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Fulminant myocarditis (FM) is a form of acute myocardial inflammation leading to rapid-onset hemodynamic instability due to cardiogenic shock or life-threatening arrhythmias. As highlighted by recent registries, FM is associated with high rates of death and heart transplantation, regardless of the underlying histology. Because of a paucity of evidence-based management strategies exists for this disease, an International workshop on FM was held in Wuhan, China, in October 2019, in order to share knowledge on the disease and identify areas of consensus. The present report highlights both agreements and controversies in FM management across the world, focusing the attention on areas of opportunity, FM definition, the use of endomyocardial biopsy and viral identification on heart specimens, treatment algorithms including immunosuppression and the timing of circulatory support escalation. This report incorporates the most recent recommendations from national and international professional societies. Main areas of interest and aims of future prospective observational registries and randomized controlled trials were finally identified and suggested.

"Not a guideline but a guidance" is the motto of this document of guidance by the European Society of Cardiology, which is designed as an orientation aid to learning for physicians in the coronavirus disease 2019 (COVID-19) pandemic. A total of 62 European cardiologists as authors and 29 further experts as reviewers have contributed to this 119-page document. The emphasis of the guidelines is on a cautious strategy in dealing with a pandemic, which is still characterized by many unknown factors. It is consciously limited to cardiovascular diseases. In the last update from 10 June 2020 many practical instructions for cardiovascular diagnostics and treatment under the conditions of a pandemic are given. These recommendations largely depend on the already well-known guidelines of the ESC. To recapitulate them might be helpful but much is redundant. The sections on the pathophysiology and pathomechanisms by which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) could specifically affect the cardiovascular system, are informative but sometimes in need of supplementation. It is counterproductive to recommend that pathohistological and molecular investigations of tissues from affected and deceased patients should be avoided. This document of guidance is an ambitious attempt of a learning recommendation that needs some further improvement. It needs an early update if it intends to do justice to the ambitions.

Inflammatory dilated cardiomyopathy (DCMi) is a syndrome, not an etiological disease entity. The infective etiology and the immunopathology can be best determined through endomyocardial biopsy with a complete work-up by light microscopy, immunohistology, and polymerase chain reaction for microbial agents. This review focuses on the methodological advances in diagnosis in the past few years and exemplifies the importance of an etiology-orientated treatment in different case scenarios. In fulminant nonviral myocarditis, immunosuppressive treatment together with hemodynamic stabilization of the patient via mechanical circulatory support (e.g., microaxial pumps, extracorporeal membrane oxygenation, left ventricular assist device) can be life-saving. For viral inflammatory cardiomyopathy, intravenous immunoglobulin treatment can resolve inflammation and often eradicate the virus.

After 2 years and 5 waves of the coronavirus disease 2019 (COVID-19) pandemic in Germany and experience with superspreader events worldwide, we know that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a rapidly mutating virus with changing clinical phenotypes. Besides infections of the respiratory tract, which in severe cases are accompanied by pneumonia requiring mechanical ventilation, the involvement of the heart with myocarditis and pericarditis as well as the kidneys have short-term and also long-term consequences. We have learnt to deal with myocarditis and pericarditis in acute infections and after vaccinations, which in rare cases can also lead to myocarditis and pericarditis. Myocarditis with myocytolysis in autopsy specimens or endomyocardial biopsy specimens is rare. In contrast, elevated troponin levels and suspicious cardiac magnetic resonance imaging (MRI) findings are much more frequent. The best preventive measure is a complete double basic vaccination and booster vaccination with an mRNA vaccine. For patients and medical personnel precise information is given with respect to personal protective equipment and behavior (distancing-hygiene-mask-airing rule).Nach 2 Jahren und 5 Wellen der COVID-19(„coronavirus disease 2019“)-Pandemie in Deutschland und der weltweiten Erfahrung mit „Superspreader-Events“ wissen wir, dass SARS-CoV‑2 („severe acute respiratory syndrome coronavirus 2“) ein stark mutierendes Virus mit wechselndem klinischen Phänotyp ist. Neben der Infektion des Respirationstrakts, die in schweren Fällen mit beatmungspflichtigen Pneumonien einhergeht, sind die Beteiligung des Herzens mit Myokarditis und Perikarditis sowie der Niere sowohl von kurzfristiger als auch langfristiger Bedeutung. Wir haben gelernt, mit Myokarditis und Perikarditis bei der akuten Infektion und nach einer Impfung, bei der es in seltenen Fällen auch zu Myokarditis und Perikarditis kommen kann, umzugehen. Eine Myokarditis mit Myozytolyse im Sektionsgut oder bei einer Endomyokardbiopsie ist selten. Dagegen finden sich erhöhte Troponinspiegel und suspekte Kardio-MRT(Magnetresonanztomographie)-Befunde wesentlich häufiger. Die beste präventive Maßnahme ist eine komplette zweifache Grundimpfung und Boosterung mit einem mRNA-Impfstoff. Für Patienten und ärztliches Personal werden konkrete Hinweise zu Ausstattung und Verhalten (AHA-L-Regel) gegeben.

The AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guidelines 2021 on thoracic pain focusses on chest pain as a single but important symptom. The guidelines fall back on many guidelines on cardiac disease entities, such as myocardial infarction with (STEMI) or without ST segment elevation (NSTEMI), chronic coronary artery disease (CAD), pericarditis and aortic dissection. They also refer to guidelines on cardiac syndromes, such as acute coronary syndrome (ACS) or ACS without persisting ST segment elevation (NSTE-ACS), in which angina pectoris is an integral component. The guideline separates acute from stable angina pectoris. It gives a comprehensive overview on risk stratification and clinical work-up of chest pain. It stretches the main theme to angina equivalents, such as dyspnoe. They meticulously weigh up the noninvasive against the invasive diagnostic methods under the aspects of a cost-benefit analysis. In this context, a clear trend towards evidence-based, cost-effective noninvasive methods in recent years is unmistakable.Die AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR-Leitlinie 2021 zum Thoraxschmerz wählt den Brustschmerz als ein einziges, aber wichtiges Symptom zum zentralen Thema. Sie greift dabei zurück auf zahlreiche Leitlinien zu kardialen Krankheitsentitäten wie dem Myokardinfarkt mit (STEMI) oder ohne ST-Strecken-Hebung (NSTEMI), die chronische koronare Herzkrankheit (KHK), die Perikarditis oder die Aortendissektion. Oder sie nimmt Bezug auf Leitlinien zu kardialen Syndromen wie dem akuten Koronarsyndrom (ACS) oder dem ACS ohne persistierende ST-Strecken-Hebungen (NSTE-ACS), in denen Angina pectoris integraler Bestandteil ist. Sie differenziert zwischen akutem, instabilem Brustschmerz einerseits und stabilem Thoraxschmerz andererseits und berücksichtigt auch Anginaäquivalente wie Dyspnoe im Kontext von kardialen und nichtkardialen Erkrankungen. Sie wägt die nicht-invasiven und invasiven diagnostischen Methoden unter dem Gesichtspunkt einer Kosten-Nutzen-Analyse sorgfältig gegeneinander ab. Dabei ist der Trend zu evidenzbasierten, kostengünstigen nicht-invasiven Methoden in den letzten Jahren unverkennbar.

