gold standard sequence, a mean deviation of − 0.46 ± 1.84% was observed. The in vivo measurements proved high reproducibility of myocardial T1ρ mapping. The mean T1ρ in the left ventricle was 39.5 ± 1.2 ms for different animals and the maximum deviation was 2.1% in the successive measurements. The myocardial T1ρ dispersion slope, which was measured for the first time in one animal, could be determined to be 4.76 ± 0.23 ms/kHz.ConclusionThis new and fast T1ρ quantification technique enables high-resolution myocardial T1ρ mapping and even dispersion quantification within the limited time of an in vivo study and could, therefore, be a reliable tool for improved tissue characterization.

Role of myocardial inflammation and fibrosis in the development of ventricular arrythmias in patients with inflammatory cardiomyopathy (results of 1-year follow-up)

Abstract Background Myocardial inflammatory and fibrotic changes are the most frequent and significant causes of ventricular rhythm disorders that could result in development of life threatening arrythmias and increase the risk of sudden cardiac death, especially in young patients with inflammatory cardiomyopathy (ICM). The purpose – to estimate association of myocardial inflammation and fibrosis with development of ventricular arrythmias in patients with ICM during 12-months of follow-up. Material and methods The study was performed on 70 patients with ICM, average age was (35,2±2,7) years. Initially all patients had cardiomegaly with reduced left ventricular (LV) ejection fraction - &amp;lt;40% and absolute value of longitudinal global systolic strain &amp;lt;9,0%. By 24-hour ECG monitoring we studied frequency of ventricular premature beats (VPB) and incidence of non-sustained ventricular tachycardia (NSVT) paroxysms. All patients underwent for cardiac MRI with evaluation of early T1- and T2-weighted images for the detection of inflammatory changes and T1-weighted delayed images for detection of myocardial fibrosis. Results of cardiac MRI were estimated by Lake Louise criteria and also we performed quantification of segments involved according to standard 17-segment LV model. Initial examination was carried out within the 1st month from the clinical onset of disease and subsequent evaluation of studied parameters was performed after 12 months of follow-up. Results After 12 months of follow-up average frequency of VPB reduced to (1,42±0,14) % from (2,32±0,27) % on initial examination (p&amp;lt;0,01), similarly reduced the incidence of NSVT paroxysms – to 11,4% after 12 months from 28,6% initially. Mean quantity of LV segments, affected by inflammatory process and characterized by presence of edema and/or hyperemia, reduced to (2,12±0,22) segm. after 12 months of follow up from (6,12±0,71) segm. on the 1st month (p&amp;lt;0,01). Also we observed increase of LV segments amount with the presence of delayed enhancement which indicates myocardial fibrosis – from (2,04±0,21) segm. on initial examination to (4,79±0,38) segm. after 12 months (p&amp;lt;0,01). Using binary regression analysis we defined that initial presence of inflammatory lesions in ≥5,0 LV segments was associated with frequent VPB (≥1,0%) and NSVT paroxysms. Wherein, after 12 months presence of inflammatory lesions had no association with ventricular rhythm disorders but the same relation was observed between the presence of delayed enhancement in ≥4,0 LV segments and frequent VPB (≥1,0%) as also with NSVT paroxysms. Conclusion At the time of clinical onset of inflammatory cardiomyopathy ventricular rhythm disorders (particularly VPB and NSVT paroxysms) were associated with larger quantity of LV segments involved into inflammatory process. After 12 months of follow-up ventricular rhythm disorders were associated predominantly with the presence of fibrotic lesions in several (≥4,0) segments of LV. Funding Acknowledgement Type of funding source: None

Detection of Myocardial Fibrosis and Left Ventricular Dysfunction with Cardiac MRI in a Hypertensive Swine Model.

