Although the overall survival of patients with dilated cardiomyopathy (DCM) has improved significantly in the last decades, a non-negligible proportion of DCM patients still shows an unfavorable prognosis. DCM patients not only need imaging techniques that are effective in diagnosis, but also suitable for long-term follow-up with frequent re-evaluations. The exponential growth of echocardiography’s technology and performance in recent years has resulted in improved diagnostic accuracy, stratification, management and follow-up of patients with DCM. This review summarizes some new developments in echocardiography and their promising applications in DCM. Although nowadays cardiac magnetic resonance (CMR) remains the gold standard technique in DCM, the echocardiographic advances and novelties proposed in the manuscript, if properly integrated into clinical practice, could bring echocardiography closer to CMR in terms of accuracy and may certify ultrasound as the technique of choice in the follow-up of DCM patients. The application in DCM patients of novel echocardiographic techniques represents an interesting emergent research area for scholars in the near future. The current definition of dilated cardiomyopathy (DCM) could appear relatively simple; namely, a heart muscle disease characterized by left ventricular (LV) or biventricular dilation and systolic dysfunction in the absence of pressure or volume overloads or coronary artery disease sufficient to explain the dysfunction ,2. ActuaEchocardiography is crucial in the diagnosis, stratification, management and follow-up of patients with DCM ,8. NearlEchocardiographic DCM diagnostic criteria traditionally consisted of the presence of LV ejection fraction (EF) <45% and/or fractional shortening <25% and left ventricular end diastolic dimension (LVEDD) >112% of predicted value corrected for age and body surface area (BSA) . ActuallThe EF and fractional shortening are part of the standard echocardiographic parameters used to assess LV dimensions, geometry and systolic function, among which there are also: dP/dT and cardiac output , tissue doppler mitral annulus velocity and speckle tracking strain (less load dependent). EF is defined as stroke volume (SV) indexed to EDV and is a pillar of clinical practice, even if is deeply influenced by preload, afterload, heart rate and ventricular geometry. The biplane Simpson’s rule is generally recommended to calculate EF, although there are significant limitations: suboptimal endocardial definition in up to 15% of patients, poor reproducibility of measurements and inability to reflect regional LV function. A better description of LV mechanics derives from a non-invasive evaluation of myocardial deformation, namely myocardial strain [Global longitudinal strain (GLS) is a dimensionless variable and represents the percent change in myocardial length between two points over the cardiac cycle. The measurements of myocardial segments’ length change are performed by tracking the shift of myocardial speckles via an algorithm . Since tThe great improvement in DCM prognosis in the last decades  seems toThree-dimensional (3D) echocardiography. This technique improves reproducibility of LV volumes with an accuracy similar to CMR . It is aNon-invasive left ventricular pressure-strain loop (PSL) and global work index (GWI). Myocardial work (MW) is a new parameter that considers both myocardial deformation and after-load. It is calculated combining LV strain and non-invasively estimated LV pressure curves. The area within the PSL represent an index of MW, and the following parameters can be determined : GWI, asReverse remodeling index. Although DCM is classically defined as above, conventional geometric parameters used have not been demonstrated to have a prognostic value ,40,41,42Post-systolic shortening (PSS) and early systolic lengthening (ESL). Objective measures of cardiac function are supplied by PSS and ESL , both paMitral valve complex (MVC) tissue longitudinal elongation. It is clear that LV sphericity is associated with impaired LVEF, functional mitral regurgitation (MR) and poor prognosis ,54 in DCArtificial intelligence and machine learning (ML). AI is historically defined as the ability of computer systems to perform tasks that would usually require human levels of intelligence . AI has More recent refinements in LV echocardiographic characterization could be found in the following echo parameters and techniques:2, and peak tricuspid regurgitation (TR) velocity >2.8 m/sec. However, diastolic function can be determined only when more than half of these parameters are concordant. Between 11% and 22% of scans are labeled indeterminate according to real-world clinical data [LV diastolic function plays an important role in determining LV filling and stroke volume in DCM. Diastolic dysfunction is associated with worse outcomes, including total mortality and hospitalizations due to HF ,68. The cal data ,72.The application of bidimensional STE, mainly used for the objective quantification of systolic myocardial deformation, has been recently studied also for the evaluation of diastolic function. New echo-parameters have been found to correlate well with LV filling pressure; this could help in the “grey-zone” when diastolic function is indeterminate. LV global longitudinal diastolic strain (Ds) rate (DSr) measurements during the isovolumic relaxation period and during early diastole by STE are the two variables that best correlate with the time constant of LV relaxation (t) . DokainiMore recently, assessment of LV torsion using 2D STE has been proposed as a novel marker of LV relaxation. LV untwisting, the rapid reversal of rotation during early diastole, represents the rapid release of LV restoring forces and should be delayed and reduced in magnitude in patients with diastolic dysfunction. However, literature shows conflicting results regarding its usefulness for detecting diastolic dysfunction ,83,84. TFinally, a novel technique to evaluate diastolic function comes from AI. ML is a powerful tool able to process large datasets, like echocardiographic parameters of diastolic function, combined with detailed clinical and demographic features . While ERight ventricle (RV) has been considered for many years the “forgotten chamber”. However, recent scientific literature highlighted the potential impact of right ventricular function on outcome of patients with DCM ,94. AsseA simple new parameter is the RV systolic to diastolic duration ratio (S/D ratio), assessed by continuous Doppler imaging using the TR envelope to calculate the durations of RV systole and diastole. Boqing Xu et al.  showed tStrain imaging has been initially used to evaluate global LV function, but it is also able to provide a non-geometric approach to RV assessment. Recently 2D strain imaging using STE has been explored and RV global longitudinal strain (RVGLS) and global longitudinal strain rate (RVGLSR) have been shown to correlate well with RVEF measured by CMR . RV straThe 2D echo techniques are only surrogates for the true RV volume, due to its crescent shaped. Instead, 3D echo evaluation is independent of the RV’s exact shape and does not rely on assumptions about the total structure. Indeed, 3D echo RV volumetric measurements correlate well with CMR measurements ,109. VîjMoreover, the recovery of RV function under therapy is frequent and can already be observed at 6 months. It precedes LVRR and is emerging as an early therapeutic target and an independent prognostic predictor . EchocarLV contraction is the result of its coordinated mechanical activation following the propagation of the electrical impulse through the specialized conducting system. LVD can be defined as a significant delay of contraction between the different segments. It may or may not be secondary to electrical conduction tissue disturbance .Asynchronous LV contraction has been hypothesized to play a key role in the likelihood of response to cardiac resynchronization therapy (CRT), even more important than QRS interval duration, especially in patients with DCM . CompariTDI is one of the most used technique. Limitations of TDI are its angle-dependence, its being prone to noise and artifacts and the inability to distinguish between active and passive movements. When compared with more recent and technically complex methods such as STE longitudinal strain, TDI has showed better predictive value for chronic reverse remodeling in patients with LVD undergoing CRT . The appApical transverse motion (ATM), a TDI-derived parameter defined as the apex motion perpendicular to the LV long-axis, quantifies the phenomenon of apical rocking as an integrative surrogate of both temporal and functional inhomogeneities within the LV. ATM has proven its superiority over conventional evaluation  and was Three-dimensional (3D) echocardiography, evaluating data on all the three basic components of LV function , could accurately assess LVD. Nevertheless, 3D echocardiography suffers from the disadvantages associated with semi-automatic measurement and limited spatial resolution. Many studies have shown that 3D echocardiography is superior to TDI in assessing LV reverse remodeling and predicting response to CRT in DCM ,124. A cSTE has shown, through a more accurate analysis of radial dyssynchrony, a high sensitivity in identifying long-term responses to CRT . It measA relatively recently analyzed echocardiographic parameter of mechanical dispersion as a possible marker of response to CRT is the systolic aortic root motion (SARM). It is a measure of the displacement of the aortic root during the cardiac cycle and is obtained through M-mode echocardiography. It has been shown to be able to predict non-response to CRT also in DCM patients .Several attempts have been made to overcome the limitations inherent the methods previously described. One of them uses ML to combine different echocardiographic data, LVD parameters (ATM and SPE indices) and the duration of the QRS interval to try to predict the likelihood of LV reverse remodeling after CRT. It has been studied in 323 patients with heart failure (both ischemic and non-ischemic DCM) and it has been shown to improve the predicting value of standard imaging in the response to CRT . FurtherSecondary or functional MR develops in absence of structural anomalies  of the mitral valve. It is a disease of the atrium or the ventricle due to an imbalance between the tension acting on the mitral leaflets and the closing forces generated by the LV. Adverse LV remodeling leads to the apically displacement, tethering and restriction in mobility of the leaflets resulting in incomplete mitral valve closure ,132. In Two-dimensional (2D) transthoracic echocardiography (TTE) and trans-esophageal echocardiography (TOE) supported by color-flow Doppler are the core methods used to analyze MR. The echocardiographic criteria to define the severity of MR only mildly differ between primary and secondary MR. Qualitative parameters include the presence of severe tenting and poor leaflet coaptation , a largThree dimensional (3D) TTE and TOE allow a more precise prediction of regurgitation severity based on a comprehensive evaluation of valve morphology and leaflet coaptation, an accurate quantification of LV dimensions, a detailed geometry of vena contracta area and effective regurgitant orifice area and an automated quantitation of flow and regurgitant volume by 3D color-flow Doppler ,140. Thr2D techniques were able to correctly quantified MR severity in less than two-thirds of cases while 3D technique showed higher accuracy in identifying severe MR compared to cardiac CMR . NeverthSecondary TR is the most common cause of tricuspid insufficiency caused by dilation of the RV and/or of the tricuspid annulus due to left-sided heart valve diseases, pulmonary hypertension, congenital heart defects, and cardiomyopathy . Most DoAI-based valve assessment software algorithms integrating 2D and 3D echocardiographic parameters with automated quantification of disease severity have shown to reduce time to analyze cardiac structures and provide good reproducibility with minimal user intervention. Their implementation could improve diagnostic and prognostic stratification for surgical and interventional procedures ,147.Autopsy  and echoIn DCM patients, myocardial fibrosis (MF) is commonly found and contributes to the weakening and dilatation of the ventricular walls, affects the mechanical-electrical activity of cardiomyocyte and it is associated with deteriorating cardiac function and high long-term mortality ,159. TheContrast-enhanced (CE) 3D Echo. Montant et al. tested CE-3D echo versus CMR-LGE and found that second-harmonic imaging (with transmission/receive 1.6/3.2 Mhz) at a mechanical index of 0.5 was the best combination to differentiate normal myocardium from fibrotic scar .Three dimensional (3D) speckle tracking echocardiography. A study conducted in DCM patients prior to heart transplant comparing STE versus histological findings found that 3D GLS may be an optimal surrogate marker for reflecting MF  .Pulse cancellation ultrasound technique (eSCAR). The echo machine built-in setting for LV opacification used without CE, thanks to cancellation of “linear” signals back from normal myocardium, is incidentally very efficient to enhance signals from abnormal myocardial tissue, such as fibrotic  and calcRadiomics-based texture analysis. Using a ML pipeline to integrate and process ultrasound images texture features the presence of MF is predictable with an AUC of 0.84 (sensitivity 86.4% and specificity 83.3%) .Four new echo techniques, mostly studied in ischemic patients, are now available to identify and quantify MF and may be usefully applied in DCM:Exponential growth of echocardiography’s technology and performance in recent years has not only resulted in improved diagnostic accuracy of DCM but highlighted the complexities of DCM characterization that extend beyond simplistic volumetric, flow and pressure determination. Although nowadays CMR remains the gold standard technique in DCM, the echocardiographic advances and novelties summarized, if properly integrated into clinical practice in the coming years, could bring echocardiography closer to CMR in terms of accuracy. Furthermore, unlike CMR, the use of affordable, accessible echocardiographic techniques applicable in unstable, arrhythmic and claustrophobic patients could prove in the future to be the new gold standard to track the longitudinal follow-up of patients affected by DCM. The application in DCM patients of the aforementioned echocardiographic advances must further be corroborated by large clinical studies, mapping out an interesting emergent research area for scholars in the near future.