"Not a guideline but a guidance" is the motto of this document of guidance by the European Society of Cardiology, which is designed as an orientation aid to learning for physicians in the coronavirus disease 2019 (COVID-19) pandemic. A total of 62 European cardiologists as authors and 29 further experts as reviewers have contributed to this 119-page document. The emphasis of the guidelines is on a cautious strategy in dealing with a pandemic, which is still characterized by many unknown factors. It is consciously limited to cardiovascular diseases. In the last update from 10 June 2020 many practical instructions for cardiovascular diagnostics and treatment under the conditions of a pandemic are given. These recommendations largely depend on the already well-known guidelines of the ESC. To recapitulate them might be helpful but much is redundant. The sections on the pathophysiology and pathomechanisms by which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) could specifically affect the cardiovascular system, are informative but sometimes in need of supplementation. It is counterproductive to recommend that pathohistological and molecular investigations of tissues from affected and deceased patients should be avoided. This document of guidance is an ambitious attempt of a learning recommendation that needs some further improvement. It needs an early update if it intends to do justice to the ambitions.„No guideline but guidance“ ist das Motto dieses Leitfadens der European Society of Cardiology (ESC), der als lernende Orientierungshilfe für Ärzte in der Coronapandemie konzipiert ist. 62 europäische Kardiologen haben als Autoren und 29 weitere Experten als Reviewer zu dem 119 Seiten starken Dokument beigetragen. Der Leitfaden ist geprägt von einer vorsichtigen Strategie im Umgang mit einer Pandemie, von der vieles noch nicht bekannt ist. Er beschränkt sich bewusst auf kardiovaskuläre Erkrankungen. In seiner letzten Fassung vom 10. Juni 2020 gibt er zahlreiche praktische Anleitungen zur kardiovaskulären Diagnostik und Therapie unter Pandemiebedingungen. Die Empfehlungen sind oft redundante Rückgriffe auf die bekannten Leitlinien der ESC. Informativ, aber in Teilen ergänzungsbedürftig sind die Abschnitte zur Pathophysiologie und zu den Pathomechanismen, über die SARS-CoV‑2 („severe acute respiratory syndrome coronavirus 2“) spezifisch auf das Herz-Kreislauf-System wirken dürfte. Kontraproduktiv ist die Empfehlung, auf pathohistologische und molekulare Untersuchungen von Gewebe betroffener oder verstorbener Patienten zu verzichten. Den hohen Ansprüchen an einen sich immer wieder ergänzenden Leitfaden genügt die letzte verfügbare Fassung dennoch in weiten Teilen. Sie benötigt aber eine baldige Aktualisierung, wenn sie ihren Ambitionen gerecht werden will.

For myocarditis and inflammatory cardiomyopathy, an etiologically driven treatment is today the best option beyond heart failure therapy. Prerequisites for this are noninvasive and invasive biomarkers including endomyocardial biopsy and polymerase chain reaction on cardiotropic agents. Imaging by Doppler echocardiography and cardiac magnetic resonance imaging as well as cardiac biomarkers such as C‑reactive protein, N‑terminal pro-B-type natriuretic peptide , and troponins can contribute to the clinical work-up of the syndrome but not toward elucidating the underlying cause or pathogenetic process. This review summarizes the phases and clinical features of myocarditis and gives an up-to-date short overview of the current treatment options starting with heart failure and antiarrhythmic therapy. Although inflammation in myocardial disease can resolve spontaneously, often specific treatment directed against the causative agent is required. For fulminant, acute, and chronic autoreactive myocarditis, immunosuppressive treatment has proven to be beneficial in the TIMIC and ESETCID trials; for viral cardiomyopathy and myocarditis, intravenous immunoglobulin IgG subtype and polyvalent intravenous immunoglobulins IgG, IgA, and IgM can frequently resolve inflammation. However, despite the elimination of inflammation, the eradication of parvovirus B19 and human herpesvirus-6 is still a challenge, for which ivIg treatment can become a future key player.

Interventional procedures for pericardial diseases include pericardiocentesis, drainage of pericardial effusion, intrapericardial therapy, and percutaneous balloon pericardiotomy or percutaneous pericardiostomy. Echocardiographic and fluoroscopic guidance have greatly increased safety and feasibility. Several devices for pericardiocentesis have been tested (PerDucer, PeriAttacher, visual puncture systems, Grasper, Scissors, and Reverse slitter), mainly to facilitate access to the pericardium in the absence of effusion for epicardial ablations or left atrial appendage ligation. In selected patients with pericardial effusions that cannot be managed medically or with prolonged drainage, various medications can be applied intrapericardially to prevent further recurrences or induce sclerosis of the pericardial space.

