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Non-caseating granulomatous infiltration of the myocardium is the hallmark of cardiac sarcoidosis (CS). CS manifests clinically as conduction disturbance, ventricular arrhythmia, sudden cardiac death and/or heart failure with reduced ejection fraction. Other than confirmation through endomyocardial biopsy, a diagnosis of probable CS can be established by histological evidence of systemic sarcoidosis in addition to characteristic clinical or advanced imaging findings. Cardiac Magnetic Resonance imaging (CMR) and 18F-flurodeoxyglycose positron emission tomography (FDG-PET) are imaging modalities indispensable in the diagnosis and monitoring of CS. FDG-PET is the method of choice for identifying the active inflammatory phase of CS and in the monitoring and modifying of immunosuppressive treatment. CMR is better suited for assessing cardiac morphology and function. Both modalities are more effective in detecting CS when used in combination than either is alone. Management of CS is primarily based upon observational data of low quality due to a paucity of randomized controlled trials. Corticosteroid therapy and/or tiered-immunosuppression are the mainstays of treatment in reducing myocardial inflammation. Steroid-sparing agents aim to limit the unfavorable side-effects of a significant steroid burden. Antiarrhythmics and guideline-directed medical therapies are utilized for control of ventricular arrhythmia and left ventricular dysfunction respectively. CS necessitates multidisciplinary care in specialized centers to most effectively diagnose and manage the disease. Additional randomized trials are warranted to further our understanding of medical optimization in CS.

A nationwide population-based study in Korea found that patients with newly diagnosed psoriatic disease have a higher risk of incident inflammatory heart diseases (IHD) and autoimmune neural diseases compared to individuals without psoriatic disease. The study included over 350,000 patients with psoriatic disease and their matched comparators. The risk of IHD, particularly acute myocarditis, was significantly higher in patients with psoriatic disease. Additionally, the risk of autoimmune neural diseases affecting both the peripheral nervous system (PNS) and central nervous system (CNS) was also significantly higher in patients with psoriatic disease. The study suggests that systemic inflammation driven by IL-17 in psoriatic disease may contribute to the development of these conditions. [Extracted from the article]

Myocarditis is a disease caused by cardiac inflammation that can progress to dilated cardiomyopathy, heart failure, and eventually death. Several etiologies, including autoimmune, drug-induced, and infectious, lead to inflammation, which causes damage to the myocardium, followed by remodeling and fibrosis. Although there has been an increasing understanding of pathophysiology, early and accurate diagnosis, and effective treatment remain challenging due to the high heterogeneity. As a result, many patients have poor prognosis, with those surviving at risk of long-term sequelae. Current diagnostic methods, including imaging and endomyocardial biopsy, are, at times, expensive, invasive, and not always performed early enough to affect disease progression. Therefore, the identification of accurate, cost-effective, and prognostically informative biomarkers is critical for screening and treatment. The review then focuses on the biomarkers currently associated with these conditions, which have been extensively studied via blood tests and imaging techniques. The information within this review was retrieved through extensive literature research conducted on major publicly accessible databases and has been collated and revised by an international panel of experts. The biomarkers discussed in the article have shown great promise in clinical research studies and provide clinicians with essential tools for early diagnosis and improved outcomes. [ABSTRACT FROM AUTHOR]

Cardiac sarcoidosis (CS) results from epithelioid cell granulomas infiltrating the myocardium and predisposing to conduction disturbances, ventricular tachyarrhythmias, and heart failure. Manifest CS, however, constitutes only the top of an iceberg as advanced imaging uncovers cardiac involvement 4 to 5 times more commonly than what is clinically detectable. Definite diagnosis of CS requires myocardial biopsy and histopathology, but a sufficient diagnostic likelihood can be achieved by combining extracardiac histology of sarcoidosis with clinical manifestations and findings on cardiac imaging. CS can appear as the first or only organ manifestation of sarcoidosis or on top of pre-existing extracardiac disease. Due to the lack of controlled trials, the care of CS is based on observational evidence of low quality. Currently, the treatment involves corticosteroid-based, tiered immunosuppression to control myocardial inflammation with medical and device-based therapy for symptomatic atrioventricular block, ventricular tachyarrhythmias, and heart failure. Recent outcome data indicate 90% to 96% 5-year survival in manifest CS with the 10-year figures ranging from 80% to 90%. Major progress in the care of CS awaits the key to its molecular–genetic pathogenesis and large-scale controlled clinical trials. [ABSTRACT FROM AUTHOR]