Hey1, a transcriptional repressor. Bioinformatic analyses located putative binding sites for the HEY1 protein upstream of the Gdf11 gene in the mouse and human genomes. In contrast, serum myostatin concentrations were more heritable (0.57) than GDF11 concentrations, and mapping identified a significant locus near the gene FoxO1, which has binding motifs within the promoter regions of human and mouse myostatin genes. Together, these findings more precisely define the independent cardiovascular effects of GDF11 and myostatin, as well as their distinct regulatory pathways. Hey1 is a compelling candidate for the regulation of GDF11 and will be further evaluated in future studies.Growth differentiation factor 11 (GDF11) is a member of the TGF-β protein family that has been implicated in the development of cardiac hypertrophy. While some studies have suggested that systemic GDF11 protects against cardiomyocyte enlargement and left ventricular wall thickening, there remains uncertainty about the true impact of GDF11 and whether its purported effects are actually attributable to its homolog myostatin. This study was conducted to resolve the statistical and genetic relationships among GDF11, myostatin, and cardiac hypertrophy in a mouse model of human genetics, the Diversity Outbred (DO) stock. In the DO population, serum GDF11 concentrations positively correlated with cardiomyocyte cross-sectional area, while circulating myostatin levels were negatively correlated with body weight, heart weight, and left ventricular wall thickness and mass. Genetic analyses revealed that serum GDF11 concentrations are modestly heritable (0.23) and identified a suggestive peak on murine chromosome 3 in close proximity to the gene  The heart adapts to excessive loading stresses by eccentric or concentric hypertrophy. Eccentric cardiac hypertrophy, a typical response to excessive ventricular preload, is characterized by dilatation of the affected ventricular chamber . Heart fIn recent years, evidence has shown that age-related cardiac hypertrophy is governed, at least in part, by systemic factors. Using heterochronic parabiosis, Loffredo and colleagues demonstrated that blood from young mice reverses signs of cardiac hypertrophy in aged animals  stock, a translationally relevant model of human genetic diversity, vastly expanding upon previous results gathered using inbred mice. Overall, we discovered unique relationships among GDF11, myostatin, and indicators of cardiac hypertrophy, as well as distinct loci and candidate genes behind each phenotype, and our results point to molecular pathways that will be interrogated in future studies of GDF11 and the heart.N = 225) were purchased from The Jackson Laboratory  . Data from eight mice that died or were euthanized before the end of the study due to injuries sustained in fights or other health issues were not included in final histological analyses.DO mice  with a 30-MHz probe. Mice were anesthetized with inhaled 1–2% isoflurane in oxygen and placed in a supine position on a heating platform. M-mode recordings of the left ventricle were obtained from a short-axis view at the level of the mitral valve chordal attachments to the papillary muscles. From these images, measurements from the average of 3–5 consecutive beats were used to calculate the following parameters: interventricular septal thickness at end-diastole and end-systole , left ventricular internal diameter at end-diastole and end-systole  and left ventricular posterior wall thickness at end-diastole and end-systole . Ejection fraction, fractional shortening, left ventricular mass, and LV volume at end-diastole and end-systole  were calculated from these measurements. This procedure was approved by the Institutional Animal Care and Use Committee of the University of Georgia.At 5–6 months of age, mice were euthanized, and hearts were isolated and fixed in neutral-buffered 10% formalin for 24 h at room temperature and then paraffin embedded using routine methods. Tissue was serially sectioned and stained using hematoxylin and eosin , Gordon and Sweet’s reticulin stain , and Masson’s trichrome stain (for determination of percent fibrosis). Left ventricular wall thickness, cardiomyocyte cross-sectional area, and percent fibrosis were measured using FIJI software (ImageJ).Tail tips were collected and sent to NEOGEN Genomics  for DNA isolation and genotyping via the Giga Mouse Universal Genotyping Array (GigaMuga) . Mappinghttp://genome.ucsc.edu/, last accessed Aug. 2021) using the Human Assembly Dec. 2013 (GRCh38/hg38) and Mouse Assembly December 2011 (GRCm38/mm10) versions for the human and mouse genomes, respectively.Bioinformatics was used to illuminate likely binding sites for HEY1 and FOXO1 upstream of their putative target genes. Coordinates of the transcription factors were determined in both the human (hg38) and mouse genome (mm10) through the Integrative Genomics Viewer software (version 2.8.2)  emerged. In the 64 DO mice  randomly selected to undergo echocardiography, no significant correlations between GDF11 and measures of heart size or function were noted , heart weight standardized to tibial length , and left ventricular heart wall thickness  = 3.72, P < 0.001], and similarly, heart wall thickness tended to be lower in females [t(217) = −8.65, P < 0.001; r = −0.34, P < 0.001), a trend that aligns with past evidence that myostatin negatively regulates body mass , and percent fibrotic area . Females showed a negative relationship between myostatin and total body weight , heart weight , and the ratio of heart weight to tibia length . When separated by sex, the only significant correlation appeared in males: a negative correlation between serum myostatin and LVM  and may serve as the foundation for future aging studies. Second, LC-MS/MS was used to quantify serum GDF11 and myostatin levels. This technique is highly specific and more sensitive for distinguishing between GDF11 and myostatin than antibody-based methods  and a moderate heritability for myostatin levels (0.57). The GDF11 heritability estimation is lower than the estimate (0.75) previously reported by our group, which could be explained in part by the fact that the prior study used an ELISA test that likely failed to fully discriminate between GDF11 and myostatin, resulting in a higher heritability estimate reflecting that of myostatin  and the other suggestive  (N = 217 vs N = 547). Meanwhile, mapping serum GDF11 levels revealed a suggestive peak (P < 0.1) on murine chromosome 3 within the Bayesian credible interval 3.039589–9.983782 Mbp . Stmn2 is another reasonable candidate as it is expressed in both murine and human heart tissue throughout development and into adulthood , located 13,933 base pairs upstream from the GDF11 gene and 12,613 base pairs from the flanking promoter region  transcription factor has documented activator activity  on murine chromosome 3 within the Bayesian credible interval of 52.26269–52.71985 Mbp  gene itself and within the flanking promoter region . The Reagent Table can be found in the Supplementary information on FigShare, as can the raw, uncorrected phenotypic data (Supplementary Table S1), the GeneSeek data containing the genotypes from each mouse (Supplementary File S1), genotype probabilities (Supplementary File S2), and the script used (Supplementary File S3). The phenotype QTL viewers are available at https://churchilllab.jax.org/qtlviewer/pazdrodoheart (last accessed Aug. 2021). Marker information containing the genetic map (cM) and physical map (Mbp) for the GigaMUGA, the eight founder strain genotypes, the GigaMUGA founder genetic maps (cM) and physical maps (Mbp) for each chromosome (Supplementary File S4), and the genetic mapping reports (Supplementary File S5) can also be found on figshare: https://doi.org/10.25387/g3.14248718.The DO stock is available through The Jackson Laboratory (Bar Harbor, ME;


