Non-ischemic Pattern Research Articles

Exploring cardiovascular involvement in IgG4-related disease: a case series approach with cardiovascular magnetic resonance

BackgroundIgG4-related disease (IgG4-RD) is a relapsing–remitting, fibroinflammatory, multisystem disorder. Cardiovascular involvement from IgG4-RD has not been systematically characterised. In this study, we sought to evaluate consecutive patients with IgG4-RD using...

Baseline C-reactive protein as a predictor of non-ischemic LGE in myocarditis

Abstract Background Identifying reliable early indicators of myocardial injury in myocarditis is a pressing concern in cardiology. Despite their established role in detecting myocardial necrosis, traditional markers like high-sensitivity cardiac troponin (hs-cTn) may not fully capture the extent of myocardial damage identified by non-ischemic late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) Purpose To identify early admission biomarkers associated with non-ischemic LGE in patients with myocarditis, offering the potential for improved risk stratification and therapeutic targeting. Methods In this retrospective study, we analyzed 59 myocarditis patients admitted to a high-volume medical center from 2017 to 2023, who underwent CMR to evaluate LGE. 41 patients (69.5%) exhibited non-ischemic LGE and 18 (30.5%) did not. We assessed baseline laboratory and echocardiographic parameters, employing Pearson correlation, logistic regression, and ROC curve analyses to elucidate the potential association of baseline biomarkers with non-ischemic LGE, while also discerning subepicardial from midwall patterns. Results Baseline C-reactive Protein (CRP) levels were significantly correlated with non-ischemic LGE (Pearson's r=0.301, p<0.05). Logistic regression analysis substantiated CRP as a predictor of non-ischemic LGE (OR=1.41, p<0.05), corroborated by a multivariate approach even after accounting for age and sex (OR=1.33; p<0.05). Among non-ischemic patterns, subepicardial LGE exhibited the strongest correlation with CRP (Pearson's r=0.321, p<0.05). In contrast, hs-cTn levels showed no significant association with non-ischemic LGE. The ROC analysis revealed that while both CRP and hs-cTn provide valid predictive values for non-ischemic LGE, with AUCs of 0.7333 and 0.6898 respectively, CRP demonstrated a higher discriminative performance, indicating that CRP may offer a more reliable assessment in this clinical context. Additionally, diabetic status emerged as the most significant condition associated with increased CRP levels, with diabetic patients presenting a substantial elevation in baseline CRP compared to non-diabetic patients (8.75 mg/dl vs 3.21 mg/dl; p<0.05). Conclusion CRP appears as a key early biomarker for non-ischemic LGE in myocarditis, with its predictive value being particularly evident in the subepicardial pattern and notably more pronounced among diabetic patients who demonstrate an increased inflammatory burden. These findings suggest a critical role for CRP in risk stratification right from the point of hospital admission and underline the potential for tailored therapeutic approaches that warrant further investigations. Figure 1: ROC curves comparison for CRP and hs-cTn in predicting non-ischemic LGE in myocarditis patients. Figure 2: Patients with diabetes (DM) exhibit significantly higher CRP levels (mean 8.75 mg/dl, SE = 5.54 mg/dl) than those without DM (mean 3.21 mg/dl, SE = 0.49 mg/dl).ROC curves comparisonCPR in patients with and without DM

Characterizing myocardial edema and fibrosis in hypertensive crisis with cardiovascular magnetic resonance imaging.

A hypertensive crisis is associated with an increased risk of cardiovascular events. Although altered cardiac structure, function, and myocardial architecture on cardiovascular magnetic resonance (CMR) have been associated with increased adverse events in hypertensive patients, the studies did not include patients with hypertensive crisis. Our study aimed to determine myocardial tissue characteristics in patients with hypertensive crisis using CMR imaging. Participants underwent comprehensive CMR imaging at 1.5T. The imaging protocol included cine-, T2-weighted-, contrasted- and multi-parametric mapping images. Blood and imaging biomarkers were compared in hypertensive emergency and hypertensive urgency. Predictors of myocardial edema was assessed using linear regression. The predictive value of T1- and T2 mapping for identifying hypertensive emergency (from urgency) was assessed with receiver operator characteristics curves. Eighty-two patients (48.5 ± 13.4 years, 57% men) were included. Hypertensive emergency constituted 78%. Native T1 was higher in patients with LVH compared to those without (1056 ± 33 vs. 1013 ± 40, P < 0.001), and tended to be higher in hypertensive emergency than urgency (1051 ± 37 vs. 1033 ± 40, P = 0.077). T2-w signal intensity (SI) ratio and T2 mapping values were higher in hypertensive emergency (1.5 ± 0.2 vs. 1.4 ± 0.1, P = 0.044 and 48 ± 2 vs. 47 ± 2, P = 0.004), and in patients with than without LVH (1.5 ± 0.2 vs. 1.4 ± 0.1, P = 0.045 and P = 0.030). A trend for higher extracellular volume was noted in hypertensive emergency compared to urgency (25 ± 4 vs. 22 ± 3, P = 0.050). Native T1 correlated with T2 mapping (rs = 0.429, P < 0.001), indexed LV mass (rs = 0.493, P < 0.001), cardiac troponin (rs = 0.316, P < 0.001) and NT-proBNP (rs = 0.537, P < 0.001), while T2 correlated with cardiac troponin (rs = 0.390, P < 0.001), and NT-proBNP (rs = 0.348, P < 0.001). Non-ischemic LGE pattern occurred in 59% and was 21% more prevalent in the hypertensive emergency group (P = 0.005). Our findings demonstrate that hypertensive crisis is associated with distinct myocardial tissue alterations, including increased myocardial edema and fibrosis, as detected on CMR. Patients with hypertensive emergency had a higher degree of myocardial oedema than hypertensive urgency. Further research is necessary to explore the prognostic value of these findings.