Background Cardiac involvement can be an initial manifestation in sarcoidosis. However, little is known about the association between various clinical phenotypes of cardiac sarcoidosis (CS) and outcomes. We aimed to analyze the relation of different clinical manifestations with outcomes of CS and to investigate the relative importance of clinical features influencing overall survival. Methods and Results A retrospective cohort of 141 patients with CS enrolled at 2 Swedish university hospitals was studied. Presentation, imaging studies, and outcomes of de novo CS and previously known extracardiac sarcoidosis were compared. Survival free of primary composite outcome (ventricular arrhythmias, heart transplantation, or death) was assessed. Machine learning algorithm was used to study the relative importance of clinical features in predicting outcome. Sixty‐two patients with de novo CS and 79 with previously known extracardiac sarcoidosis were included. De novo CS showed more advanced New York Heart Association class (P=0.02), higher circulating levels of NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) (P

Background: Giant cell myocarditis (GCM) and cardiac sarcoidosis (CS) are, in contrast to acute non-fulminant myocarditis (ANFM), rare inflammatory diseases of the myocardium with poor prognosis. Although echocardiography is the first-line diagnostic tool in these patients, their echocardiographic appearance has so far not been systematically studied. Methods: We assessed a total of 71 patients with endomyocardial biopsy-proven GCM (n = 21), and CS (n = 25), as well as magnetic resonance-verified ANFM (n = 25). All echocardiographic examinations, performed upon clinical presentation, were reanalysed according to current guidelines including a detailed assessment of right ventricular (RV) dysfunction. Results: In comparison with ANFM, patients with either GCM or CS were older (mean age (±SD) 55 ± 12 or 53 ± 8 vs 25 ± 8 years), more often of female gender (52% or 24% vs 8%), had more severe clinical symptoms and higher natriuretic peptide levels. For both GCM and CS, echocardiography revealed more frequently signs of left ventricular (LV) dysfunction in form of a reduced ejection fraction (p

There is considerable variability in practice among pediatric centers for treatment of myocarditis. We report outcomes using high dose steroids in conjunction with IVIG. This is a single center retrospective study of children < 21 years of age diagnosed with myocarditis and treated with high dose steroids and IVIG from January 2004-April 2021. Diagnostic criteria for myocarditis included positive endomyocardial biopsy, cardiac magnetic resonance (CMR) imaging meeting Lake Louise criteria, or strictly defined clinical diagnosis. Forty patients met inclusion criteria. Median age at diagnosis was 11.6 years (0.7–14.6). Diagnosis was made clinically in 70% of cases (N = 28), by CMR in 12.5% (N = 5) and by biopsy in 17.5% (N = 7). Median ejection fraction (EF) at diagnosis was 35% (IQR 24–48). Median duration of IV steroids was 7 days (IQR 4–12) followed by an oral taper. Median cumulative dose of IV immunoglobulin (IVIG) was 2 g/kg. There were no serious secondary bacterial infections after steroid initiation. Ten patients (25%) required mechanical circulatory support. Overall transplant free survival was 92.5% with median follow-up of 1 year (IQR 0–6 years). Six patients required re-admission for cardiovascular reasons. By 3 months from diagnosis, 70% of patients regained normal left ventricular function. High dose steroids in conjunction with IVIG to treat acute myocarditis can be safe without significant infections or long-term side effects. Our cohort had excellent recovery of ventricular function and survival without transplant. Prospective comparison of a combination of high dose steroids with IVIG versus other therapies is needed. [ABSTRACT FROM AUTHOR]