This observational CMR study aims to characterize left-ventricular (LV) damage, which may be specifically attributed to COVID-19 and is distant in time from the acute phase, through serial CMR performed during the first year in patients with no prior cardiac disease.This study included consecutive patients without any prior history of cardiac disease but with a peak troponin-Ic > 50 ng/ml at the time of the first COVID-wave. All had a CMR in the first months after the acute phase, and some had an additional CMR at the end of the first year to monitor LV function, remodeling, and abnormalities evocative of myositis and myocarditis - i.e., increased T1/T2 relaxation times, increased extracellular volume (ECV), and delayed contrast enhancement.st CMR, recorded at a median 3.2 [interquartile range: 2.6–3.9] months from the troponin peak, showed (1) LV concentric remodeling in 12 patients (63%), (2) myocardial tissue abnormalities in 11 (58%), including 9 increased myocardial ECVs, and (3) 14 (74%) increased ECVs from shoulder skeletal muscles. The 2nd CMR, obtained at 11.1 [11.0–11.7] months from the troponin peak in 13 patients, showed unchanged LV function and remodeling but a return to normal or below the normal range for all ECVs of the myocardium and skeletal muscles.Nineteen consecutively admitted COVID-19 patients  were included. Eight (42%) had hypertension, six (32%) were obese, and 16 (84%) had suffered an acute respiratory distress syndrome. The 1Many patients with no history of cardiac disease but for whom an increase in blood troponin-Ic ascertained COVID-19 induced myocardial damage exhibited signs of persistent extracellular edema at a median 3-months from the troponin peak, affecting the myocardium and skeletal muscles, which resolved within a one-year time frame. Associations with long-COVID symptoms need to be investigated on a larger scale now.ClinicalTrials.gov site.NCT04753762 on the  COVID-19 induced myocardial damage is complex and exhibits features consistent with inflammation and endothelium dysfunction, and thrombosis . It has Cardiac Magnetic Resonance (CMR) already documented myocardial tissue abnormalities at the acute or sub-acute phase of COVID-19 and, more specifically, increases in myocardial T1 and T2 relaxation times and an increased extracellular volume (ECV) , 6. ThisThis observational CMR study aims to characterize the left-ventricular (LV) damage which may be specifically attributed to COVID-19 and distant in time from the acute phase, through serial CMR planned during the first year in patients with no previous history of cardiac disease but with significant increases in blood troponin-Ic during the initial COVID-19 hospitalization.th and the 31st of March 2020, which corresponded to the peak of the first COVID-19 wave in our region. Patients' COVID-19 status was ascertained by a positive reverse transcriptase-polymerase chain reaction test. Additional inclusion criteria were: (i) a peak troponin Ic > 50 ng/ml measured during hospitalization, (ii) the absence of any prior cardiac disease history, and (iii) health conditions required to endure the CMR-based monitoring which is currently prescribed for myocarditis patients in our center.The study included consecutive 18- to 80-year-old patients hospitalized in our Regional University Hospital for a COVID-19-related pathology between the 16st CMR within the first months following the acute phase and the follow-up investigations with the 2nd CMR, at the end of the first year, on a 3T PRISMA Magnet . Echocardiography and blood analysis for routine biomarkers were also performed on the CMR days. Echocardiography data were obtained according to current recommendations , 60° flip angle (FA), 41 ms repetition time (TR), 2.9 ms interecho time, 1.27 ms echo time (TE), and 14 segments.The same CMR protocol was used in all patients and for both the 1sequence , on cont−1 body weight of Dotarem®, . T1 maps were recorded with the following parameters: 1.4 x 1.4 x 8.0 mm3 voxel size, 371 x 278 mm2 FOV, 35° FA, 1 excitation, 180 ms time to inversion (TI), 267 ms TR, 1.11 ms TE, and 63 segments. For the T2 maps, these parameters were: 1.9 x 1.9 x 8.0 mm3 voxel size, 360 x 360 mm2 FOV, 12° FA, 201 ms TR, and 1.32/30/50 ms TE. For the LGE images, these parameters were: 2.1 x 2.1 x 8 mm3 voxel size, 400 x 380 mm2 FOV, 40° FA, 305 ms TI, 768 ms RT, 2.4 ms interecho time, 1.04 ms TE, and 1 excitation.According to the “2018 updated Lake Louise Criteria” , signs o® injection.CMR results were extracted with the Syngovia software , using a manual adjustment of the ventricular contours applied to determine LV mass, end-diastolic volumes, and ejection fractions . VentricThe cardiac T1 maps were additionally used to determine the T1 and ECV of the shoulder skeletal muscles setting in the field of view  with careful exclusion of perimuscular fat and intramuscular tendons from the hand-drawn ROIs , as prevNormal limits for the main CMR parameters are summarized in −2 for LV end-diastolic volume, 73 and 57 g.m−2 for LV mass, and 1.11 and 0.90 for LV mass/volume ratio. These limits are within the range of those already defined for ≥ 60 years old normal subjects in previously published CMR studies  as an increase in the signal from myocardial areas clearly distinct from the epicardial fat and cavitary blood. All transmural or sub-epicardial areas of LGE were considered as potentially related to myocarditis . This waP values were not not adjusted for possible multiple comparison effects given the exploratory nature of the present study, and p < 0.05 were considered to reflect significant differences.Statistical analyses were obtained using the SPSS statistical software (IBM Statistics version 20). Qualitative variables were expressed as numbers and percentages and quantitative variables were expressed as medians with interquartile ranges. As the number of cases was not sufficiently large to assume a normal distribution, paired comparisons of quantitative variables between the two CMR visits were assessed using a non-parametric test: the Wilcoxon sum-rank test. Paired comparisons of qualitative variables were planned with Mc Nemar tests. st CMR, the median age was 66 [59–71] years, and the median from peak troponin was 3.2 [2.6–3.9] months. Seventeen patients (89%) were male, 11 (58%) had previously been identified with hypertension or obesity (6 with obesity and 8 with hypertension), and as many as 16 (84%) had been affected by an acute respiratory distress syndrome (ARDS) requiring mechanical ventilation at the acute phase.Among the 222 COVID-19 patients hospitalized during the study period, 45 exhibited a peak troponin Ic > 50 ng/ml, and 19 fulfilled all study inclusion criteria. As detailed in st CMR, recorded at a median 3.2 [interquartile range: 2.6–3.9] months from the troponin peak, showed a > 50% LV ejection fraction in all but 2 patients for whom it was only slightly lower (46% and 48%). However, as many as 12 (63%) exhibited LV concentric remodeling , which was associated with LV hypertrophy  in 9 cases. Myocardial tissue damage was documented in 11 patients (58%), including 9 increased myocardial ECVs, 3 abnormal T1, 1 abnormal T2, and 2 evocative late gadolinium enhancements (LGE). No pattern suggestive of myocardial infarction was observed .The 12).For the shoulder skeletal muscles, abnormal values were observed for T1 in 2 cases (11%) and for ECV in 14 (74%). As detailed in nd CMR was performed in 13 out of the 19 patients, at a median of 11.1 [11.0–11.7] months from peak troponin. LV function and remodeling parameters were unchanged between the 1st and 2nd CMR, but significant decreases in heart rate, myocardial T1, and particularly ECV from skeletal muscles and myocardium were observed (The 2observed . Late coAs illustrated by a schematic representation in st CMR), and (iii) is then no longer associated with any evident signs of active damage or inflammation .CMR already documented an increased myocardial ECV at the acute or sub-acute phase of COVID-19 and associated with increases in myocardial T1 and T2 , 6. ThisInterestingly, the decrease in ECV at 1 year was observed in our COVID patients irrespective of the presence or absence of an abnormal ECV at 3-months see . This deThis increased ECV was not associated with any evident deterioration of cardiac function, with LV ejection fractions and volumes remaining normal or below the normal range during follow-up according to the CMR, as well as the echocardiography data see . As manyA main limitation is the small sample size of the present study population, and further studies will be required to confirm the results.The present serial CMR study shows a slow return to normal of the extracellular volume of the myocardium and skeletal muscles in many patients with no history of cardiac disease, but for whom an increase in blood troponin-Ic ascertained COVID-19 induced myocardial damage. This observation is likely due to a delayed resolution of the interstitial edema, which is known to affect severe COVID-19 patients. Associations with long-COVID symptoms  need to The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.The studies involving human participants were reviewed and approved by Ethics Committee of the Nancy University Hospital. Written informed consent for participation was not required for this study in accordance with the national legislation and the institutional requirements.Seven authors contributed significantly to the analysis and interpretation of the data , and/or to the writing or revision of the manuscript , the four others collaborated in the study implementation, and/or management of the included subjects . All authors contributed to the article and approved the submitted version.This study was funded by CHRU-Nancy, Nancy, France. Hospital's own funds were used for the study organization.The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.