The Correlation between Cardiac Magnetic Resonance Findings and Post-COVID-19: The Impact of Myocardial Injury on Quality of Life.

In the post-COVID-19 era, there is growing concern regarding its impact on cardiovascular health and the following effects on the overall quality of life of affected individuals. This research seeks to investigate cardiac magnetic resonance (CMR) findings following COVID-19 and their impact on the quality of life of affected individuals. An observational, cross-sectional study was conducted in consecutive patients with persistent cardiovascular symptoms after COVID-19 who were referred to CMR due to suspected myocardial injury. In addition, patients completed a questionnaire about symptoms and the quality of life during the post-COVID-19 period. In this study, 85 patients were included. The study population consisted of patients with a mean age of 42.5 ± 13.4 years, predominantly women, who made up 69.4% of the study population, while men made up 30.6%. CMR findings showed non-ischemic myocardial injury in 78.8% of patients and myocardial edema in 14.1% of patients. Late pericardial enhancement was present in 40% of patients and pericardial effusion in 51.8% of patients. Pericardial effusion (p = 0.001) was more prevalent in patients who reported more pronounced symptoms in the post-COVID-19 period compared to the acute infection phase. Predictors of lower quality of life in the post-COVID-19 period were the presence of irregular heartbeat (p = 0.039), cardiovascular problems that last longer than 12 weeks (p = 0.018), and the presence of pericardial effusion (p = 0.037). Acute myocarditis was observed in a minority of patients after COVID-19, while non-ischemic LGE pattern and pericardial effusion were observed in the majority. Quality of life was worse during the post-COVID-19 period in patients with CMR abnormalities, primarily in patients with pericardial effusion. Also, irregular heartbeat, cardiovascular symptoms that last longer than 12 weeks, as well as pericardial effusion were independent predictors of lower quality of life during the post-COVID-19 period.

Cardiovascular magnetic resonance reveals myocardial involvement in patients with active stage of inflammatory bowel disease.

Active inflammatory bowel disease (A-IBD) but not remission (R-IBD) has been associated with an increased risk of cardiovascular death and hospitalization for heart failure. Using cardiovascular magnetic resonance (CMR), this study aims to assess adverse myocardial remodeling in patients with IBD in correlation with disease activity. Forty-four IBD patients without cardiovascular disease (24 female, median-age: 39.5years, 26 A-IBD, 18 R-IBD) and 44 matched healthy volunteers (HV) were prospectively enrolled. The disease stage was determined by endoscopic and patient-reported criteria. Participants underwent CMR for cardiac phenotyping: cine imaging and strain analysis were performed to assess ventricular function. T1 mapping, extracellular volume and late-gadolinium enhanced images were obtained to assess focal and diffuse myocardial fibrosis. Simultaneous T1 and T2 elevation (T1 > 1049.3ms, T2 > 54ms) was considered to indicate a myocardial segment was inflamed. 16/44 (16.4%) IBD patients described dyspnea on exertion and 10/44 (22.7%) reported chest pain. A-IBD patients showed impaired ventricular function, indicated by reduced global circumferential and radial strain despite preserved left-ventricular ejection fraction. 16% of all IBD patients had focal fibrosis in a non-ischemic pattern. A-IDB patients had increased markers of diffuse left ventricular fibrosis (T1-values: A-IBD: 1022.0 ± 34.83ms, R-IBD: 1010.10 ± 32.88ms, HV: 990.61 ± 29.35ms, p < .01). Significantly more participants with A-IDB (8/26, 30.8%) had at least one inflamed myocardial segment than patients in remission (0/18) and HV (1/44, 2.3%, p < .01). Markers of diffuse fibrosis correlated with disease activity. This study, using CMR, provides evidence of myocardial involvement and patterns of adverse left ventricular remodeling in patients with IBD. ISRCTN30941346.

Myocardial Fibrosis in Young and Veteran Athletes: Evidence from a Systematic Review of the Current Literature.

Background: Exercise is associated with several cardiac adaptations that can enhance one's cardiac output and allow one to sustain a higher level of oxygen demand for prolonged periods. However, adverse cardiac remodelling, such as myocardial fibrosis, has been identified in athletes engaging in long-term endurance exercise. Cardiac magnetic resonance (CMR) imaging is considered the noninvasive gold standard for its detection and quantification. This review seeks to highlight factors that contribute to the development of myocardial fibrosis in athletes and provide insights into the assessment and interpretation of myocardial fibrosis in athletes. Methods: A literature search was performed using the PubMed/Medline database and Google Scholar for publications that assessed myocardial fibrosis in athletes using CMR. Results: A total of 21 studies involving 1642 endurance athletes were included in the analysis, and myocardial fibrosis was found in 378 of 1595 athletes. A higher prevalence was seen in athletes with cardiac remodelling compared to control subjects (23.7 vs. 3.3%, p < 0.001). Similarly, we found that young endurance athletes had a significantly higher prevalence than veteran athletes (27.7 vs. 19.9%, p < 0.001), while male and female athletes were similar (19.7 vs. 16.4%, p = 0.207). Major myocardial fibrosis (nonischaemic and ischaemic patterns) was predominately observed in veteran athletes, particularly in males and infrequently in young athletes. The right ventricular insertion point was the most common fibrosis location, occurring in the majority of female (96%) and young athletes (84%). Myocardial native T1 values were significantly lower in athletes at 1.5 T (p < 0.001) and 3 T (p = 0.004), although they had similar extracellular volume values to those of control groups. Conclusions: The development of myocardial fibrosis in athletes appears to be a multifactorial process, with genetics, hormones, the exercise dose, and an adverse cardiovascular risk profile playing key roles. Major myocardial fibrosis is not a benign finding and warrants a comprehensive evaluation and follow-up regarding potential cardiac disease.