Die 2015 von der ESC und der AHA veroffentlichten Leitlinien zur infektiosen Endokarditis stutzen sich in der Diagnostik auf die modifizierten Duke-Kriterien. Diese beruhen auf dem Nachweis endokarditistypischer Erreger und dem Nachweis der endokarditischen Lasion in der Bildgebung, die sich neben der transthorakalen und transosophagealen Echokardiographie auch PET/CT, Kardio-CT und nuklearmedizinischer Methoden bedienen kann. Das Management soll durch ein interdisziplinares Endokarditisteam im dafur ausgewiesenen Referenzzentrum weiter verbessert werden. Die medikamentose Behandlung stutzt sich weitgehend unverandert auf bewahrte Antibiotika in Mono- oder Kombinationstherapie. Lediglich bei Staphylokokkenendokarditis kann auf Gentamycin verzichtet werden. Bis zu 50 % der Falle mussen fruher oder spater einer herzchirurgischen Masnahme zugefuhrt werden. Die Dringlichkeit dieses Eingriffs hangt ab vom Ausmas der Herzinsuffizienz, der Erregerpersistenz trotz Antibiose und den neurologischen Komplikationen.

The individual amount of alcohol consumed acutely or chronically decides on harm or benefit to a person’s health. Available data suggest that one to two drinks in men and one drink in women will benefit the cardiovascular system over time, one drink being 17.6 ml 100 % alcohol. Moderate drinking can reduce the incidence and mortality of coronary artery disease, heart failure, diabetes, ischemic and hemorrhagic stroke. More than this amount can lead to alcoholic cardiomyopathy, which is defined as alcohol toxicity to the heart muscle itself by ethanol and its metabolites. Historical examples of interest are the Munich beer heart and the Tübingen wine heart. Associated with chronic alcohol abuse but having different etiologies are beriberi heart disease (vitamin B1 deficiency) and cardiac cirrhosis as hyperdynamic cardiomyopathies, arsenic poising in the Manchester beer epidemic, and cobalt intoxication in Quebec beer drinker’s disease. Chronic heavy alcohol abuse will also increase blood pressure and cause a downregulation of the immune system that could lead to increased susceptibility to infections, which in turn could add to the development of heart failure. Myocardial tissue analysis resembles idiopathic cardiomyopathy or chronic myocarditis. In the diagnostic work-up of alcoholic cardiomyopathy, the confirmation of alcohol abuse by carbohydrate deficient transferrin (CDT) and increased liver enzymes, and the involvement of the heart by markers of heart failure (e.g., NT-proBNP) and of necrosis (e.g., troponins or CKMb) is mandatory. Treatment of alcoholic cardiomyopathy consists of alcohol abstinence and heart failure medication.

Cardiac tamponade is a pericardial syndrome characterized by compression of the heart by the exudate accumulating within the pericardial space and impairing diastolic filling and cardiac output. Pericardial diseases of any aetiology but also haemorrhage during interventional procedures may cause tamponade. If pericardial effusion accumulates slowly, 2000 mL or more could be tolerated (unless precipitated by dehydration, loop diuretics, vasodilators, anticoagulants, or thrombolytics), but acute accumulation of more than 250 mL is fatal.

In developed countries, more than 80% of cases of acute pericarditis remain without an established diagnosis after a conventional and standard diagnostic approach. These cases are generally labelled as 'idiopathic', i.e. without a known cause. This lack of information is a matter of concern for both patients and clinicians. Some years ago, this term reflected the state of the art of scientific knowledge on the topic. Advances have changed this point of view, in light of available molecular techniques like polymerase chain reaction able to identify viral cardiotropic agents in pericardial fluid and biopsies. Furthermore, the remarkable efficacy of interleukin-1 antagonists, a therapy targeting the innate immune response, suggests clinical and pathogenic similarity between a proportion of patients with idiopathic recurrent pericarditis and classical autoinflammatory diseases. So, it seems useful to discuss the pros and cons of using the term "idiopathic" in light of the new knowledge.