To examine the use of positron emission tomography (PET) for imaging post-infarct myocardial inflammation and repair.Dysregulated immune responses after myocardial infarction are associated with adverse cardiac remodelling and an increased likelihood of ischaemic heart failure. PET imaging utilising novel tracers can be applied to visualise different components of the post-infarction inflammatory and repair processes. This approach could offer unique pathophysiological insights that could prove useful for the identification and risk-stratification of individuals who would ultimately benefit most from emerging immune-modulating therapies. PET imaging could also bridge the clinical translational gap as a surrogate measure of drug efficacy in early-stage clinical trials in patients with myocardial infarction. The use of hybrid PET/MR imaging, in particular, offers the additional advantage of simultaneous in vivo molecular imaging and detailed assessment of myocardial function, viability and tissue characterisation.Further research is needed to realise the true clinical translational value of PET imaging after myocardial infarction. Myocardial infarction is a major global cause of morbidity and mortality, both due to acute complications arising at the time of initial presentation, as well as longer-term sequelae including chronic heart failure. After myocardial infarction, inflammation and its resolution play key roles in the promotion of healing responses and ultimately act to limit the degree of acute cardiac injury and the severity of subsequent adverse cardiac remodelling.Indeed, inflammation is an automatic and necessary by-product of ischaemic myocyte necrosis, which seeks to clear and organise the damaged tissue. A broadly biphasic immune response to myocardial infarction occurs, wherein an initial ‘pro-inflammatory phase,’ characterised by the sequential mobilisation of various pro-inflammatory cell types, is followed by a ‘reparative phase’ where the main role of the immune system is to facilitate wound healing, involving myofibroblast proliferation, neovascularisation, fibrosis and scar formation . HoweverIn the light of the landmark CANTOS and COLCOT trials, which established the proof-of-principle that certain anti-inflammatory therapies can reduce cardiovascular events in patients with prior myocardial infarction and initial data indicating an additional signal for reduction in heart failure–related events, the tantalising prospect is thus presented that pharmacological manipulation of immune responses in the post-infarct period could be clinically beneficial , 4, 5••.Given the variation in clinical presentations and the heterogeneity of inflammatory cell phenotypes at play within the infarcted heart, it is likely that targeted immunosuppressive therapies applied in specific high-risk patient populations would yield far greater overall benefit than more ‘blanket’ broad-spectrum approaches that have been trialled in the past ., and to directly investigate the effects of novel therapies on myocardial inflammation. This article provides a focused review of recent progress in the use of PET imaging for imaging post-infarct myocardial inflammation and related processes.In this regard, positron emission tomography (PET) imaging presents a unique opportunity to probe and visualise molecular mechanisms occurring after myocardial infarction in vivoAn understanding of the cellular biology of post-infarct inflammation is important for contextualising the significance of cardiac PET signals, although detailed consideration of this topic is beyond the scope of this article. The reader is directed to more comprehensive reviews elsewhere , 7, 8.The cardiomyocyte necrosis that follows cardiac ischaemia sets in motion a chain of events closely linked to immune activation and resolution, which ultimately results in the formation of stable fibrotic scar tissue. However, if this balanced and coordinated immune response fails, uncontrolled initial or resurgent inflammation, fuelled by dysregulation of the mononuclear phagocytic network, can contribute to the risk of developing long-term heart failure .In the initial pro-inflammatory phase, neutrophils are among the first leucocytes to migrate to the site of injury whereupon they phagocytose cellular debris, degrade extra-cellular matrix via the release of matrix metalloproteinases and generate reactive oxygen species. Monocytes are also recruited from the splenic reservoir and bone marrow via adrenergic signalling, whereupon they differentiate into tissue macrophages and likewise undertake phagocytosis, proteolysis and promote inflammation through generation of reactive oxygen species and secretion of pro-inflammatory cytokines . Monocyte recruitment occurs as early as 30 min after the onset of ischaemia and up to 40% of the monocytes recruited within the first 24 h originate from the spleen , 11. B ahi monocytes , which have a life span of about 20 h, predominate at days 1–4 post-infarction [lo monocytes , which give rise to macrophages whose secretory cytokine profile includes IL-10, TGFβ and VEGF. These cytokines exert anti-inflammatory actions including downregulation of Th1 cell responses, and promotion of angiogenesis and fibrosis through interactions with endothelial cells and fibroblasts, respectively. This well-characterised transition in monocyte phenotype was also observed in a human post-mortem study [+CD16− cells in the infarct border zone during the acute inflammatory phase, and comparable numbers of CD14+CD16− and non-classical CD14+CD16+ cells in the infarct core at later time points, which coincided with depletion of splenic monocytes. Although several studies have shown different correlations with peripheral blood monocytes in patients with myocardial infarction, the role of non-classical monocytes in this context remains largely unknown.In mouse models, flow cytometry performed after coronary ligation has shown that pro-inflammatory Ly-6Cfarction . By day +CD16− monocytes measured after acute myocardial infarction were negatively associated with the likelihood of longer-term left ventricular functional recovery [In another study of 36 patients, increased peak levels of peripheral CD14recovery . Increasrecovery –19. The recovery .+ and CCR2− macrophages have also been described [+ macrophages are pro-inflammatory, tissue-resident CCR2− macrophages have non-redundant cardioprotective roles in tissue remodelling and cardiac regeneration, and largely self-renew via local proliferation [Divergent subsets of cardiac CCR2escribed . While mferation . During feration .+ macrophages have been associated with improvement in left ventricular systolic function in patients with severe heart failure undergoing left ventricular assist device implantation, as has also been shown in mice [Lower numbers of CCR2 in mice , 24. In  in mice , 26.+/CCR2− macrophages [Traditionally, the functions of the broadly divergent macrophage types in the post-infarct myocardium have been ascribed to ‘M1-like’ and ‘M2-like’ macrophages. However, it is important to note that this classification system is based on a spectrum of in vitro activation profiles rather than the broader transcriptional repertoire of macrophages that is now known to exist . There irophages . Indeed,rophages . The occrophages .Apoptosis and the clearance of apoptotic cells (efferocytosis) are another important component of post-infarction damage resolution, and experimental suppression of efferocytosis has been shown to result in larger myocardial infarct size and greater systolic dysfunction .Because these key inflammatory processes are vital for determining the extent of myocardial damage and likelihood of long-term heart failure after myocardial infarction, there is a role for molecular imaging techniques such as PET to study these disease mechanisms in efforts to inform the design and use of new therapeutic strategies for ischaemic heart failure.Molecular imaging of myocardial inflammation with PET offers the advantage of enabling the in situ visualisation, in real-time, of post-infarction processes. Moreover, by utilising novel PET tracers that are specific for particular inflammatory cell types or processes, individual components of the initial inflammatory and subsequent healing responses can potentially be interrogated.18F-fluorodeoxyglucose (18F-FDG) is the most commonly used PET tracer for inflammation imaging in clinical medicine, and several studies of post-infarct imaging testify to the general feasibility of this imaging approach.18F-FDG uptake within infarcted myocardium on day 5 post-infarct compared to control animals, which co-localised with delayed gadolinium enhancement on MRI [18F-FDG signals were observed at the infarct border zone, which corresponded with the site of peak monocyte/macrophage recruitment in some cases. Increased tracer uptake was also confirmed in monocytes/macrophages isolated from the infarcted mouse hearts, compared to the surrounding infarct tissue.Using PET/CT in a mouse model of myocardial infarction, one study showed increased t on MRI . The hig18F-FDG have been observed in several clinical studies. For example, one study including 15 patients imaged within 7 days of a first myocardial infarction showed the metabolic rate of 18F-FDG uptake to be increased in infarcted versus remote myocardium [18F-FDG uptake in the chronic infarct compared to remote zone. Another study that analysed 39 patients with ST-segment elevation myocardial infarction found that elevated infarct-related 18F-FDG uptake in the first week after myocardial infarction was associated with an increased likelihood of left ventricular impairment on MRI after 6 months, independent of infarct size [18F-FDG uptake in the infarcted myocardium was also correlated with 99mTc-sestamibi SPECT-defined area at risk and peripheral blood counts of CD14highCD16+ monocytes.Similar findings for ocardium . The PETrct size •. In thi18F-FDG is nonetheless challenging due to avid physiological background uptake. Pre-scan patient preparation for cardiac 18F-FDG imaging requires cumbersome myocardial suppression protocols, which are often ineffective. The effect of dietary manipulation on the already altered metabolic state of viable, post-ischaemic cardiac myocytes is also unknown. Moreover, while 18F-FDG is a clinically useful measure of metabolic activity in inflammatory cells such as macrophages in several cardiovascular diseases, its uptake is not cell-specific.However, despite these encouraging data, myocardial imaging using 18F-FDG have been investigated for use in myocardial imaging  receptor is situated in the outer mitochondrial membrane and is expressed in activated mononuclear cells and other inflammatory cells. In a translational study, PET imaging with the TSPO tracer  infarct •. Early 2) occurs in activated macrophages, offering another novel inflammation imaging target that may be useful in range of cardiovascular diseases [68Ga-DOTATATE has the highest binding affinity for SST2. Although one preclinical study observed rapid blood clearance of 68Ga-DOTATATE following injection with no myocardial binding after coronary ligation in mice, initial clinical data appears more promising for this approach. In a study that included 6 patients with myocardial infarction who were imaged using the somatostatin receptor PET tracer 68Ga-DOTATOC within 3 to 10 days of symptoms, focal myocardial signals were observed in all patients [68Ga-DOTATOC signal and infarcted myocardial segments with late gadolinium enhancement and oedema on MRI. In an exploratory post hoc analysis of 12 patients with myocardial infarction who underwent prospective cardiovascular 68Ga-DOTATATE PET imaging, infarct-related myocardial SST2 signals were increased in patients with recent myocardial infarction [68Ga-DOTATATE