COVID-19 related myocardial injury is associated with immune dysregulation in symptomatic patients with cardiac MRI abnormalities.

While acute cardiovascular complications of COVID-19 are well-described, less is known about longer-term cardiac sequelae. For many individuals with cardiac signs or symptoms arising after COVID-19 infection, the aetiology remains unclear. We examined immune profiles associated with magnetic resonance imaging (MRI) abnormalities in patients with unexplained cardiac injury after COVID-19. Twenty-one participants (mean age 47 [SD 13] years, 71% female) with long COVID (n=17), raised troponin (n=2), or unexplained new-onset heart failure (n=2), who did not have pre-existing heart conditions or recent steroid/immunosuppression treatment were enrolled a mean 346 (SD 191) days after COVID-19 infection in a prospective observational study. Cardiac MRI and blood sampling for deep immunophenotyping using mass cytometry by time of flight and measurement of proteomic inflammatory markers was performed. Nine of 21 (43%) participants had MRI abnormalities (MRI(+)), including non-ischaemic patterns of late gadolinium enhancement and/or visually overt myocardial oedema in 8 people. One patient had mildly impaired biventricular function without fibrosis or oedema, and 2 had severe left ventricular impairment. MRI(+) individuals had higher blood CCL3, CCL7, FGF-23 and CD4 Th2 cells, and lower CD8 T effector memory (TEM) cells, than MRI(-). Cluster analysis revealed lower expression of inhibitory receptors PD1 and TIM3 in CD8 TEM cells from MRI(+) patients than MRI(-) patients, and functional studies of CD8 T αβ cells showed higher proportions of cytotoxic granzyme B+ secreting cells upon stimulation. CD8 TEM cells and CCL7 were the strongest predictors of MRI abnormalities in a LASSO regression model (composite AUC 0.96, 95%CI 0.88-1.0). CCL7 was correlated with diffuse myocardial fibrosis/oedema detected by quantitative T1 mapping (r=0.47, p=0.04). COVID-19 related cardiac injury in symptomatic patients with non-ischaemic myocarditis-like MRI abnormalities is associated with immune dysregulation, including decreased peripheral CD8 TEM cells and increased CCL7, persisting long after the initial infection.

Quantification of myocardial scar of different etiology using dark- and bright-blood late gadolinium enhancement cardiovascular magnetic resonance

Dark-blood late gadolinium enhancement (LGE) has been shown to improve the visualization and quantification of areas of ischemic scar compared to standard bright-blood LGE. Recently, the performance of various semi-automated quantification methods has been evaluated for the assessment of infarct size using both dark-blood LGE and conventional bright-blood LGE with histopathology as a reference standard. However, the impact of this sequence on different quantification strategies in vivo remains uncertain. In this study, various semi-automated scar quantification methods were evaluated for a range of different ischemic and non-ischemic pathologies encountered in clinical practice. A total of 62 patients referred for clinical cardiovascular magnetic resonance (CMR) were retrospectively included. All patients had a confirmed diagnosis of either ischemic heart disease (IHD; n = 21), dilated/non-ischemic cardiomyopathy (NICM; n = 21), or hypertrophic cardiomyopathy (HCM; n = 20) and underwent CMR on a 1.5 T scanner including both bright- and dark-blood LGE using a standard PSIR sequence. Both methods used identical sequence settings as per clinical protocol, apart from the inversion time parameter, which was set differently. All short-axis LGE images with scar were manually segmented for epicardial and endocardial borders. The extent of LGE was then measured visually by manual signal thresholding, and semi-automatically by signal thresholding using the standard deviation (SD) and the full width at half maximum (FWHM) methods. For all quantification methods in the IHD group, except the 6 SD method, dark-blood LGE detected significantly more enhancement compared to bright-blood LGE (p < 0.05 for all methods). For both bright-blood and dark-blood LGE, the 6 SD method correlated best with manual thresholding (16.9% vs. 17.1% and 20.1% vs. 20.4%, respectively). For the NICM group, no significant differences between LGE methods were found. For bright-blood LGE, the 5 SD method agreed best with manual thresholding (9.3% vs. 11.0%), while for dark-blood LGE the 4 SD method agreed best (12.6% vs. 11.5%). Similarly, for the HCM group no significant differences between LGE methods were found. For bright-blood LGE, the 6 SD method agreed best with manual thresholding (10.9% vs. 12.2%), while for dark-blood LGE the 5 SD method agreed best (13.2% vs. 11.5%). Semi-automated LGE quantification using dark-blood LGE images is feasible in both patients with ischemic and non-ischemic scar patterns. Given the advantage in detecting scar in patients with ischemic heart disease and no disadvantage in patients with non-ischemic scar, dark-blood LGE can be readily and widely adopted into clinical practice without compromising on quantification.