Non-caseating granulomatous infiltration of the myocardium is the hallmark of cardiac sarcoidosis (CS). CS manifests clinically as conduction disturbance, ventricular arrhythmia, sudden cardiac death and/or heart failure with reduced ejection fraction. Other than confirmation through endomyocardial biopsy, a diagnosis of probable CS can be established by histological evidence of systemic sarcoidosis in addition to characteristic clinical or advanced imaging findings. Cardiac Magnetic Resonance imaging (CMR) and 18 F-flurodeoxyglycose positron emission tomography (FDG-PET) are imaging modalities indispensable in the diagnosis and monitoring of CS. FDG-PET is the method of choice for identifying the active inflammatory phase of CS and in the monitoring and modifying of immunosuppressive treatment. CMR is better suited for assessing cardiac morphology and function. Both modalities are more effective in detecting CS when used in combination than either is alone. Management of CS is primarily based upon observational data of low quality due to a paucity of randomized controlled trials. Corticosteroid therapy and/or tiered-immunosuppression are the mainstays of treatment in reducing myocardial inflammation. Steroid-sparing agents aim to limit the unfavorable side-effects of a significant steroid burden. Antiarrhythmics and guideline-directed medical therapies are utilized for control of ventricular arrhythmia and left ventricular dysfunction respectively. CS necessitates multidisciplinary care in specialized centers to most effectively diagnose and manage the disease. Additional randomized trials are warranted to further our understanding of medical optimization in CS., Competing Interests: 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., (© 2024 Aftab, Szeto, Aftab and Bokhari.)

The goal of this study was to evaluate a three-dimensional compressed sensing (3D-CS) LGE prototype sequence for the detection and quantification of myocardial fibrosis in patients with chronic myocardial infarction (CMI) and myocarditis (MYC) compared with a 2D-LGE standard. Patients with left-ventricular LGE due to CMI (n = 33) or MYC (n = 20) were prospectively recruited. 2D-LGE and 3D-CS images were acquired in random order at 1.5 Tesla. 3D-CS short axis (SAX) images were reconstructed corresponding to 2D SAX images. LGE was quantitatively assessed on patient and segment level using semi-automated threshold methods. Image quality (4-point scoring system), Contrast-ratio (CR) and acquisition times were compared. There was no significant difference between 2D and 3D sequences regarding global LGE (%) (CMI [2D-LGE: 11.4 ± 7.5; 3D-LGE: 11.5 ± 8.5; p = 0.99]; MYC [2D-LGE: 27.0 ± 15.7; 3D-LGE: 26.2 ± 13.1; p = 0.70]) and segmental LGE-extent (p = 0.63). 3D-CS identified papillary infarction in 5 cases which was not present in 2D images. 2D-LGE acquisition time was shorter (2D: median: 06:59 min [IQR: 05:51–08:18]; 3D: 14:48 min [12:45–16:57]). 3D-CS obtained better quality scores (2D: 2.06 ± 0.56 vs. 3D: 2.29 ± 0.61). CR did not differ (p = 0.63) between basal and apical regions in 3D-CS images but decreased significantly in 2D apical images (CR basal: 2D: 0.77 ± 0.11, 3D: 0.59 ± 0.10; CR apical: 2D: 0.64 ± 0.17, 3D: 0.53 ± 0.11). 3D-LGE shows high congruency with standard LGE and allows better identification of small lesions. However, the current 3D-CS LGE sequence did not provide PSIR reconstruction and acquisition time was longer. [ABSTRACT FROM AUTHOR]