To quantitatively evaluate the dynamic changes of extracellular volume (ECV) and native T1 in hypertensive swine over time using histologic findings as standard of reference. Eighteen hypertensive (hypertension group) and six healthy (control group) swine aged 6-12 months were studied. Both groups underwent cardiac MRI, including pre- and postcontrast T1 mapping and late gadolinium enhancement (LGE) imaging at three time points: baseline, 1 month, and 3 months after hypertensive model induction. The left ventricular function, strain, and strain rate were also calculated using the cine images. Animals were killed after the last MRI examination. Histopathologic examination of the heart was performed later. Analysis of the relationship between strain, ECV, and native T1 was carried out by Pearson correlation and linear regression models. The mean systolic and diastolic pressure increased from 111 mg Hg and 68 mm Hg to 160 mm Hg and 97 mm Hg, respectively, over 3 months during developing hypertension (P = .03, .02, respectively). There was no LGE detected at any of three imaging times. The ECV and native T1 value of myocardium in the hypertension group increased over 3 months (ECV, increased from 21.5% ± 4.4 to 27.3% ± 5.4; native T1, increased from a mean of 1056 msec ± 32 [standard deviation] to 1218 msec ± 66; all P < .001). The collagen volume fraction (CVF) was calculated and correlated with ECV (r = 0.63, P = .01) and native T1 (r = 0.80, P < .001). In addition, ECV was associated with longitudinal diastolic strain rate (r =-.34, P = .04). Native T1 was associated with radial strain (r = -0.62, P < .001) as well as circumferential strain (r = 0.57, P < .001). Native T1 and ECV correlated significantly with the CVF, indicating that early myocardial interstitial fibrosis exists in hypertensive heart disease. As hypertension progresses, the values of ECV fraction and T1 native increase. Supplemental material is available for this article. © RSNA, 2020.

1642 Mitral annulus disjunction, a rare form of focal arrhythmogenic cardiomyopathy

Abstract Funding Acknowledgements Project no. NVKP_16-1-2016-0017 has been implemented with the support provided from the National Research, Development and Innovation Fund of Hungary The rate of sudden cardiac death in mitral valve prolapse (MVP) patients is roughly twice that observed in the general population. Arrhythmogenic bileaflet MVP syndrome has been recently described and mitral annulus disjunction (MAD) has been found associated with papillary muscle fibrosis and ventricular arrhythmias even without severe mitral regurgitation. An underlying primary structural myocardial disease might be expected and the non-invasive imaging techniques are playing an increasingly important role in the detection of myocardial fibrosis as a focal arrhythmogenic substrate. Standard 2D-, 3D- and speckle tracking echocardiography and cardiac MRI can help to differentiate between the benign and malignant forms of MVP. A 52-year-old man with a history of hypertension was referred for evaluation of frequent palpitations and presyncope. Ambulatory Holter monitoring showed paroxysmal atrial fibrillation and non-sustained ventricular tachycardias. Dilated left ventricle (LVEDD: 65mm, LVESD: 45 mm) and left atrium (LAVi: 52mL/m2), moderately reduced left ventricular (LV) systolic function (LVEF: 42%), and reduced LV global longitudinal strain (GLS: -13.5%) with severely decreased segmental longitudinal strain in the basal inferolateral segment were measured by transthoracic echocardiography. The diastolic function was preserved, however Pickelhaube sign was noticed in the lateral mitral annulus TDI curves. MAD (17 mm) and curling motion of the inferolateral basal segment of the left ventricle was observed. Transesophageal echocardiography showed bileaflet mitral valve prolapse with the involvement of all the six scallops (mitral valve prolapse volume: 10.2 mL). Severe mitral regurgitation (3D vena contracta area: 1cm2) and extremely dilated and dyskinetic mitral annulus (diameters: 55x72x12 mm, area: 34 cm2) was measured by 3D echocardiography. MRI showed transmural late gadolinium enhancement in the underlying myocardium of both papillary muscles and midmyocardial enhancement in the basal inferior, inferolateral and anteroseptal LV segments. During electrophysiology study ventricular fibrillation was easily induced and ICD was placed for primary prevention of sudden cardiac death. The patient was referred to the heart surgeon for mitral valve replacement. This case highlights the importance of early recognition of MAD and arrhythmogenic MVP syndrome using novel non-invasive imaging techniques. The presence of MAD, the curling motion of the inferolateral basal LV segment, the Pickelhaube sign, the decreased LVEF and GLS, the characteristic segmental longitudinal strain pattern and the presence of late enhancement in the papillary muscles and the surrounding myocardium could be warning signs of the malignant form of MVP. Abstract 1642 Figure. CMR images of arrhythmogenic MAD