Unrecognized myocardial scar by late-gadolinium-enhancement cardiovascular magnetic resonance: Insights from the population-based Hamburg City Health Study

The presence of myocardial scar is associated with poor prognosis in several underlying diseases. Late-gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging reveals clinically silent "unrecognized myocardial scar" (UMS), but the etiology of UMS often remains unclear. This population-based CMR study evaluated prevalence, localization, patterns, and risk factors of UMS. The study population consisted of 1064 consecutive Hamburg City Health Study participants without a history of coronary heart disease or myocarditis. UMS was assessed by standard-phase-sensitive-inversion-recovery LGE CMR. Median age was 66 [quartiles 59, 71] years and 37% (388/1064) were females. UMS was detected in 244 (23%) participants. Twenty-five participants (10%) had ischemic, and 217 participants (89%) had non-ischemic scar patterns, predominantly involving the basal inferolateral left-ventricular (LV) myocardium (75%). Two participants (1%) had coincident ischemic and non-ischemic scar. The presence of any UMS was independently associated with LV ejection fraction (odds ratios (OR) per standard deviation (SD) 0.77 (confidence interval (CI) 0.65-0.90), p=0.002) and LV mass (OR per SD 1.54 (CI 1.31-1.82), p<0.001). Ischemic UMS was independently associated with LV ejection fraction (OR per SD 0.58 (CI 0.39-0.86), p=0.007), LV mass (OR per SD 1.74 (CI 1.25-2.45), p=0.001), and diabetes (OR 4.91 (CI 1.66-13.03), p=0.002). Non-ischemic UMS was only independently associated with LV mass (OR per SD 1.44 (CI 1.24-1.69), p<0.001). UMS, in particular with a non-ischemic pattern, is frequent in individuals without known cardiac disease and predominantly involves the basal inferolateral LV myocardium. Presence of UMS is independently associated with a lower LVEF, a higher LV mass, and a history of diabetes.

Association Between Left Ventricular Scar and Ventricular Ectopy in People Living With and Without HIV

BackgroundPeople living with HIV (PLWH) have greater risk for arrhythmic sudden death and heart failure than people without HIV (PWOH), though risk identifiers remain understudied. Higher ventricular ectopy (VE) burden reflects increased arrhythmic susceptibility and cardiomyopathy risk. ObjectivesThe purpose of this study was to test if myocardial scar measured by late gadolinium-enhancement cardiovascular magnetic resonance (LGE-CMR) associates with VE by ambulatory electrocardiographic monitoring among PLWH and PWOH with risk factors for HIV, and if the association differs by HIV. MethodsParticipants from 3 cohorts of PLWH and PWOH underwent electrocardiographic monitoring (median wear time 8.3 days) and CMR. Using multivariable regression, we assessed: 1) associations between scar metrics and VE, adjusting for demographics, HIV serostatus, substance use, cardiovascular risk factors, and left ventricular (LV) function/structure; and 2) effect measure modification by HIV. ResultsOf 329 participants (median age 55 years, 30% women, 62% PLWH), 109 had LGE (62% PLWH). Ischemic or major nonischemic pattern LGE was associated with high VE burden (adjusted OR: 2.32, P = 0.004) and more PVCs/day (141% higher, P < 0.001). Among people with LGE, greater scar mass correlated with more PVCs/day (P = 0.028). Associations persisted after adjustment for LV function/structure and when excluding PLWH with HIV viremia and showed no effect measure modification by HIV. ConclusionsIschemic or major nonischemic pattern LGE and greater scar mass correlated with higher VE burden, independently of LV structure/function, HIV serostatus, and HIV viremia. The findings highlight specific scar characteristics common to PLWH and PWOH with risk factors for HIV that may portend higher risk for arrhythmias and heart failure.

Investigating the cardiac manifestations of IgG4-related disease using cardiac magnetic resonance imaging