BackgroundAcute myocarditis and acute coronary syndrome (ACS) are important differential diagnoses in patients with new-onset chest pain. To date, no clinical score exists to support the differentiation between these two diseases. The aim of this study was to develop such a score to aid the physician in scenarios where discrimination between myocarditis and ACS appears difficult.Materials and MethodsPatients with ACS (n = 233) and acute myocarditis (n = 123) were retrospectively enrolled. Least absolute shrinkage and selection operator (LASSO) regression was conducted to identify parameters associated with the highest or least probability for acute myocarditis. Logistic regression was conducted using the identified parameters and score points for each level of the predictors were calculated. Cutoffs for the prediction of myocarditis were calculated. Validation was conducted in a separate cohort of 90 patients.ResultsA score for prediction of acute myocarditis was calculated using six parameters [age, previous infection, hyperlipidemia, hypertension, C-reactive protein (CRP), and leukocyte count]. Logistic regression analysis showed a significant association between total score points and the presence of myocarditis (B = 0.9078, p < 0.0001). Cutoff #1 for the prediction of myocarditis was calculated at ≥ 4 (Sens.: 90.3%, Spec.: 93.1%; 46.3% predicted probability for acute myocarditis), cutoff #2 was calculated at ≥ 7 (Sens.: 73.1%, Spec.: > 99.9%; 92.9% pred. prob.). Validation showed good discrimination [area under the curve (AUC) = 0.935] and calibration of the score.ConclusionOur clinical score showed good discrimination and calibration for differentiating patients with acute myocarditis and ACS. Thus, it could support the differential diagnosis between these two disease entities and could facilitate clinical decisions in affected patients.

Abstract Giant cell myocarditis is a rare form of autoimmune myocarditis with high morbidity and mortality that affects mainly middle‐aged adults. We report a case study of a 70‐year‐old man on chronic immunosuppression who presented with sustained ventricular tachycardia and symptoms of acute systolic heart failure, both with poor response to standard measures. A decision to pursue endomyocardial biopsy established the diagnosis of GCM and lead to initiation of immunosuppressive therapy and a favourable outcome. Our case illustrates that a low threshold for endomyocardial biopsy in new onset heart failure can lead to actionable information even in patients of advanced age.

Background Cardiac sarcoidosis (CS) and giant cell myocarditis (GCM) share many histopathologic and clinical features. Whether they are parts of a one‐disease continuum has been discussed. Methods and Results We compared medical record data of 351 CS and 28 GCM cases diagnosed in Finland since the late 1980s and followed until February 2018 for a composite end point of cardiac death, aborted sudden death, and heart transplantation. Heart failure was the presenting manifestation in 50% versus 15% (P

• Electrocardiography (ECG) is valuable and ubiquitously available for screening for cardiac sarcoidosis. • Patients with an extra-cardiac manifestation should frequently be evaluated by ECG. • QRS broadening, fragmentation, and T-Wave abnormalities may be promising. Sarcoidosis is a multisystem granulomatous disease of unknown etiology characterized by noncaseating granulomas. Cardiac involvement is often limiting patients' prognosis. Cardiac sarcoidosis can manifest with variant cardiac arrhythmias, of which atrioventricular (AV)-block-related bradycardia and ventricular tachycardias are the most common. Although cardiac sarcoidosis remains a histopathological diagnosis, the significance of imaging modalities, especially cardiac magnetic resonance imaging is increasing rapidly but mainly remains reserved for patients with a high suspicion due to a previous arrhythmia or unknown cardiomyopathy. Thus, there is a need for screening in daily clinical practice so that possible characteristic electrocardiographic (ECG) findings may guide the way to detect the disease. We therefore evaluated the ECG as a potential tool for screening of cardiac sarcoidosis and present different electrophysiological manifestations of cardiac sarcoidosis based on a literature review. The ECG is a valuable tool for screening of cardiac involvement in patients with sarcoidosis. Several parameters have been shown to be associated with cardiac involvement in sarcoidosis such as higher-degree AV-block, QRS complex fragmentation and widening, as well as certain T wave abnormalities that may indicate cardiac involvement, of which the latter two are most promising and specific. However, prospective studies examining a large number of trials are desirable. [ABSTRACT FROM AUTHOR]