P599Native T1 mapping is useful for detection of myocardial fibrosis in cases with ischemic and non-ischemic myocardial diseases

Abstract Background Evaluation of myocardial fibrosis (MF) as late gadolinium enhancement (LGE) on MRI is useful for differential diagnosis of various myocardial diseases and prediction of future adverse cardiac events in some specific myocardial diseases. Gadolinium contrast is contraindicated for cases with severe renal dysfunction, therefore non contrast MRI is necessary for detection of MF in cases with both myocardial disease and severe renal dysfunction. Purpose We aimed to evaluate diagnostic accuracy of native T1 mapping for detection of MF compared with LGE in cases with various myocardial diseases, including ischemic and non-ischemic myocardial diseases. Methods We selected consecutive 40 patients who were suspected of having various myocardial diseases and underwent cardiac MRI, using 1.5T MRI (Ingenia, Philips) in 10 cases (25%) or 3T MRI (Ingenia, Philips) in 30 cases (75%), including native T1 mapping (without contrast) and LGE using contrast media from Jan 2018 to Feb 2019 in our institution. We evaluated diagnostic accuracy for detection of MF in left ventricular myocardium (LVM) of native T1 mapping image compared with LGE as the gold standard, in a patient-based and segment-based analysis. In T1 mapping images, segmental high T1 lesions were defined as MF. In a segment-based analysis, MF was evaluated using 17 LVM segments model in American Heart Association. Results MF was detected in 139 LVM segments in 25 (63%) cases. Sensitivity, specificity, positive predictive value, negative predictive value and diagnostic accuracy of native T1 mapping for detection of MF were 90%, 89%, 95%, 80% and 90% in a patient-based analysis, and 63%, 96%, 84%, 89% and 88% in a segment-based analysis (left figure). Native T1-values of LVM with MF were significantly higher than LVM without LGE (1351±79 vs 1093±124 in 1.5T and 1562±131 vs 1291±43 in 3T) (p&lt;0.05 and p&lt;0.01). Interobserver agreement of native T1 mapping and LGE were not significantly different (0.88 and 0.89, P=0.70). Overall diagnostic accuracy of native T1 mapping for detection of MF in a patient-based analysis, was not significantly different in between the cases with ischemic (n=18) and non-ischemic (n=22) myocardial disease (90% and 83.3%, P=0.10). Conclusion Native T1 mapping (without contrast) is useful for detection of MF in various myocardial diseases and high diagnostic accuracy is expected especially in a patient-based analysis.

Myocardial Fibrosis as a Pathway of Prediction of Ventricular Arrhythmias and Sudden Cardiac Death in Patients With Nonischemic Dilated Cardiomyopathy.

The mechanism of sudden cardiac death (SCD) in patients with nonischemic dilated cardiomyopathy (NIDCM) is mostly due to sustained ventricular tachycardia and ventricular fibrillation. The clinical guidelines for the therapeutic management of this set of patients are mostly based on left ventricular ejection fraction value which has a low specificity to differentiate the risk of SCD from the risk of mortality associated with heart failure or other comorbidities. Moreover, since SCD can occur in patients with normal or mildly depressed ejection fraction, it is necessary to identify new markers to improve the prognostic stratification of SCD. Several studies that analyzed the ventricular arrhythmia substrate found that myocardial fibrosis plays an important role in the genesis of ventricular arrhythmias in patients with NIDCM. The surrounding zone of the area of fibrosis is a heterogeneous medium, where tissue with different levels of fibrosis coexists, resulting in both viable and nonviable myocardium. This myocardial fibrosis may constitute a substrate for ventricular arrhythmias, where slow and heterogeneous conduction may favor the genesis of reentry mechanism increasing the chance to develop sustained ventricular tachycardia or ventricular fibrillation. Therefore, the evaluation of ventricular fibrosis by late gadolinium enhancement (LGE) cardiac magnetic resonance imaging has been suggested as an indicator for SCD risk stratification. Indeed, LGE in patients with NIDCM is associated with increased risk of all-cause mortality, heart failure hospitalization, and SCD. Detection of myocardial fibrosis as LGE by cardiac magnetic resonance imaging can be considered as a useful pathway of prediction of malignant ventricular arrhythmias since it has excellent prognostic characteristics and may help guide risk stratification and management in patients with NIDCM.