Abstract Introduction IgG4-related disease (IgG4-RD) is a relapsing-remitting immune-mediated condition that affects multiple organ systems. Case reports of suspected cardiovascular involvement in IgG4-RD have emerged though no study has systematically assessed the cardiovascular phenotype of IgG4-RD using cardiac magnetic resonance (CMR) imaging. Purpose We systematically assessed patients with IgG4-RD using CMR to identify the cardiovascular manifestations, and compared them to controls. Methods We recruited 11 patients with histologically-confirmed IgG4-RD (6 female, 61±11 years, 9 with active disease (8 with pancreatic involvement, 3 parotid, 5 bile ducts, 5 kidneys and 3 cardiovascular)). Patients underwent CMR at 1.5T including cine, myocardial tagging, native T1-mapping, late gadolinium enhancement (LGE), extracellular volume (ECV) and quantitative stress perfusion mapping. Results were compared to 10 healthy controls with no cardiac disease (50% female, 35±8 years). Results are presented as mean ± standard deviation (SD) unless otherwise stated. Results Patients with IgG4-RD had similar cardiac geometry to the reference group (Table 1), with similar biventricular and bi-atrial volumes. However, despite similar biventricular ejection fractions compared to controls (patient LVEF: 55-67%, RVEF: 51-65%), IgG4-RD patients showed significantly reduced global longitudinal strain (GLS) (-16.8 ± 2.3% vs -18.7 ± 1.6%, p=0.045). Furthermore, 64% (7/11) of IgG4-RD patients showed LGE, 6 of whom showed non-ischaemic patterns (Figure 1). Male IgG4-RD patients (n=5) as a group showed a significantly higher average myocardial T1 value relative to the reference group, with 3/5 male patients having an abnormally high myocardial T1 (above the 2SD limit of normal). Female IgG4-RD patients (n=6) had similar and normal myocardial T1 values to the reference group. ECV did not significantly differ between the two groups. IgG4-RD patients showed a significantly reduced global myocardial perfusion reserve (MPR), including two patients with a qualitative inducible perfusion defect. Only 3 out of the 11 IgG4-RD patients had a completely normal CMR. Conclusion Patients with IgG4-RD show frequent cardiac abnormalities as revealed by advanced CMR phenotyping. These include subclinical systolic dysfunction, ischaemic and non-ischaemic myocardial fibrosis, reduced myocardial perfusion reserve, and elevated myocardial T1 times. These abnormalities have been described in inflammatory cardiovascular diseases, supporting a plausible pathophysiological link with IgG4-RD. Future work in larger and multicentre cohorts is warranted, to systematically define the novel cardiovascular phenotype of IgG4-RD.Table 1Figure 1

Multimodality imaging and immunophenotyping of COVID-19 related myocardial injury (the MIIC-MI Study)

Abstract Background Cardiac injury is a well-recognised complication of acute COVID-19 infection, with varied aetiologies ranging from myocarditis to endothelial dysfunction, micro-embolic phenomena, and acute coronary syndromes. While persistent cardiac symptoms in patients with post-acute COVID-19 syndrome are also common, the underlying mechanisms remain unclear. A better understanding of immune-mediated drivers of chronic cardiac injury after COVID-19 infection is urgently needed to inform the management of patients with, or at risk of, long-term sequelae. Purpose To examine immune mechanisms associated with clinically detectable imaging abnormalities across a spectrum of patients with unexplained cardiac injury and/or symptoms after COVID-19 infection. Methods Participants with a history of COVID-19 infection and suspected cardiac involvement based on: a) troponin I elevation (&amp;gt;99th percentile upper reference limit), b) new-onset heart failure not attributable to another cause, or c) persistence of unexplained cardiac symptoms, were enrolled at a single centre in the United Kingdom between October 2020 and February 2022. Individuals with prior myocardial infarction or heart failure and those treated with immunosuppression within the past four weeks, were excluded. Cardiac magnetic resonance imaging (MRI) was performed on a 1.5T scanner following a standard clinical protocol. In parallel to cardiac imaging, peripheral blood samples were analysed for immunophenotyping using cytometry by time of flight (Fluidigm, 32 marker panel) and proteomic analysis (Olink, Target 96 Inflammation panel). Results Twenty-one patients (mean age 47 (SD 13) years, 71% female) were enrolled who had unexplained cardiac symptoms (n=17), raised troponin I (n=2), or new-onset heart failure (n=2). In total, 9/21 (43%) patients had MRI abnormalities, including a non-ischaemic pattern of late gadolinium enhancement (Figure 1a; arrow) and/or visually overt myocardial oedema on T2-weighted imaging (Figure 1b; arrow) in 8 patients, and one with impaired ventricular function in the absence of fibrosis. Patients with MRI abnormalities had higher CCL3, CCL7 (MCP-3), FGF21, and CD4 Th2 cells, and lower CD8 T effector memory cells (Figure 2, volcano plot), compared to those without. CCL7 (MCP-3) levels were correlated with native T1 mapping (r=0.45, p&amp;lt;0.05) and these along with CD8 T effector memory cell counts were the strongest predictors of MRI abnormalities in a LASSO regression model incorporating all clinical, cell phenotyping and proteomic data (composite AUC 0.96, CI 0.88-1). Conclusion Here we show for the first time that COVID-19 related cardiac injury in patients with MRI abnormalities is associated with increased CCL7 (MCP-3), a chemokine known to be important in viral myocarditis1, as well as decreased CD8 T effector memory cells. These findings provide novel insights into the immune-mediated mechanisms underlying non-ischemic cardiac complications of COVID-19.Fig. 1.Post-COVID imaging abnormalitiesFig. 2.Immunophenotyping and proteomics

Abstract 17881: A Predictive Algorithm to Identify Late Gadolinium Enhancement Using Echocardiography