Inflammatory heart disease (IHD) is a group of diseases that includes pericarditis, myocarditis, and endocarditis. Although males appear to be more commonly affected than females, IHD can be seen in any age group. While the disease can be self-limiting leading to full recovery, affected individuals can develop chronic disease, suggesting that identification of primary triggers is critical for successful therapies. Adding to this complexity, however, is the fact that IHD can be triggered by a variety of infectious and non-infectious causes that can also occur as secondary events to primary insults. In this review, we discuss the immunological insights into the development of IHD as well as a mechanistic understanding of the disease process in animal models.

Giant cell myocarditis is a rare form of autoimmune myocarditis with high morbidity and mortality that affects mainly middle‐aged adults. We report a case study of a 70‐year‐old man on chronic immunosuppression who presented with sustained ventricular tachycardia and symptoms of acute systolic heart failure, both with poor response to standard measures. A decision to pursue endomyocardial biopsy established the diagnosis of GCM and lead to initiation of immunosuppressive therapy and a favourable outcome. Our case illustrates that a low threshold for endomyocardial biopsy in new onset heart failure can lead to actionable information even in patients of advanced age. [ABSTRACT FROM AUTHOR]

The objective of this study was to describe a cohort of patients with clinical myocarditis and normal left ventricular (LV) systolic function on admission. A retrospective chart review at seven tertiary pediatric hospitals identified patients aged < 19 years admitted with an ICD-9 code of myocarditis between 2008 and 2012. Patients were excluded if admission LV systolic ejection fraction was < 50%, fractional shortening (FS) was < 28% or if the admitting or consulting cardiologist did not suspect myocarditis. A total of 75 patients met inclusion criteria. The median age was 15.5 years with an Interquartile Range (IQR) of 13.6–16.6. 33% were female. Patients presented most commonly with chest pain (75%) and dyspnea (24%). On admission, median B-type natriuretic peptide (BNP) was 132 pg/mL (IQR 57–689) and median troponin I (TnI) was 8.4 ng/mL (IQR 2.0–20.3). Electrocardiogram revealed ST elevation in the majority (55%). Magnetic resonance imaging was obtained on 40%, with 63% of those showing evidence of inflammation. Therapies included inotropic support (15%), mechanical ventilation (12%), antiarrhythmic medications (9%), and Extracorporeal Membrane Oxygenation (5%). Those with poor outcomes were noted to have significantly higher BNP, TnI, and creatine kinase levels on presentation. One patient was transplanted and 35% were discharged on heart failure medications. At one year follow-up one patient had died of unspecified causes, 15% required readmission for cardiac reasons, and 21% continued on heart failure medications. The risk associated with clinical myocarditis in the setting of normal ventricular function at presentation may be higher than previously suspected. [ABSTRACT FROM AUTHOR]

ABSTRACT: Background and objective: Molecular biomarkers are needed to refine prognostication and phenotyping of pulmonary hypertension (PH) patients. S100A12 is an emerging biomarker of various inflammatory diseases. This study aims to determine the prognostic value of S100A12 in PH. Methods: Exploratory microarray analysis performed on peripheral blood mononuclear cells (PBMC) collected from idiopathic pulmonary fibrosis (IPF) patients suggested an association between S100A12 and both PH and mortality. So the current study was designed to evaluate for an association between S100A12 in peripheral blood collected from two well‐phenotyped PH cohorts in two other centres to derive and validate an association between S100A12 protein serum concentrations and mortality. Results: The majority of the patients in the discovery and validation cohorts were either World Health Organization (WHO) group 1 (pulmonary arterial hypertension (PAH)) or 3 (lung disease‐associated) PH. In the discovery PH cohort, S100A12 was significantly increased in patients with PH (n = 51) compared to controls (n = 22) (29.8 vs 15.7 ng/mL, P < 0.001) and negatively correlated with cardiac output (r = −0.58, P < 0.001) in PH patients. When S100A12 data were pooled from both cohorts, PAH and non‐PAH PH patients had higher S100A12 compared to healthy external controls (32.6, 30.9, 15.7 ng/mL; P < 0.001). S100A12 was associated with an increased risk in overall mortality in PH patients in both the discovery (n = 51; P = 0.008) and validation (n = 40; P < 0.001) cohorts. Conclusion: S100A12 levels are increased in PH patients and are associated with increased mortality. [ABSTRACT FROM AUTHOR]