signals were observed in damaged myocardial segments with echocardiographic regional wall motion abnormalities in patients with old myocardial infarction. Infarct-related 68Ga-DOTATATE signals were also correlated with increased metabolic bone marrow activity measured by 18F-FDG PET. A pre-specified sub-study of an ongoing prospective observational study aiming to characterise the natural history of coronary and myocardial 68Ga-DOTATATE inflammatory signals after myocardial infarction  will shed further light on these initial observations.Upregulation of somatostatin receptor subtype-2 2) occurs68Ga-pentixafor peaked in the infarct region 3 days post-myocardial infarction in mice and corresponded with a flow cytometry-based peak of circulating CD45+ leukocytes and histological staining of macrophages and granulocytes within the infarct [68Ga-pentixafor PET/CT and cardiac MRI within 8 days of an ST-segment elevation myocardial infarction. In these patients, CXCR4 PET signals were higher in the infarct region than remote myocardium and were correlated with CXCR4 signals in the bone marrow and spleen.The C-X-C motif chemokine receptor type 4 (CXCR4) is expressed on the surface of several inflammatory cell types, including macrophages, neutrophils and lymphocytes. In one study, uptake of the CXCR4-targeted tracer  infarct . As with68Ga-pentixafor PET imaging within 5–10 days of the event, only 3 of the 7 patients showed focal uptake in the infarct as defined by MRI [68Ga-pentixafor uptake in 17 of 22 patients imaged within the first 2 weeks after the event [68Ga-pentixafor uptake at this late timepoint could represent leucocyte involvement in the healing process, but without direct histological comparison, this notion remains speculative.In a small clinical study of 7 patients with myocardial infarction who underwent d by MRI  Fig. 1)68Ga-penthe event . In this68Ga-pentixafor PET signals occurring beyond 3 days after coronary ligation were observed more often in animals that died of left ventricular rupture than those who survived and were associated with worse cardiac function at 6 weeks [68Ga-pentixafor uptake co-localised with CD68+ inflammatory cells and was also associated with increased numbers of both Ly6Chigh and Ly6Clow peripheral monocyte counts. These findings were confirmed in 50 patients with myocardial infarction. In these patients, CXCR4 signals showed a weak-to-moderate inverse correlation with left ventricular function at baseline and after follow-up of approximately 7 months.In another translational study involving 180 mice, persistent myocardial  6 weeks •. Moreov68Ga-pentixafor uptake in mediastinal lymph nodes in patients after myocardial infarction because of T cell accumulation [Another study showed increased mulation . The finmulation .64Cu-DOTA-ECL1i was shown to bind CCR2+ monocytes and macrophages within donor hearts, demonstrating increased tracer uptake compared to native hearts [64Cu-labelled tracer to data from a previous study on 68Ga-DOTA-ECL1i [C-C chemokine receptor type 2 (CCR2) is another important inflammatory cell marker involved in monocyte/macrophage recruitment, which has been evaluated for imaging myocardial inflammation using PET. In an ischaemia-reperfusion heterotopic heart transplantation mouse model, the PET tracer e hearts . SpecifiTA-ECL1i .+ macrophage depletion has demonstrated beneficial effects on cardiac function post-infarction in mouse models, CCR2-targeted PET tracers could also be useful for the clinical evaluation of CCR2 inhibitors in future early-stage clinical trials [As CCR2l trials .64Cu-Macrin is a 20-nm spherical dextran nanoparticle tracer designed specifically to target macrophages. In a preclinical study, 64Cu-Macrin was shown to report on the accumulation of macrophages within the infarcted myocardium in experiments using mice, rabbits and pigs [64Cu-Macrin PET signals were also observed in mouse models of sepsis and pneumonia, in newborn mice exhibiting higher macrophage content than adults, and in atherosclerotic plaques in rabbits. Comparison of a near-infrared fluorescent version of the nanoparticle with flow cytometry and confocal staining showed that the tracer uptake occurred predominately in MHCIIhigh CCR2high tissue macrophages. In contrast, 64Cu-Macrin uptake was negligible in neutrophils, fibroblasts and endothelial cells.and pigs •. Increa11C-methionine is thought to accumulate in macrophages, but not healthy myocytes. In a small clinical study, 11C-methionine PET was performed in 9 patients with left anterior descending artery myocardial infarctions treated by percutaneous coronary intervention, within 2 weeks of the event [11C-methionine signal was observed in areas of low or absent 201Thallium SPECT and 18F-FDG PET signal in the myocardium indicating tissue infarction, and subsequent reductions in 11C-methionine signals were seen in 2 patients imaged at 3 or 6 months. In another study, 11C-methionine PET imaging performed in mice showed increased tracer uptake in the infarcted myocardium at day 3 post-coronary ligation, compared to the remote myocardium and healthy control animals, which was associated with macrophage infiltration on histology [11C-methionine PET signal declined by day 7 and was also inhibited by treatment with anti-integrin antibodies that lowered macrophage content. In the same study, 11C-methionine uptake was shown to occur more in M1 than M2 polarised macrophages. Further spatiotemporal profiling of infarct-related 14C-methionine signal was investigated in a rat model, which showed peak tracer uptake occurring at days 3 to 7 post-infarct, with a gradual decline until day 28 [per se.Radio-labelled amino acid analogues represent another potential approach for imaging the metabolic activity of inflammatory cells after myocardial infarction. For example, the PET tracer he event . In thesistology . The 11Cl day 28 . Lower tvβ3 expressed by endothelial cells (as well as macrophages and other cells) has been examined for use as a PET imaging target for detecting neoangiogenesis. In one study, myocardial accumulation of the avβ3-targeted PET tracer 18F-Galacto-RGD was observed from 3 days post-infarction in rats, with peak tracer uptake in the infarct between 1 and 3 weeks [vβ3 PET signal intensity was associated with increased histological vascular density in post-infarct tissue specimens. In a clinical study, increased myocardial avβ3 PET signal was also observed using 68Ga-PRGD2 in 20 out of 23 patients imaged within 1 week after their event [18F-Fluciclatide, which also binds avβ3, showed higher PET signals at the site of acute infarction in patients within 2 weeks of their event, compared to remote myocardium and patients with old infarction or healthy volunteers [18F-Fluciclatide uptake was also associated with an increased probability of subsequent functional left ventricular recovery after 9 months.Integrin a 3 weeks . avβ3 PEir event . Anotherlunteers • 68Ga-FAPIh cancer .18F-ML-10 and 18F-ML-8 demonstrated focal infarct-related myocardial tracer accumulation on days 1 to 3 after coronary ligation in rats in regions devoid of 18F-FDG uptake and histologically confirmed apoptosis [18F-ML-8 was taken up by apoptotic, but not necrotic or normal cells, presenting a potential advantage over Annexin V and synaptotagmin-I targeted SPECT tracers, which bind exposed phosphatidylserine in both apoptotic and necrotic cells.Other pathogenic processes occurring after myocardial infarction that have been targeted for molecular imaging with PET tracers include apoptosis and microcalcification. Indeed, given the importance of efferocytosis on post-infarct repair and inflammation resolution, detection of defective or delayed clearance of apoptotic cells by PET imaging could represent an important imaging target. A study of the novel apoptosis tracers poptosis . In this18F-NaF, which binds to areas of microcalcification and exposed hydroxyapatite in atherosclerosis, was increased more in areas of myocardial infarction with scar than the remote myocardium [18F-NaF PET signals occurring 1 day after myocardial infarction in rats were found to closely match histological markers of apoptosis, but not calcification.Microcalcification is also thought to occur as part of the healing process after myocardial infarction. In one study of 10 patients, signal from the PET tracer ocardium . However68Ga-DOTA chelate, and for imaging myocardial oxidative metabolism, such as 11C-acetate, have also been investigated in preclinical studies and could be useful in this setting [Among the other molecular targets that have been examined for post-myocardial infarction PET imaging is glucagon-like peptide-1 (GLP-1) . This ta setting , 64.Among the potential clinical translational applications of post-infarct myocardial PET imaging are as follows: (i) to identify and risk-stratify patients with maladaptive initial or ‘residual’ inflammatory responses contributing an increased likelihood of long-term heart failure, and (ii) to inform the design and use of emerging immune-modulatory therapies for cardiovascular disease. This type of mechanistic research may also yield valid, non-PET biomarkers that can be more easily rolled out in the clinic.18F-FDG inflammatory signals, along with histological grading of M1 macrophage and neutrophil infiltration, and improved myocardial viability after myocardial infarction [Several preclinical studies have shown that PET imaging, for example with tracers targeting TSPO or CXCR4, can quantify changes in myocardial inflammation after treatment with conventional heart failure therapies, such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers , 65, 66.farction . Results18F-GE180 infarct-related uptake at day 7 compared to control myocardial infarction due to lower CD68+ macrophage content, but increased 68Ga-pentixafor signal because of sustained recruitment of Ly6G+ neutrophils, as well as active calcification of intracavity thrombus detected by 18Na-NaF [Multi-tracer studies can potentially help further tease out individual inflammatory pathways or healing responses to improve the precision of therapeutic targeting after myocardial infarction. For example, a study published as an abstract showed that peripheral macrophage depletion in mice resulted in reduced 18F-FDG PET/MRI within 5 days of revascularisation for myocardial infarction [18F-FDG uptake, T1 mapping and extracellular volume tended to overlap anatomically within the infarcts of individual patients, a lack of quantitative correlation meant that these measures were reporting on different underlying biological processes or tissue properties. In another preclinical study, dual-imaging with 18F-Macroflor PET (a dextran nanoparticle similar to 18F-Macrin) and MRI with MPO-Gd, which detects myeloperoxidase activity in neutrophils and Ly-6Chigh monocytes, was performed at day 2 and 6 post-infarct in mice. This study showed divergent temporal changes in PET and MRI signals in keeping with the well-characterised biphasic monocyte/macrophage phenotypic response after myocardial infarction [Moreover, the use of multi-modality multi-parametric imaging, and in particular hybrid PET/MRI, offers the ability to combine molecular imaging of inflammation and adjunct processes with detailed tissue characterisation. The potential value of this combined approach was shown in a study of 25 patients who underwent hybrid farction . This stfarction .Dysregulated post-infarction inflammation and remodelling confer adverse outcomes in patients after myocardial infarction. PET imaging of these processes can potentially be utilised in both the development and deployment of novel immunomodulatory therapies for this indication. Further research efforts should be directed towards realising the full potential of these novel molecular imaging techniques.