Background: Late gadolinium enhancement (LGE) on cardiac MRI (CMR) correlates with fibrosis and arrhythmic risk, but cannot be used in several clinical settings compared the availability of echocardiography (TTE). Aim: To develop and evaluate a machine learning (ML) model that uses standard clinical and echocardiography (TTE) variables to identify LGE on paired CMR. Methods: Amongst 725 patients (mean age 56.9 ± 16.5 years, 40.3% female) with TTE and CMR within 3 months at our institution, 2018-2023, we derived and tested several ML models (recursive partitioning, random forest, boosted tree, neural networks, LASSO/Elastic Net) to identify LGE on CMR using age and 24 TTE features. Ten-fold cross validation was used for internal validation. Results: A total of 165 (23%) had the presence of LGE (40% ischemic, 60% nonischemic pattern). Of tested models, a boosted neural network performed best (validation area under the curve [AUC] = 0.98; Figure ). In the validation cohort, the algorithm had a sensitivity and specificity of 93.8% and 94.6% for identifying presence of LGE. Accuracy remained high regardless of gender (M vs. F, AUC, 0.987 vs. 0.988) or race (blacks vs. whites, AUC, 0.987 vs. 0.984) and was not related to time between studies (r = -0.06, p = 0.09). Accuracy was better for ischemic LGE (AUC = 0.94) than nonischemic LGE (AUC = 0.90). Left ventricular size, age, fractional shortening, and wall thickness, were amongst the top predictors of LGE presence in the model. Conclusions: In this single center study, a boosted neural network using TTE features identified LGE on paired CMR with high sensitivity and specificity. If confirmed in external data, this suggests possible utility of ML for improving the diagnostic value of TTE for LGE assessment.

Cardiac Morphology, Function, and Left Ventricular Geometric Pattern in Patients with Hypertensive Crisis: A Cardiovascular Magnetic Resonance-Based Study.

(1) Background: Altered cardiac morphology and function are associated with increased risks of adverse cardiac events in hypertension. Our study aimed to assess left ventricular (LV) morphology, geometry, and function using cardiovascular magnetic resonance (CMR) imaging in patients with hypertensive crisis. (2) Methods: Patients with hypertensive crisis underwent CMR imaging at 1.5 Tesla to assess cardiac volume, mass, function, and contrasted study. Left ventricular (LV) function and geometry were defined according to the guideline recommendations. Late gadolinium enhancement (LGE) was qualitatively assessed and classified into ischemic and nonischemic patterns. Predictors of LGE was determined using regression analysis. (3) Results: Eighty-two patients with hypertensive crisis (aged 48.5 ± 13.4 years, and 57% males) underwent CMR imaging. Of these patients, seventy-eight percent were hypertensive emergency and twenty-two percent were urgency. Diastolic blood pressure was higher under hypertensive emergency (p = 0.032). Seventy-nine percent (92% of emergency vs. 59% of urgency, respectively; p = 0.003) had left ventricular hypertrophy (LVH). The most prevalent LV geometry was concentric hypertrophy (52%). Asymmetric LVH occurred in 13 (22%) of the participants after excluding ischemic LGE. Impaired systolic function occurred in 46% of patients, and predominantly involved hypertensive emergency. Nonischemic LGE occurred in 75% of contrasted studies (67.2% in emergency versus 44.4% in urgency, respectively; p < 0.001). Creatinine and LV mass were independently associated with nonischemic LGE. (5) Conclusion: LVH, altered geometry, asymmetric LVH, impaired LV systolic function, and LGE are common under hypertensive crisis. LVH and LGE more commonly occurred under hypertensive emergency. Longitudinal studies are required to determine the prognostic implications of asymmetric LVH and LGE in hypertensive crisis.

Differentiation of acute non-ST elevation myocardial infarction and acute infarct-like myocarditis by visual pattern analysis: a head-to-head comparison of different cardiac MR techniques

ObjectivesParametric cardiac magnetic resonance (CMR) techniques have improved the diagnosis of pathologies. However, the primary tool for differentiating non-ST elevation myocardial infarction (NSTEMI) from myocarditis is still a visual assessment of conventional signal-intensity-based images. This study aimed at analyzing the ability of parametric compared to conventional techniques to visually differentiate ischemic from non-ischemic myocardial injury patterns.MethodsTwenty NSTEMI patients, twenty infarct-like myocarditis patients, and twenty controls were examined using cine, T2-weighted CMR (T2w) and late gadolinium enhancement (LGE) imaging and T1/T2 mapping on a 1.5 T scanner. CMR images were presented in random order to two experienced fully blinded observers, who had to assign them to three categories by a visual analysis: NSTEMI, myocarditis, or healthy.ResultsThe conventional approach (cine, T2w and LGE combined) had the best diagnostic accuracy with 92% (95%CI: 81–97) for NSTEMI and 86% (95%CI: 71–94) for myocarditis. The diagnostic accuracies using T1 maps were 88% (95%CI: 74–95) and 80% (95%CI: 62–91), 84% (95%CI: 67–93) and 74% (95%CI: 54–87) for LGE, and 83% (95%CI: 66–92) and 73% (95%CI: 53–87) for T2w. The accuracies for cine (72% (95%CI: 52–86) and 60% (95%CI: 38–78)) and T2 maps (62% (95%CI: 40–79) and 47% (95%CI: 28–68)) were significantly lower compared to the conventional approach (p < 0.001 and p < 0.0001).ConclusionsThe conventional approach provided a reliable visual discrimination between NSTEMI, myocarditis, and controls. The diagnostic accuracy of a visual pattern analysis of T1 maps was not significantly inferior, whereas the diagnostic accuracy of T2 maps was not sufficient in this context.Clinical relevance statementThe ability of parametric compared to conventional CMR techniques to visually differentiate ischemic from non-ischemic myocardial injury patterns can avoid potentially unnecessary invasive coronary angiography and help to shorten CMR protocols and to reduce the need of gadolinium contrast agents.Key Points•A visual differentiation of ischemic from non-ischemic patterns of myocardial injury is reliably achieved by a combination of conventional CMR techniques (cine, T2-weighted and LGE imaging).•There is no significant difference in accuracies between visual pattern analysis on native T1 maps without providing quantitative values and a conventional combined approach for differentiating non-ST elevation myocardial infarction, infarct-like myocarditis, and controls.•T2 maps do not provide a sufficient diagnostic accuracy for visual pattern analysis for differentiating non-ST elevation myocardial infarction, infarct-like myocarditis, and controls.