Combined PET/MRI is a novel imaging method integrating the advances of functional and morphological MR imaging with PET applications that include assessment of myocardial viability, perfusion, metabolism of inflammatory tissue and tumors, as well as amyloid deposition imaging. As such, PET/MRI is a promising tool to detect and characterize ischemic and non-ischemic cardiomyopathies. To date, the greatest benefit may be expected for diagnostic evaluation of systemic diseases and cardiac masses that remain unclear in cardiac MRI, as well as for clinical and scientific studies in the setting of ischemic cardiomyopathies. Diagnosis and therapeutic monitoring of cardiac sarcoidosis has the potential of a possible 'killer-application' for combined cardiac PET/MRI. In this article, we review the current evidence and discuss current and potential future applications of cardiac PET/MRI. [ABSTRACT FROM AUTHOR]

Background Cardiac involvement can be an initial manifestation in sarcoidosis. However, little is known about the association between various clinical phenotypes of cardiac sarcoidosis (CS) and outcomes. We aimed to analyze the relation of different clinical manifestations with outcomes of CS and to investigate the relative importance of clinical features influencing overall survival. Methods and Results A retrospective cohort of 141 patients with CS enrolled at 2 Swedish university hospitals was studied. Presentation, imaging studies, and outcomes of de novo CS and previously known extracardiac sarcoidosis were compared. Survival free of primary composite outcome (ventricular arrhythmias, heart transplantation, or death) was assessed. Machine learning algorithm was used to study the relative importance of clinical features in predicting outcome. Sixty-two patients with de novo CS and 79 with previously known extracardiac sarcoidosis were included. De novo CS showed more advanced New York Heart Association class ( P =0.02), higher circulating levels of NT-proBNP (N-terminal pro-B-type natriuretic peptide) ( P <0.001), and troponins ( P <0.001), as well as a higher prevalence of right ventricular dysfunction ( P <0.001). During a median (interquartile range) follow-up of 61 (44-77) months, event-free survival was shorter in patients with de novo CS ( P <0.001). The top 5 features predicting worse event-free survival in order of importance were as follows: impaired tricuspid annular plane systolic excursion, de novo CS, reduced right ventricular ejection fraction, absence of β-blockers, and lower left ventricular ejection fraction. Conclusions Patients with de novo CS displayed more severe disease and worse outcomes compared with patients with previously known extracardiac sarcoidosis. Using machine learning, right ventricular dysfunction and de novo CS stand out as strong overall predictors of impaired survival.

Genetic factors play an important role in the development of cardiac sarcoidosis and may determine disease pattern, severity, and prognosis. A 55‐year‐old African American male presented with new onset of congestive heart failure. This patient was diagnosed with pulmonary sarcoidosis eleven years prior and initially treated with prednisone. He was lost to follow‐up until this index admission. He had a monozygotic twin brother who was diagnosed with pulmonary and cardiac sarcoidosis, and passed away from severe biventricular dysfunction. Surveillance, with echocardiography or cardiac MRI, in siblings at high risk of sarcoidosis may allow for early detection and treatment. [ABSTRACT FROM AUTHOR]