We used an experimental murine model of severe ischemic cardiomyopathy through the ligation of the left coronary artery without reperfusion, and after 7 days randomly assigned mice showing large anterior MI (>4 akinetic segments), increased left ventricular (LV) dimensions ([LVEDD] > 4.4 mm), and reduced function (LV ejection fraction < 40%) to a diet that was enriched with OLT1177® admixed with the chow in the diet at 3.75 g/kg (Group 1 [n = 10]) or 7.5 g/kg (Group 2 [n = 9]), or a standard diet as the no-treatment control group (Group 3 [n = 10]) for 9 weeks. We measured the cardiac function and contractile reserve with an isoproterenol challenge, and the diastolic function with cardiac catheterization at 10 weeks following the MI surgery. When compared with the control (Group 3), the mice treated with OLT1177 (Group 1 and 2) showed significantly greater preservation of their contractile reserve  and of diastolic function measured as the lower left ventricular end-diastolic pressure . No differences were noted between the resting LVEF of the MI groups. These effects were independent of the effects on the ventricular remodeling after MI. NLRP3 inflammasome inhibition with OLT1177® can preserve β-adrenergic responsiveness and prevent left ventricular diastolic dysfunction in a large non-reperfused anterior MI mouse model. OLT1177® could therefore be used to prevent the development of heart failure in patients with ischemic cardiomyopathy.Interleukin-1β (IL-1β), a product of the NLRP3 inflammasome, modulates cardiac contractility and diastolic function. We proposed that OLT1177 The NLRP3  inflammasome is an intracellular macromolecular structure involved in sensing danger signals, activating caspase-1, and the pyroptotic release of pro-inflammatory cytokines that initiate the sterile inflammatory response to injury that has been identified as a central mechanism in both the response to damage and the healing process of acute myocardial infarction (MI) ,3,4.Interleukin-1β (IL-1β) is a cytokine that is produced and released by the cells due to the activation of the NLRP3 inflammasome ,3,4. As Treatment before an MI and before cardiac dysfunction ensues is typically not possible, and unfortunately, patients may already show signs of HF as they are waiting for treatment. In order to address these concerns, multiple experimental studies are investigating the efficacy of utilizing pharmacological strategies to mitigate NLRP3-modulated inflammatory signals that promote further myocardial injury in cardiovascular diseases. In a mouse model of HF due to large non-reperfused anterior MI, IL-1β blockade preserved contractile reserve and diastolic function even after the adverse remodeling of the left ventricle had ensued . ConsequIn addition to studies investigating the anti-inflammatory effects resulting from the targeting of the IL-1 receptor, IL-1β and IL-6, several NLRP3 inhibitors, which are upstream mediators of the neutralizing biologics, are under development in a variety of experimental conditions to target and inhibit the upstream NLRP3 inflammasome formation process, thereby resulting in less caspase-1 being activated, less IL-1β being produced, and an overall decrease in the sterile inflammatory response.®, also known as dapansutrile (3-methanesulfonyl-propionitrile), is effective in in vitro and in vivo studies, and is currently being evaluated to help treat acute gout flares, Schnitzler’s syndrome, Alzheimer’s disease, cardiovascular diseases and others /LVEDD3), as previously described [All of the mice underwent transthoracic echocardiography at 3 and 70 days after surgery. The echocardiograms were obtained in order to assess and monitor the change in LV systolic function, infarct size, cardiac remodeling, and wall motion abnormalities between the groups of mice. The echocardiography was performed using a Vevo770 High Resolution  along with a transducer probe with a high transmission frequency of 30 MHz . Brieflyescribed ,6,9. TheWe assessed the contractile reserve 70 days after the MI surgery through an echocardiogram assessment of LVEF and isoproterenol challenge. Isoproterenol (20 ng/mouse) is a synthetic short-acting β-adrenergic receptor agonist ; it was administered intraperitoneally to each anesthetized mouse in order to assess the contractile reserve/β-adrenergic sympathetic response ,41. LVEF® on the left ventricular diastolic pressure, as previously described [® Pressure Transducer Catheter  into the right carotid artery, through the aorta, and into the left ventricle allowed the measurement and recording of the intracardiac LV pressure-volume tracings. The effect of the treatment on the left ventricular diastolic pressure was characterized by comparing the left ventricular end-diastolic pressures (LVEDP) of the experimental groups to the control group. The values (mmHg) from this pressure probe catheter were recorded in real-time and measured using Labchart Pro 5 . The LV catheterization, as well as the assessment of LVEDP, were performed by an investigator blinded to treatment allocation.Between 48 and 72 h after the isoproterenol challenge, all of the mice underwent anesthesia using pentobarbital (70 mg/kg) before LV catheterization, a terminal procedure utilized to determine the effect of the OLT1177p-values are reported throughout, with statistical significance set at the two-tailed 0.05 level (p < 0.05). Prism 9.1.0  for Mac was used.The data and values derived from these procedures and techniques are presented as the mean and the standard error of the mean. The normality of the data distribution was determined using the Kolmogorov–Smirnov test. For the differences between the mouse treatment groups, comparisons were made utilizing a two-tailed Student’s T-test, whereas comparisons of the two different doses and the control condition were assessed using one-way analysis of variance (ANOVA) followed by Bonferroni’s post-hoc test for multiple comparisons. The missing data  was excluded from our experimental results and analyses. The unadjusted ® (dapansutrile), administered orally, preserved the contractile reserve and diastolic function in a preclinical model of severe ischemic heart failure in mice after 10 weeks of treatment. The data presented support the notion that NLRP3 inhibition with OLT1177 may improve the cardiac function and reserve of patients with HF.The inhibition of NLRP3-dependent IL-1β with OLT1177


The prognosis of patients with ventricular ectopy and a normal heart, as evaluated by echocardiography, is virtually unknown. Cardiac magnetic resonance (CMR) can detect focal ventricular anomalies that could act as a possible site of origin for premature ventricular contractions (PVCs). The aim of this study was to investigate the presence of cardiac anomalies in patients with normal findings at echocardiogram. Methods: Fifty-one consecutive patients  with very high PVC burden  and normal findings at standard echocardiography and exercise test were examined with CMR. The outcome was pathologic findings, defined as impaired ejection fraction, regional wall motion abnormalities, abnormal ventricular volume, myocardial edema and fibrosis. Results: Sixteen out of 51 patients (32%) had structural ventricular abnormalities at CMR. In five patients CMR showed impairment of the left ventricular and/or right ventricular systolic function, and six patients had a dilated left and/or right ventricle. Regional wall motion abnormalities were seen in six patients and fibrosis in four. No patient had CMR signs of edema or met CMR criteria for arrhythmogenic right ventricular cardiomyopathy. Five patients had extra-ventricular findings . Conclusions: In this study 16 out of 51 patients with a high PVC burden and normal findings at echocardiography showed signs of pathology in the ventricles with CMR. These findings indicate that CMR should be considered in evaluating patients with a high PVC burden and a normal standard investigation. Premature ventricular complexes (PVCs) are common clinical findings, both in patients with and without structural heart disease, and the reported prevalence, although it varies among different studies, is high ,3,4,5,6 While the general recommendations in the diagnostic pathway for PVC patients include echocardiography , in 1997The aim of this study was to assess the occurrence of structural pathology at CMR in a cohort of consecutive patients with a high burden of PVCs and normal findings at echocardiography and exercise test, regardless of the PVC morphology.We prospectively included 51 consecutive patients between 2016 and 2018 with at least 10,000 PVCs per day according to Holter recording. All the patients were evaluated at our Arrhythmia Outpatient Clinic by an experienced cardiologist and underwent an exercise test and echocardiography with a normal result. No patient had a history of previous structural heart disease or sustained ventricular tachycardia. In a majority (42 of 51) of patients we also had access to PVC on 12-lead ECG. The only exclusion criteria were contraindications to CMR or inability to perform the exam .The Holter data were analyzed manually by an experienced physician to ensure accuracy. The recording time was at least 24 h, and the first 24 h were considered for inclusion.A normal exercise test was defined as absence of exercise-induced depression of the ST segment on ECG and absence of exercise-induced arrhythmia .A normal echocardiogram was defined as left ventricular ejection fraction (LVEF) equal to or higher than 55%, visually normal right ventricular ejection fraction (RVEF), absence of moderate to severe valve dysfunction, absence of local dyskinesia, normal ventricular dimension, and normal wall thickness. Echocardiographic exams were reviewed by two additional independent and blinded examiners. In case of conflicting evaluations of the echocardiographic findings, the exam was considered normal if two of three examiners had assessed the exam as such, and pathologic if two of the three examiners had found signs of pathology. As a result of this process, we excluded one of the 52 originally included patients.CMR examinations were performed using a 1.5 T Signa HDxt scanner  with a cardiac phased array 32 channel coil out of which 16 channels were used. All patients were in sinus rhythm during the investigation. For the assessment of regional wall motion abnormalities (RWMA) and left ventricular (LV) and right ventricular (RV) volumes, cine images were used with a steady-state free precession (FIESTA) cine sequence in long axis views and short-axis stack . In patients with PVCs of unknown QRS morphology or morphology suggestive of RV origin a transaxial cine stack , sagittal RVOT and RV in-/outflow views were added. The following acquisition parameters were typically applied: 30 phases, 24 views per segment adjusted for heart rate, NEX 1, FOV 35 cm, a matrix of 256 × 224, a 40–45 °C flip angle, TR/TE approximately equal to 3.5/1.5, and a bandwidth of 125 kHz.For evaluation of edema, black blood T2w images (STIR) were performed in long axes views and short axis stack .Late gadolinium enhancement (LGE) was performed using a gadolinium dose of 0.2 mmol/kg bodyweight, but decreased to 0.1 mmol/kg in patients with GFR 30–60 mL/min. For LGE a standard 2D–IR GRE sequence was performed in long and short axis views using the same slice thickness and gap as for SSFP cines.We used dedicated software  for post-processing, and functional parameters were obtained from the short-axis images. For both LV and RV, end-diastolic and end-systolic volume indexes and ejection fraction were reported and compared to the respective reference values for class age and sex . SegmentPathology at CMR was defined as one or more of the following: abnormal LV or RV volume, abnormal wall thickness, regional dyskinesia, myocardial edema, fibrosis and ejection fraction (EF) lower than 55%.p-value of ≤0.05 was considered statistically significant. Continuous data were presented as mean ± standard deviation or median ± interquartile range (IQR) when appropriate. Nominal data are presented as number of cases (percent).No power calculation was done