In this position statement of the ESC Working Group on Myocardial and Pericardial Diseases an expert consensus group reviews the current knowledge on clinical presentation, diagnosis and treatment of myocarditis, and proposes new diagnostic criteria for clinically suspected myocarditis and its distinct biopsy-proven pathogenetic forms. The aims are to bridge the gap between clinical and tissue-based diagnosis, to improve management and provide a common reference point for future registries and multicentre randomised controlled trials of aetiology-driven treatment in inflammatory heart muscle disease.

In biology, classification systems are used to promote understanding and systematic discussion through the use of logical groups and hierarchies. In clinical medicine, similar principles are used to standardise the nomenclature of disease. For more than three decades, heart muscle diseases have been classified into primary or idiopathic myocardial diseases (cardiomyopathies) and secondary disorders that have similar morphological appearances, but which are caused by an identifiable pathology such as coronary artery disease or myocardial infiltration (specific heart muscle diseases). In this document, The European Society of Cardiology Working Group on Myocardial and Pericardial Diseases presents an update of the existing classification scheme. The aim is to help clinicians look beyond generic diagnostic labels in order to reach more specific diagnoses.

In patients with transthyretin amyloid cardiomyopathy, tafamidis was associated with reductions in all-cause mortality and cardiovascular-related hospitalizations and reduced the decline in functional capacity and quality of life as compared with placebo. (Funded by Pfizer; ATTR-ACT ClinicalTrials.gov number, NCT01994889 .).

ESC Guidelines for the diagnosis and management of syncopeThe Task Force for the diagnosis and management of syncope of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA)

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In this paper the Working Group on Myocardial and Pericardial Disease proposes a revised definition of dilated cardiomyopathy (DCM) in an attempt to bridge the gap between our recent understanding of the disease spectrum and its clinical presentation in relatives, which is key for early diagnosis and the institution of potential preventative measures. We also provide practical hints to identify subsets of the DCM syndrome where aetiology directed management has great clinical relevance.

Background-Diffuse myocardial fibrosis is a final end point in most cardiac diseases. It is missed by the cardiovascular magnetic resonance (CMR) late gadolinium enhancement technique. Currently, quantifying diffuse myocardial fibrosis requires invasive biopsy, with inherent risk and sampling error. We have developed a robust and noninvasive technique, equilibrium contrast CMR (EQ-CMR) to quantify diffuse fibrosis and have validated it against the current gold standard of surgical myocardial biopsy. Methods and Results-The 3 principles of EQ-CMR are a bolus of extracellular gadolinium contrast followed by continuous infusion to achieve equilibrium; a blood sample to measure blood volume of distribution (1Ϫhematocrit); and CMR to measure pre-and postequilibrium T1 (with heart rate correction). The myocardial volume of distribution is calculated, reflecting diffuse myocardial fibrosis. Clinical validation occurred in patients undergoing aortic valve replacement for aortic stenosis or myectomy in hypertrophic cardiomyopathy (nϭ18 and nϭ8, respectively). Surgical biopsies were analyzed for picrosirius red fibrosis quantification on histology. Key Words: magnetic resonance imaging Ⅲ cardiomyopathy Ⅲ imaging Ⅲ endomyocardial fibrosis Ⅲ collagen F ibrosis is a final common end point in virtually all pathological processes in human organs and tissues. In the heart, focal fibrosis (scar) as a result of myocardial infarction is the leading cause of death and heart failure in the world. 1 Cardiovascular magnetic resonance (CMR) using the late gadolinium enhancement (LGE) contrast technique is the gold standard method for its assessment. 2,3 Focal fibrosis also occurs in other diseases, including cardiomyopathy, 4 myocarditis, 5 and infiltrative diseases. 6 Scar leads to an increased volume of distribution for gadolinium and slower contrast kinetics, 7 leading to late enhancement of scar by CMR. Clinical Perspective on p 144Diffuse myocardial fibrosis is a covert process that occurs as a part of normal aging. 8 -10 It is accelerated in diseases such as hypertension, aortic stenosis, and cardiomyopathy, 11Ϫ13 where it contributes to breathlessness, heart failure, and arrhythmia. 14 -16 Unlike scar, however, it may be reversible and is a treatment target. 17,18 Currently, the only method to quantify diffuse fibrosis is invasive biopsy, which carries significant morbidity and is prone to sampling error. 19 The LGE technique cannot be used to visualize diffuse fibrosis because "normal" myocardium with diffuse fibrosis is "nulled" to highlight focal scar, thereby losing all information of any background interstitial expansion. Recently, attempts to quantify diffuse fibrosis with CMR have been made, but they have required complex kinetic modeling and have not definitively excluded confounding factors such as heart rate, body composition, and renal clearance variability. Histological validation, where present, has In this study, we describe a potentially clinically applicable, robust, noninvasive method to quantify diffuse myo...

This study demonstrates that patients with multiple risk factors have a substantially increased risk of SD sufficient to warrant consideration for prophylactic therapy.