Myocarditis is defined as inflammation of the myocardium according to clinical, histological, biochemical, immunohistochemical, or imaging findings. Inflammation can be categorized histologically by cell type or pattern, and many causes have been implicated, including infectious, most commonly viral, systemic autoimmune diseases, vaccine-associated processes, environmental factors, toxins, and hypersensitivity to drugs. Sarcoid myocarditis is increasingly recognized as an important cause of cardiomyopathy and has important diagnostic, prognostic, and therapeutic implications in patients with systemic sarcoidosis. The clinical presentation of myocarditis may include an asymptomatic, subacute, acute, fulminant, or chronic course and may have focal or diffuse involvement of the myocardium depending on the cause and time point of the disease. For most causes of myocarditis except sarcoidosis, myocardial biopsy is the gold standard but is limited due to risk, cost, availability, and variable sensitivity. Diagnostic criteria have been established for both myocarditis and cardiac sarcoidosis and include clinical and imaging findings particularly the use of cardiac magnetic resonance and positron emission tomography. Beyond diagnosis, imaging findings may also provide prognostic value. This case-based review focuses on the current state of multimodality imaging for the diagnosis and management of myocarditis and cardiac sarcoidosis, highlighting multimodality imaging approaches with practical clinical vignettes, with a discussion of knowledge gaps and future directions. [ABSTRACT FROM AUTHOR]

Background: Giant cell myocarditis (GCM) and cardiac sarcoidosis (CS) are, in contrast to acute non-fulminant myocarditis (ANFM), rare inflammatory diseases of the myocardium with poor prognosis. Although echocardiography is the first-line diagnostic tool in these patients, their echocardiographic appearance has so far not been systematically studied., Methods: We assessed a total of 71 patients with endomyocardial biopsy-proven GCM (n = 21), and CS (n = 25), as well as magnetic resonance-verified ANFM (n = 25). All echocardiographic examinations, performed upon clinical presentation, were reanalysed according to current guidelines including a detailed assessment of right ventricular (RV) dysfunction., Results: In comparison with ANFM, patients with either GCM or CS were older (mean age (±SD) 55 ± 12 or 53 ± 8 vs 25 ± 8 years), more often of female gender (52% or 24% vs 8%), had more severe clinical symptoms and higher natriuretic peptide levels. For both GCM and CS, echocardiography revealed more frequently signs of left ventricular (LV) dysfunction in form of a reduced ejection fraction (p < 0.001), decreased cardiac index (p < 0.001) and lower global longitudinal strain (p < 0.001) in contrast to ANFM. The most prominent increase in LV end-diastolic volume index was observed in CS. In addition, RV dysfunction was more frequently found in both GCM and CS than in ANFM (p = 0.042)., Conclusions: Both GCM and CS have an echocardiographic and clinical appearance that is distinct from ANFM. However, the method cannot further differentiate between the two rare entities. Consequently, echocardiography can strengthen the initial clinical suspicion of a more severe form of myocarditis, thus warranting a more rigorous clinical work-up., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Author(s).)

Background: Acute myocarditis and acute coronary syndrome (ACS) are important differential diagnoses in patients with new-onset chest pain. To date, no clinical score exists to support the differentiation between these two diseases. The aim of this study was to develop such a score to aid the physician in scenarios where discrimination between myocarditis and ACS appears difficult., Materials and Methods: Patients with ACS ( n = 233) and acute myocarditis ( n = 123) were retrospectively enrolled. Least absolute shrinkage and selection operator (LASSO) regression was conducted to identify parameters associated with the highest or least probability for acute myocarditis. Logistic regression was conducted using the identified parameters and score points for each level of the predictors were calculated. Cutoffs for the prediction of myocarditis were calculated. Validation was conducted in a separate cohort of 90 patients., Results: A score for prediction of acute myocarditis was calculated using six parameters [age, previous infection, hyperlipidemia, hypertension, C-reactive protein (CRP), and leukocyte count]. Logistic regression analysis showed a significant association between total score points and the presence of myocarditis ( B = 0.9078, p < 0.0001). Cutoff #1 for the prediction of myocarditis was calculated at ≥ 4 (Sens.: 90.3%, Spec.: 93.1%; 46.3% predicted probability for acute myocarditis), cutoff #2 was calculated at ≥ 7 (Sens.: 73.1%, Spec.: > 99.9%; 92.9% pred. prob.). Validation showed good discrimination [area under the curve (AUC) = 0.935] and calibration of the score., Conclusion: Our clinical score showed good discrimination and calibration for differentiating patients with acute myocarditis and ACS. Thus, it could support the differential diagnosis between these two disease entities and could facilitate clinical decisions in affected patients., Competing Interests: 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., (Copyright © 2022 Mirna, Schmutzler, Topf, Sipos, Hehenwarter, Hoppe and Lichtenauer.)