Evaluation of diastolic dysfunction in children with hypertrophic cardiomyopathy and its relationship with development of myocardial fibrosis

BackgroundPatients with hypertrophic cardiomyopathy may develop symptoms of shortness of breathing due to diastolic dysfunction which is not related to the severity of left ventricular outflow tract obstruction. As these patients usually develop a non-ischemic pattern of myocardial fibrosis, this may represent a mechanism for increased myocardial stiffness leading to impaired diastolic filling. The study aimed to determine the prevalence of myocardial fibrosis assessed by magnetic resonance imaging in children with hypertrophic cardiomyopathy and to evaluate its relationship with echocardiographic parameters including left ventricle diastolic dysfunction and to find echocardiographic indices which correlates with myocardial fibrosis as detected by cardiac magnetic resonance. A cross-sectional study was done for data of 50 children with hypertrophic cardiomyopathy from July 2018 to July 2021, patients were divided into (group 1) having myocardial fibrosis and (group 2) with no myocardial fibrosis, and results of echocardiographic parameters were compared between the two groups.ResultsResults showed strong relationship between presence of myocardial fibrosis and each of the following: Interventricular septum thickness, lower lateral and septal early diastolic tissue velocities (E′), E/E′ ratio, presence of left ventricular out flow tract obstruction and the grade of diastolic dysfunction.ConclusionsThe trans-mitral lateral and septal E/E′ (early mitral inflow to early diastolic mitral annular velocity ratio) allows early detection of left ventricular diastolic dysfunction in children with hypertrophic cardiomyopathy. The prevalence of diastolic dysfunction is higher in obstructive hypertrophic cardiomyopathy. The diastolic dysfunction severity is higher in patients with myocardial fibrosis.

The role of T1 mapping and Extracellular Volume (ECV) in predicting cardiac reverse remodelling and response to Heart Failure with reduced Ejection Fraction (HFrEF) therapy

Abstract Funding Acknowledgements Type of funding sources: None. Background Adverse cardiac remodelling results from an insult such as myocardial infarction, or as seen in Heart Failure (HF), maladaptive neurohormonal activation. Reverse remodelling describes improvement in cardiac geometry; the left ventricle (LV) recovers more normal structure with improved function and prognosis. Cardiovascular Magnetic Resonance imaging (CMR) allows gold standard assessment of LV volumes and function, diffuse and focal fibrosis and estimation of extracellular volume (ECV) by T1 mapping. Purpose Elevated T1 and ECV values are associated with worse outcome in many cardiac conditions. We conducted the first prospective study to investigate whether T1 mapping and ECV can predict cardiac reverse remodelling in response to treatment, in a cohort of patients hospitalised with a new HF diagnosis. Methods This was a single centre observational study. Inclusion criteria were admission with new HF, LVEF ≤50% or elevated NTproBNP and being treated with intravenous furosemide. Only patients with Heart Failure with reduced Ejection Fraction (HFrEF) and EF &amp;lt;40% on baseline echocardiography were included in this analysis. 36 consecutive eligible participants were included and had both echocardiogram and CMR studies to establish anatomy, function, and myocardial tissue characteristics at baseline. Participants were treated according to international HF guidelines and underwent reviews and repeat echocardiography at 6, 12–18 and 24–30 months. "Responders" to guideline directed HFrEF therapy were defined as those who had an increase in LVEF of ≥10% to a value of ≥40% between their baseline and latest follow-up echocardiogram. Baseline CMR volumes, function, presence of Late Gadolinium Enhancement (LGE), septal and whole heart T1 and ECV values were compared between responder and non-responder groups. Results Median follow-up was 26 months. 27 (75%) participants were responders to therapy. There were no differences in baseline characteristics between groups. There was high uptake of HFrEF medical therapy in both groups. (Table 1) There was no significant difference found between septal or whole heart T1 or ECV values between responder and non-responder groups. There was a trend towards lower whole heart ECV values (29% vs. 35%; p = 0.06) in the responder group but this did not reach statistical significance. (Figure 1) Overall, there was no difference in rates of LGE presence between groups but there was a significantly higher proportion of participants with non-ischaemic LGE pattern in the responder group compared to non-responder group (48% vs 11%; p = 0.05). Conclusions In this cohort of patients hospitalised with a new HFrEF diagnosis, the majority demonstrated reverse remodelling in response to therapy by 26 months. Whole heart ECV (%) as a surrogate marker for fibrosis calculated by whole heart T1 mapping may play a role in understanding which patients are likely to respond to HF therapy but further larger studies are required.

P366 FULMINANT MYOCARDITIS WITH SPONTANEOUS RESOLUTION AFTER COVID 19 AND ALLERGIC EPISODE: MIS–A OR ALLERGIC MYOCARDITIS?