before inclusion, as this is regarded as a descriptive pilot study. Calculation of mean values was done in Excel . Categorical variables were compared using Chi-squared with Yates’ correction. A two-sided A total of 51 patients, 23 females and 28 males, was included. The median age was 62 years (IQR = 44–73). Patient characteristics are summarized in Holter recording was available for all patients, while PVCs recorded on 12-lead ECG were available in 42 patients. We determined the PVC site of origin by assessing the direction of depolarization on the sagittal and the frontal plan, using a comprehensive paper from 2015 as guidance . The morAll patients completed the CMR protocol without complications. Sixteen patients (31%) had pathologic findings at CMR, with three patients (6%) having more than one pathological finding. The most common findings were RWMA, dilated left ventricle and fibrosis, while no patient had edema. The results are summarized in All cases with RMWA and dyskinetic areas were found in the right ventricle, while fibrosis was only seen in the left ventricle. In the two cases of fibrosis in which we had access to 12-lead ECG there was a correlation between topographic localization of the finding and the PVC morphology .p = 0.44).We ran a logistic regression with the number of PVCs as predictor variable and any CMR finding as the outcome variable, showing no statistically significant correlation , we had PVC recorded on a 12-lead ECG in four, and found both a right ventricular and a left ventricular morphology in two cases.p-value > 0.05.The relationships between findings and PVC morphology are summarized in CMR could also identify extraventricular pathology; three patients had enlarged atria , one had an enlarged thoracic aorta and one had pericardial exudate.In this study CMR showed signs of pathology in 16 of 51 patients (31%) with high PVC burden, despite normal findings at a standard investigation that included echocardiography and exercise test. The occurrence of CMR findings did not significantly vary with PVC morphology, but we did notice that focal or local findings such as fibrosis or wall motion abnormalities tended to be present in the same area as the site of origin of PVCs.There is an increasing body of evidence recently summarized in comprehensive reviews ,28,29 abIn our study we included consecutive patients regardless of PVC morphology, all with normal findings at a thorough standard examination. In our opinion, this design makes the study an important contribution to the evidence that has accrued since, when the first two studies were published in 1997 on patients with PVCs originating from RVOT ,30. EvenA considerable proportion of our patients (45%) had unifocal PVCs originating from the right ventricle. Patients with RV–PVC have, both in clinical praxis and scientific papers, been the object of evaluation aimed at detecting diagnostic criteria for arrhythmogenic right ventricular cardiomyopathy (ARVC). However, even when diagnostic criteria for ARVC are not met, the CMR findings still may have a prognostic value. Aquaro et al. enrolled 440 patients with a burden of >1000 PVCs/day with a LBBB morphology. The participants were evaluated with CMR in search of ARVC criteria, other than PVC originating from the right ventricle. The study also had a clinical outcome consisting of a composite end point of cardiac death, resuscitated cardiac arrest and appropriate ICD shock. The patients with RV anomalies had worse clinical outcomes than patients without RV anomalies, despite a few patients with MRI anomalies fulfilling task criteria for ARVC diagnosis . There wPVC morphology was also important in the study from Nucifora , that coThe CMR findings in our study were subtle and no patients met diagnostic criteria for ARVC or other well-defined structural heart diseases. Four patients showed signs of fibrosis, but none was of ischemic origin  based on LGE pattern, localization and distribution. In a recently published study  the authDifferently from other studies ,18,21, wAs previously mentioned, the opinion about the prognostic meaning of pathologic CMR findings is divided, with a majority of the few published articles claiming them to be a negative risk marker. It is currently uncertain whether PVCs themselves have a pathogenetic role or are merely markers of an active disease of the myocardium, even when no signs of structural pathology can be seen at imaging. It is reasonable to believe that both phenomena exist. The large multicenter study by Muser et al.  deservesOur findings revealed a possible relation between the site of fibrosis at CMR and PVC morphology, indicating that PVCs had their origin in the fibrotic area, which points toward them being an effect of a previous disease. However, in patients with impaired ventricular function or dilated ventricles, there was no correlation between the diseased ventricle and the origin of PVCs, possibly meaning that PVCs per se lead to unfavorable effects on ventricular functions. The mechanisms leading to these unfavorable effects are unknown, although several theories have been formulated including electromechanical dyssynchrony, extrasystolic potentiation, interpolation, R–R variability and myocardial remodeling by short-coupled PVCs . DyssyncPrevious papers have shown that CMR can detect previously undiscovered ventricular anomalies in a significant share of the participants, ranging between 15–75% ,32,38,42This is a descriptive pilot study, and like most papers in the field, we did not include controls. We made this decision based on the recommendations from the International Society for Magnetic Resonance in Medicine , which uAs frequent PVCs can pose a challenge in evaluating CMR sequences, all our findings are based on frames with good quality. Frequent PVCs during CMR procedure may lead to false positive findings of myocardial edema, of which we had none.This study confirms previous findings showing that CMR can offer a more thorough examination of patients with high PVC burden and a normal echocardiogram. This appears to be valid regardless of PVC morphology. CMR should therefore be considered in the diagnostic work–up. The prognostic importance of these findings needs to be assessed with longitudinal studies.


Heart space-occupying lesions are a disease that occurs frequently in clinical setting, and therefore, it is important to diagnose and treat this type of pathologies properly. Angiographic echocardiography and transesophageal sonogram are widely used for clinical diagnosis. Their application provides a guarantee for the diagnosis of cardiac space-occupying lesions. In this paper, the application of cardiac contrast echocardiography and transesophageal echocardiography in cardiac space-occupying lesions was studied. Prediction of cardiac lesions can accurately determine the nature of cardiac occupancies and provide a basis for clinical diagnosis and management judgments. The results of pathological analysis and experimental comparison showed that myocardial contrast echocardiography can accurately distinguish tumor and thrombus and make contribution to patients taking appropriate medical measures. At the same time, it can compare conventional transthoracic echocardiography and transesophageal echocardiography. The results showed that TEE could clearly show the cardiac lesions. The experimental data of 76.9% confirmed cases showed that the diagnostic accuracy is greatly improved. TEE can also clearly show small thrombus that TTE cannot, in which 2DTEE can clearly show the boundary between the space-occupying and surrounding tissues, and whether there is a clear boundary between the space-occupying and surrounding tissues is an important distinguishing point of benign and malignant tumors. In addition, the TEE probe can also be used for large angle imaging and multiangle rotation, so as to determine the tumor boundary and the spatial position relationship between the tumor and the surrounding tissue. All in all, myocardial contrast echocardiography and transesophageal echocardiography have better clinical application effect on cardiac space-occupying lesions. Space-occupying lesions are a special term in medical imaging diagnosis. The results appear in X-ray, B-ultrasound, CT, and other examinations. It points to something that is not grown out of the original part of an organ . This kiHeart-occupying lesions  are one of the heart diseases that seriously threatens the life of patients . The reaIn the study of heart-occupying lesions, many experts and scholars have conducted intensive research. Dong et al. studied four patients with space-occupying cardiomyopathy using electronic focusing high-resolution two-dimensional echocardiography . In two This article briefly introduces the damage of heart-occupying lesions to patients and the application of new medical technology, introduces the application of ultrasound technology in the medical field, and further introduces myocardial ultrasound contrast and transesophageal echocardiography technology, using practical research methods. The application of myocardial contrast echocardiography and transesophageal echocardiography in heart-occupying lesions is analyzed. The incomparable results indicated that the use of cardiomyogram echocardiography and transesophageal sonography can effectively improve the diagnosis of an occupied cardiac lesion in patients. The next surgical steps for patients had contributed a lot.Space-occupying lesions are one of the more common clinical diseases. With the population aging in China, the growing incidence of cardiovascular and the rising incidence of cardiac preoccupying lesions has caused significant concern among a number of physicians and scholars. Space-occupying lesions include benign, malignant tumors, thrombosis, hematoma, and abscesses , 10. TheWith the advancement of technology, ultrasound technology has been applied in the medical field . CompareMyocardial echocardiography (MCE) is currently a commonly used method for detecting cardiac function. In recent years, with the use of acoustic contrast agents, to observe myocardial perfusion by performing an echocardiogram has been made possible. This is known as myocardial echocardiography. It is also known as echocardiography of the corpus cavernosa. During the MCE examination, a specific microbubble contrast agent needs to be injected into the blood vessel. The microbubbles in the contrast agent are encapsulated by a high molecular weight gas (nitrogen or fluorocarbon gas) in a phospholipid or albumin shell. They cannot penetrate the endothelial cell layer and have similar dynamics to human red blood cells in blood vessels. They can be ruptured under the action of ultrasound and observed and recorded by relevant ultrasound equipment. The operation of heart echocardiography is simple, the cost is low, and there is no radiation. It is easier to be accepted by the majority of patients, and it has been gradually applied in clinical practice. In fact, the development of ultrasound contrast agents has also experienced three stages of leaping development; so far, the third generation of contrast agents has appeared , 28. TheWhile the conventional transthoracic echo cardiogram can determine most of the oncotic lesions and is by far the most widely used means of visualization of oncotic lesions, its restrictions are also very well established. In order to be able to accurately determine the heart occupying, the nature of the lesions has been gradually applied and popularized by transesophageal echocardiography. In principle, transesophageal echocardiography (TEE) refers to an ultrasound imaging method, in which an ultrasound probe is placed in the esophagus to detect changes in the morphological structure and function of the heart and blood vessels from the back of the heart and blood vessels . Its scaAt a hospital, a total of 50 patients, 28 being men and 22 being women, aged 25–85 years, diagnosed with preoccupation of the heart by transthoracic radiology, were selected for the study. Patients diagnosed with the presence of cardiac thrombus based on clinical data, etiology, and