Israel is a small country with a highly diverse population in terms of ethnicity, religion, genetics and lifestyle, which all have an impact on coronary heart disease (CHD) and metabolic risk factors. This review focuses on gender and ethnic group differences in the risk factors associated with CHD. Using the metabolic syndrome (MetSyn) as a guiding theoretical framework, 30 empirical studies from Israel published after the year 2000 were reviewed to elicit trends. Overall, the MetSyn framework appears to be less appropriate for women than for men in predicting CHD morbidity. In addition, ethnic minorities are more likely to have earlier and more severe risk factor profiles, and women are almost always disproportionately affected. Over a period of 5 to 15 years after arrival in Israel, immigrants from the former Soviet Union and Ethiopia show an increase in obesity. Recent intervention studies to reduce CHD risk have shown encouraging results when the programs are culturally tailored. [ABSTRACT FROM AUTHOR]

Abstract: Matrix metalloproteinases (MMPs) are a family of proteases best known for their capacity to proteolyse several proteins of the extracellular matrix. Their increased activity contributes to the pathogenesis of several cardiovascular diseases. MMP-2 in particular is now considered to be also an important intracellular protease which has the ability to proteolyse specific intracellular proteins in cardiac muscle cells and thus reduce contractile function. Accordingly, inhibition of MMPs is a growing therapeutic aim in the treatment or prevention of various cardiovascular diseases. Tetracyclines, especially doxycycline, have been frequently used as important MMP inhibitors since they inhibit MMP activity independently of their antimicrobial properties. In this review we will focus on the intracellular actions of MMPs in some cardiovascular diseases including ischemia and reperfusion (I/R) injury, inflammatory heart diseases and septic shock; and explain how tetracyclines, as MMP inhibitors, have therapeutic actions to treat such diseases. We will also briefly discuss how MMPs can be intracellularly regulated and activated by oxidative stress, thus cleaving several important proteins inside cells. In addition to their potential therapeutic effects, MMP inhibitors may also be useful tools to understand the biological consequences of MMP activity and its respective extra- and intracellular effects. [Copyright &y& Elsevier]

Matrix metalloproteinases (MMPs) have been shown to play significant roles in a number of physiological as well as pathological processes. Best known to proteolyse components of the extracellular matrix, MMPs have recently been discovered to also target a growing list of proteins apart from these, both inside and outside the cell. MMPs have also been traditionally thought of as enzymes involved in chronic processes such as angiogenesis, remodelling and atherosclerosis on a days-week time-scale. However they are now understood to also act acutely in response to oxidative stress on a minutes time-scale on non-extracellular matrix substrates. This review focuses on the acute actions and both extracellular and intracellular targets of two prominent MMP family members, MMP-2 and -9, in cardiovascular diseases including ischaemia/reperfusion injury, inflammatory heart disease, septic shock and pre-eclampsia. Also discussed are various ways of regulating MMP activity, including post-translational mechanisms, the endogenous tissue inhibitors of metalloproteinases and pharmacological inhibitors. A comprehensive understanding of MMP biology is necessary for the development of novel pharmacological therapies to combat the impact of cardiovascular disease.British Journal of Pharmacology (2007) 152, 189–205; doi:10.1038/sj.bjp.0707344; published online 25 June 2007 [ABSTRACT FROM AUTHOR]