Background The clinical phenotype dilated cardiomyopathy is assumed to be the endstage of a multifactorial aetiopathogenetic pathophysiology which includes a not satisfactorily defined group of patients with inflammatory cardiomyopathy. Methods Within the German Competence Network Heart Failure patients with heart failure due to dilated cardiomyopathy of viral/inflammatory (DCMi/v) and nonviral/noninflammatory (DCM) aetiology were enrolled. After 1 year 237 patients (180 male/57 female) were re-examined including complete clinical work-up. The association of different clinical courses with the time from initial diagnosis of heart failure (newly: ≤ 1 year; late: > 1 year) was investigated. Results After 1-year-follow-up New York Heart Association (NYHA) class (by −0·48 in newly diagnosed DCM and −0·82 in newly diagnosed DCMi/v in addition to −0·24 in late diagnosed DCM and −0·17 in late diagnosed DCMi/v) as well as left ventricular ejection fraction (+14% in newly diagnosed DCM and DCMi/v and +6% in later diagnosed DCM and DCMi/v) were significantly improved in all patients. In patients with early diagnosed dilated cardiomyopathy a strong improvement of NYHA class could be demonstrated. Conclusions This study demonstrates for the first time a significant interaction between duration of disease, NYHA class and left ventricular ejection fraction in patients with DCM. Our results clearly demonstrate that in patients with DCM an early diagnosis within 1 year after occurrence of clinical signs is associated with a strong improvement in the clinical course, whereas late diagnosis results in a loss of change in clinical course and outcome.

Physical training has a well-established role in the primary and secondary prevention of coronary artery disease. Moderate exercise has been shown to be beneficial in chronic stable heart failure. Competitive sports, however, is contraindicated in most forms of hypertrophic cardiomyopathy (HCM), in myocarditis, in pericarditis, and in right ventricular cardiomyopathy/dysplasia. In most European countries, the recommendations of medical societies or public bodies state that these diseases have to be ruled out by prescreening before an individual can take up competitive sports. But the intensity and quality of this health check vary considerably from country to country, from the type of sports activity, and from the individuals who want to participate in sports. Prescreening on an individual basis should also be considered for leisure sports, particularly in people who decide to start training in middle age after years of physical inactivity to regain physical fitness. In leisure sports the initiative for a medical check-up lies primarily in the hands of the "healthy" individual. If she or he plans to participate in extreme forms of endurance sports with excessive training periods such as a marathon or ultramarathon and competitive cycling or rowing, they should be aware that high-intensity endurance sports can lead to structural alterations of the heart muscle even in healthy individuals. Physical exercise in patients with heart disease should be accompanied by regular medical check-ups. Most rehabilitation programs in Europe perform physical activity and training schedules according to current guidelines. Little is known about athletes who are physically handicapped and participate in competitive sports or the Paralympics, and even less is known about individuals with intellectual disabilities (ID) who participate in local, regional, international competitions or the Special Olympics or just in leisure sport activities.

Background In heart failure (HF), traditional cardiovascular risk factors (RF) as body mass index (BMI), total cholesterol (TC) and systolic blood pressure (SBP) are associated with better survival. It is unknown at which time point along the disease continuum the adverse impact of these RF ceases and may ‘start to reverse'. We analyzed the distribution of RF and their association with survival across HF stages. Methods We pooled data from four cohort studies from the German Competence Network HF. Employing ACC/AHA-criteria, patients were allocated to stage A (n=218), B (n=1324), C1 (i.e., New York Heart Association [NYHA] classes I & II; n=1134), and C2+D (NYHA III & IV; n=639). Results With increasing HF severity median age increased (63/67/67/70years), whereas the proportion of females (56/52/37/35%), median BMI (26.1/28.8/27.7/26.6kg/m 2 ), TC (212/204/191/172mg/dl), and SBP (140/148/130/120mmHg) decreased (P 2 BMI 0.91 (95% confidence interval 0.88; 0.95); per +10mg/dl TC 0.93 (0.92; 0.95); per +5mmHg SBP 0.94 (0.92; 0.95). Conclusion In this well-characterized sample of patients representing the entire HF continuum, reverse associations were only consistently observed in symptomatic HF stages. Our data indicate that the phenomenon of a "reverse epidemiology" in HF is subject to significant selection bias in less advanced disease.