Abstract Clinical case 23–year–old male. No medical history Not vaccinated for Sars–Cov2; Recent Sars–Cov2 infection (negative antigenic swab on 03/01/22); Pharyngodynia treated with ibuprofen + ciprofloxacin and amoxicillin ac clavulanic acid(suspended for purpuric lesions on hands) After 5 days from onset of symptoms, access to PS for loss of consciousness. Laboratory: ph 7.4; Lat 3.4 EKG: sinus tachycardia HR 126 bpm ECHOCARDIOGRAM: Non–dilated left ventricle, marked reduction in FE (15%) spontaneous echocontrast in ventricular cavity chest TC: hypodense tissue in anterior mediastinum; adenopathy in peribronchial site, distended gallbladder transfer to Vanvitelli Cardiac ICU Amine support with augmented DBT for hypotension and tachycardia LAB: Tni 2193; Nt proBNP 27796; PCR 26; PCT 4; crea 1,4, Lat 1 CATH DX + EMB after 24 hours EBM: …Mixed cellularity endomyocarditis, predominantly lymphocytic, presence of eosinophils… enrollment in the MYTHS study: placebo group (saline solution) after 10 day MRI:Normal biventricular systolic function. Tissue characterization images consistent with the presence of limited area of active myocardial damage and with nonischemic pattern involving the basal segment of the infero–lateral wall of the left ventricle. Discussion The case has been a source of considerable discussion to establish the etiology of myocarditis. Although with numerous doubts, after careful evaluation of the histologic picture, the case falls under possible MIS–A (MULTISYSTEM INFLAMMATORY SYNDROME in adult) Cardiac manifestations of MIS–A include myocarditis, pericarditis, and arrhythmias, which can rapidly lead to cardiogenic shock.

P323 WELLENS PATTERN, MYOCARDIAL BRIDGING, AND BIVENTRICULAR ARRHYTHMOGENIC CARDIOMYOPATHY: A SINGLE "TRIPLE" DIAGNOSIS

Abstract Wellens‘ syndrome describes an electrocardiographic pattern characterized by T–wave changes in the antero–septal leads that make this finding highly suggestive of a lesion of the proximal segment of the anterior interventricular artery. Case report. A 58–year–old patient from China with a silent medical history presented to the emergency department with angor, dizziness, asthenia, and blurred vision. The electrocardiogram shows a Wellens type A pattern, and blood chemistry tests collected in the emergency department show liver, kidney function and blood count within normal limits. High–sensitivity troponin T values stand at 34 ng/mL. The echocardiogram shows preserved biventricular systolic function in the absence of major regional wall motion abnormality. Given the symptoms, troponin values, and electrocardiographic pattern, the patient underwent coronary angiopgraphy, which showed lesion–free epicardial coronary arteries but with a muscular bridge in the mid–proximal section of the anterior interventricular artery, with no obvious significant systolic–diastolic caliber changes at subsequent coronary CT analysis. To better assess possible myocardial ischemic damage, the patient underwent MRI (magnetic resonance), which showed an entirely unexpected result. In fact, T1 sequences revealed biventricular adipose infiltration at the anterolateral and inferolateral walls of the left ventricle, with homosedial enhancement to nonischemic pattern on late post–contrast images: this picture was considered suggestive of biventricular arrhythmogenic cardiomyopathy. In the absence of history of syncope and documented arrhythmias on prolonged rhythm monitoring during hospitalization, no indication was made for further diagnostic and therapeutic investigations from the arrhythmological point of view. Thus, beta blocker and ace inhibitor therapy was set, and the patient was started on an outpatient cardiology follow–up course and genetic counseling for him and first–degree family members was scheduled. Selecting the correct imaging method becomes crucial for a correct diagnosis, especially in cases in which symptomatology is inconclusive.

Diagnostic and prognostic role of late gadolinium enhancement in cardiomyopathies.

Late gadolinium enhancement (LGE) is the most relevant tool of cardiac magnetic resonance for tissue characterization, and it plays a pivotal role for diagnostic and prognostic assessment of cardiomyopathies. The pattern of presentation of LGE allows differential diagnosis between ischaemic and non-ischaemic heart disease with high diagnostic accuracy, and among different cardiomyopathies, specific presentation of LGE may help to make a diagnosis. Late gadolinium enhancement may be caused by conditions that significantly increase the interstitial space or, less frequently, that slow down Gd exit, like myocardial fibrosis. In chronic myocardial infarction, hypertrophic cardiomyopathies (HCM), dilated cardiomyopathy, Fabry disease, and other conditions, LGE is a marker of myocardial fibrosis, but also in patients with acute myocarditis where LGE may be also explained by the increase of interstitial space caused by interstitial oedema or by tissue infiltration of inflammatory cells. In cardiac amyloidosis, LGE represents myocardial fibrosis but the interstitial overload of amyloid proteins should also be considered as a potential cause of LGE. The identification of the pattern of presentation of LGE is also very important. In the ischaemic pattern, LGE always involves the subendocardial layer with more or less transmural extent, it is confluent, and every single scar should be located in the territory of one coronary artery. In the non-ischaemic pattern, LGE does not fulfil the previous criteria, being midwall, subepicardial, or mixed, not necessarily confluent or confined to a territory of one coronary artery. For cardiomyopathies, the exact pattern of non-ischaemic LGE is important. Quantitative analysis of LGE is required in some specific conditions as in HCM. Magnetic resonance imaging with LGE technique should be performed in every patient with suspect of cardiomyopathy. The lack of standardization of pulse sequence and mostly of quantification methods is the main limitation of LGE technique.