50173D myocardial strain analysis using 320-slice computed tomographic data is useful for the detection of myocardial fibrosis in hypertrophic cardiomyopathy

50173D myocardial strain analysis using 320-slice computed tomographic data is useful for the detection of myocardial fibrosis in hypertrophic cardiomyopathy

Micro-RNA-21 (biomarker) and global longitudinal strain (functional marker) in detection of myocardial fibrotic burden in severe aortic valve stenosis: a pilot study.

AimsMyocardial fibrosis (MF) is a deleterious consequence of aortic valve stenosis (AVS). Global longitudinal strain (GLS) is a novel left ventricular (LV) functional parameter potentially useful to non-invasively estimate MF. MicroRNAs (miRNAs) are non-coding small ribonucleic acids (RNA) modulating genes function, mainly through RNA degradation. miRNA-21 is a biomarker associated with MF in pressure overload. The aim of the present study was to find an integrated algorithm for detection of MF using a combined approach with both bio- and functional markers.MethodsThirty-six patients (75.2 ± 8 y.o.; 63 % Female) with severe AVS and preserved LV ejection fraction (EF), candidate to surgical aortic valve replacement (sAVR) were enrolled. Clinical, bio-humoral evaluation (including plasmatic miRNA-21 collected using specific tubes, PAXgene, for stabilization of peripheral RNA) and a complete echocardiographic study, including GLS and septal strain, were performed before sAVR. Twenty-eight of those patients underwent sAVR and, in 23 of them, an inter-ventricular septum biopsy was performed. Tissues were fixed in formalin and embedded in paraffin. Sections were stained with Hematoxylin and Eosin for histological evaluation and with histochemical Masson trichrome for collagen fibers. The different components were calculated and expressed as micrometers2. To evaluate tissue miRNA components, sections 2-μm thick were cut using a microtome blade for each slide. Regression analysis was performed to test association between dependent variable and various predictors included in the model.ResultsDespite a preserved EF (66 ± 11 %), patients presented altered myocardial deformation parameters (GLS −14,02 ± 3.8 %; septal longitudinal strain, SSL −9.63 ± 2.9 %; septal longitudinal strain rate, SL-Sr −0.58 ± 0.17 1/s; Septal Longitudinal early-diastolic strain rate, SL-SrE 0.62 ± 0.32 1/s). The extent of MF showed an inverse association with both GLS and septal longitudinal deformation indices (GLS: R2 = 0.30; p = 0.02; SSL: R2 = 0.36; p = 0.01; SL-Sr: R2 = 0.39; p < 0.001; SL-SrE: R2 = 0.35; p = 0.001). miRNA-21 was mainly expressed in fibrous tissue (p < 0.0001). A significant association between MF and plasmatic miRNA-21, alone and weighted for measures of structural (LVMi R2 = 0.50; p = 0.0005) and functional (SSL R2 = 0.35; p = 0.006) remodeling, was found.ConclusionsIn AVS, MF is associated with alterations of regional and global strain. Plasmatic miRNA-21 is directly related to MF and associated with LV structural and functional impairment.

From Left Ventricular Hypertrophy to Dysfunction and Failure

Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. (Circ J 2016; 80: 555-564).