TTE presentation were excluded. Of the 50 patients, 10 had previous history of malignant tumors of other organs; 45 tumors were confirmed by pathology, 5 tumors had reduced volume after chemotherapy, and 4 had reduced volume after thrombolytic therapy. Fifty patients were divided into benign tumor group (25 cases), malignant tumor group (20 cases), and thrombosis group (5 cases) according to clinicopathology and clinical diagnosis. This experiment is based on two latitudes of tumor detection time and size to determine tumor category. In general, tumors that do not change significantly in size over time are classified as benign. This example uses the most simplified two-dimensional model to visualize the sample data and produce the following graph, where the horizontal axis is the mass size, and the vertical axis is the time of detection. Each point represents the size of the tumor and the time of onset for a different patient, and the tumor is judged to be benign or malignant based on its color.Using the PhilipsiE33 ultrasound system, the patient was lying on the left side, connected to an electrocardiogram, and conventional ultrasound was used to observe the size, shape, position, internal echo, and adjacent conditions of the tumor, and to store the image. Sign the informed consent for ultrasound imaging. Select an appropriate section, so that the tumor is displayed on the same section as the ventricular septum or the left ventricular posterior wall, enable the MCE mode, the mechanical index is 0.10, the frequency is 2.5∼3.5 MHz, and slowly push the Novi contrast agent 2.5 through the left median elbow vein ml, speed 1.25 mL/min, postinjection of normal saline 5 mL to flush the injection channel, observe the tumor and normal myocardial enhancement, and store dynamic images. Instruct the patient to keep quiet and not move during the entire imaging process.y (t) = A (1 − e − Bt) + C line perfusion curve fitting, record the peak intensity A value of the space-occupying lesion and the adjacent myocardium (reflecting the blood volume of the area of interest), and record it as A1 and A2, respectively, and calculate A1/A2 ratio; the ratio is greater than 1 diagnosed as malignant tumor, the ratio is diagnosed as benign tumor or thrombosis in the range of , and the ratio is equal to 0 diagnosed as thrombosis. Use SPSS18.0 professional statistical software analysis. MCE semiquantitative index results are adopted. The absolute value indicates that the chi-square test is used to compare the semiquantitative indexes of MCE between benign and malignant heart tumor groups; the results of the quantitative indexes of MCE are described by x ± s, and the independent sample t-test is used to compare the quantitative indexes of MCE between benign and malignant heart tumor groups; P < 0.05 means that the difference was statistically significant.MCE semiquantitative analysis: visual observation: the degree of contrast enhancement of space-occupying lesions is divided into (1) high enhancement: the enhancement intensity inside the space-occupying lesion is higher than the adjacent myocardial tissue; (2) enhancement: enhancement intensity of the space-occupying lesion is equal to that of the adjacent myocardial tissue; (3) low enhancement: the enhancement intensity of the occupying lesion is lower than that of the adjacent myocardial tissue; (4) no enhancement: no enhancement agent is filled inside the occupying lesion. Diagnose malignant tumors with high-enhanced space-occupying lesions, whole-area-enhanced space-occupying lesions as normal myocardial tissue, and overall low-enhanced space-occupying lesions with benign tumors, and the morphological rules remain unchanged. The positional lesions were diagnosed as dense thrombi, and the space-occupying lesions that were significantly lobed after the angiography and had no internal enhancement were diagnosed as fresh thrombus with loose texture. The quantitative index of MCE uses the QLAB10.8 software computer region of interest ROI technology to select the region of interest and dynamically track it to obtain the contrast intensity-time curve of the heart-occupying lesion and the adjacent normal myocardium, and according to the formula 52 patients were selected for TEE examination in a hospital, 22 males and 30 females, aged 20–60 years. Of the 52 cases, 8 had no obvious symptoms, and the physical examination found that the heart occupied, and the remaining 44 had obvious symptoms and signs . Examination found that the heart occupied space. Ten of 52 patients occupy a history of malignant tumor. An occupying lesion is a general term for a group of conditions, in which the body's tissues occupy a certain spatial position. The majority of occupying heart lesions are caused by heart disease, but some are also caused by bruising inside the heart or by cysts.Ultrasonic examination uses Philips iE33 colour ultra-Doppler ultrasound diagnostic instrument, equipped with C5-1 transthoracic probe and X7-2t three-dimensional transesophageal real-time probe. Transesophageal real-time 3D has a real-time three-dimensional display mode (Live-3D) and ECG-gated three-dimensional full-volume display mode (3DFullVolume).z ± s. Use the ￡ test to compare the size of the heart-occupying lesions measured by various methods with the size of pathological specimens, and the size of the heart-occupying lesions measured by various methods, and compare the size correlation using the pathological specimens Pearson method. P < 0.05 indicates that the difference is statistically significant.TTE examination method: first, let the patient take the supine position, with the left ventricular long-axis view, left ventricular short-axis view, left ventricular apex four-chamber view, etc. as the standard part of cardiac ultrasound scanning. To measure the size of each cardiac chamber regularly and to attentiveness to the specific characteristics of the defect and its association with the surviving tissues. TEE examination method: before the examination, it is necessary to make sure that the patient has no contraindications, the consent form has been signed, and the examination room is equipped with the necessary first aid equipment. Instruct patients to fast for more than 16 hours, take the left position, connect the ECG; use X7-2t probe, 2DTEE multi-angle scanning observation, measure relevant indicators and store images and data; then, use RT3DTEE imaging; first use real-time 3D mode display, observe the position, shape, and size of the cardiac cycle, and then switch to 3DFullVolume  mode, adjust the fan angle and thickness, wide-angle display space, and surrounding structure, and continuously store 4∼7. During the cardiac cycle, rotate and cut the stored 3DFullVolume image, observe carefully, clearly show the lesion, and measure its maximum footprint. Using SPSS18.0 software analysis, the maximum meridian of the space-occupying lesion is represented by Of the 50 heart-occupying cases, 25 cases were  in the benign tumor group, including 15 cases of myxoma, 3 cases of lipoma and hemangioma, 2 cases of fibroids, and 2 cases of intracardiac leiomyoma, and 25 benign tumors were confirmed by surgery: 20 cases of malignant tumors , including 8 cases of lung cancer heart metastasis, 3 cases of malignant thymoma heart metastasis, and 3 cases of liver cancer heart metastasis and lymphoma and pericardial osteosarcoma. Pericardial angiosarcoma and neuroectodermal malignant tumors each had a heart metastasis; 20 cases of malignant tumors were confirmed by surgery in 10 cases , 7 of the remaining 10 unoperated patients had shrinkage after chemotherapy , and 3 were confirmed by biopsy under CT biopsy ; 5 cases  in the thrombus group, based on medical history  and TTE could not confirm the diagnosis of thrombosis, and they were included in this study, the volume after thrombolytic therapy is small, and final clinical diagnosis of cardiac thrombosis is applied.See P < 0.05). The results of MCE semiquantitative indicators of various tumors are shown in According to According to The quantitative index of cardiac tumor MCE is shown in As can be seen from Through the above analysis, the tumor and thrombus can be identified by MCE, and the thrombus MCE shows no enhancement; semiquantitative and quantitative indicators help judge the blood supply status of cardiac tumors: most benign tumors are of low enhancement, and there are also small ones in malignant tumors. Some have low enhancement; unevenly enhanced MCE and uneven edges have high diagnostic value for the diagnosis of malignant tumors; but for typical myxoma, the diagnostic value of conventional echocardiography is higher than MCE; for some tumors , the same pathological type shows different degrees of enhancement, so more cases need to be collected for discussion. Secondly, MCE is different from the ultrasound contrast of liver, breast, thyroid, and other organs. First, MCE takes intravenous drip, which is different from intravenous bolus injection, so the heart develops longer, and the quantitative index results are different from other organs; second, the heart is a pulsating organ, which brings difficulties to MCE quantitative analysis. Software analysis will be affected by heart beats, especially tumors with long tumor pedicles. The operation of software analysis is more complicated; third, the requirements for the cut surface are more than others. Visceral ultrasonography is high, and MCE requires that the lesion is located at the same depth as normal tissue, so the operator is required to be proficient in each section of TTE, both to select a section to display the lesion and normal tissue at the same depth, but the depth cannot be too large; otherwise, the contrast of the effect is not good, and at the same time, it is necessary to avoid adverse factors such as rib sound windows.Pathological analysis is shown in According to An example of transesophageal echocardiography is shown in The results of conventional transthoracic echocardiography and transesophageal echocardiography are shown in It can be seen that According to It has to be said that heart occupation is one of the heart diseases that seriously threatens the lives of patients, and it will cause huge interference to patients and their families. The placeholder will show different symptoms and signs due to its own characteristics. Clinically, primary heart tumors, metastases, cancer thrombi, neoplasms, thrombi, etc. are all common heart-occupying lesions.An investigation based on thermography echocardiography and transesophageal echocardiography in the clinical of occupant cardiac lesions is presented in this article. Cardiac echocardiography is simple to perform, is of low cost, and is radiation free. It is more acceptable to most patients and is gradually being used in clinical practice, but it is not possible to accurately determine the nature of the occupying cardiac lesion and to make the most accurate diagnostic modality. Using it, myocardial echocardiography and transesophageal echocardiography were in fact found to make an outstanding contribution to the diagnosis of occupying cardiac lesions.Through the application study of myocardial contrast echocardiography and transesophageal echocardiography in the clinical practice of cardiac space-occupying lesions, the following conclusions are drawn: (1) MCE can effectively distinguish tumors from thrombus and thrombus and improve the accuracy of diagnosis of space-occupying lesions. (2) TEE can clearly show the change of heart disease. The experimental data confirmed 76.9% of the cases, and the diagnosis accuracy rate is greatly improved compared with 2D TTE (the diagnosis rate is only 38.5%). (3) TEE can also clearly display small blood clots, tumor pedicles, and other details and the boundary with the surrounding tissue, which is helpful to form a more accurate judgment. In summary, the application of myocardial contrast echocardiography and transesophageal echocardiography in the clinical practice of heart-occupying lesions is conducive to more comprehensive observation and evaluation of the diagnostic accuracy of heart-occupying lesions.