We describe diagnosis, differential diagnosis, multimodality imaging and medical and invasive diagnostic treatment in patients with inflammatory cardiomyopathy and myocarditis under etiological considerations in reference to a landmark position paper of the Working Group Myocardial and Pericardial Diseases of the European Society of Cardiology together with recent developments in diagnosis and treatment. Diagnosis of the symptomatic patient is the assessment of etiology of inflammatory cardiomyopathy, followed by the clinical presentation, course, treatment option and prognosis. Viral myocarditis in its different facets can clearly be separated from autoreactive forms by histological and molecular methods in the endomyocardial biopsy, thus leading to an individualized targeted therapy beyond heart failure treatment.

Die ESC Leitlinie 2014 zur hypertrophischen Kardiomyopathie (HCM) fasst mit 133 ausformulierten und abgestimmten Empfehlungen, fur die 506 Literaturstellen hinterlegt sind, den aktuellen Erkenntnisstand zu Diagnostik, Management und Therapie des Phanotyps HCM zusammen. Neu im Vergleich zur letzten, 10 Jahre alten ACC/ESC-Leitlinie sind die Einarbeitung aktueller Erkenntnisse zur Genetik, konkrete Empfehlungen zum genetischen Screening von betroffenen Familien, die Betonung klinischer Leitsymptome (Signale) zur Zuordnung zu selteneren nichtobstruktiven HCM-Varianten, die Betonung der nicht-invasiven Bildgebung mit Echokardiographie und Kardio-MRT sowie eine Formel zur Abschatzung des Risikos fur einen plotzlichen Herztod. Dabei sollte nicht vergessen werden, dass die meisten Patienten mit einer HCM ein weitgehend normales Leben fuhren. Der hohe Detaillierungsgrad der Leitlinie erweist sich sowohl fur den Kardiomyopathieexperten als auch fur den Internisten und Allgemeinmediziner als eine ausgezeichnete, strukturierte Zusammenfassung des gegenwartigen Wissenstands.

In diesem Beitrag werden Diagnostik, Differenzialdiagnostik, multimodale Bildgebung sowie medikamentose und invasiv diagnostische Therapie der akuten und chronischen Perikarditis, der konstriktiven Perikarditis, des Perikardergusses und der Herztamponade unter atiologischen Gesichtspunkten und in Anlehnung an die Leitlinie der European Society of Cardiology (ESC) beschrieben. Ausgangspunkt des klinischen Entscheidungsbaums ist der symptomatische Patient mit echokardiographisch nachweisbarem Perikarderguss. Im Vordergrund der Diagnostik steht die atiopathogenetische Einordnung der Perikarderkrankung, die klinisches Bild, Verlauf, Therapie und Prognose pragen. Die infektiose Perikarditis (viral, bakteriell oder tuberkulos) wird von der sterilen autoreaktiven Perikarditis und vom neoplastischen Perikarderguss durch Ergusszytologie sowie (immun-)histologische und molekulare Untersuchungen der Perikard- und Epikardbiopsie abgegrenzt. Hierzu leistet die Perikardioskopie zur Erkennung suspekter Areale einen wichtigen Beitrag. Intraperikardiale Cisplatingabe bei neoplastischem Perikarderguss und Instillation von Triamcinolon bei autoreaktiver Perikarditis verhindern ebenso wie eine mehrmonatige Behandlung mit Colchicin in vielen Fallen Rezidive.

Fulminant myocarditis is a clinical syndrome with signs of acute heart failure, cardiogenic shock, or life-threating rhythm disturbances in the context of suspected myocarditis. It is not an etiological diagnosis, but may have different underlying causes and pathogenetic processes - viral, bacterial, toxic, and autoreactive. Clinical management of the disease entity at the acute stage involves hemodynamic monitoring in an intensive care unit or similar setting. Rapid routine work-up is mandatory with serial EKGs, echocardiography, cardiac MRI, heart catheterization with endomyocardial biopsy for histology, immunohistology, and molecular analysis for the underlying infection and pathogenesis. Heart failure therapy is warranted in all cases according to current guidelines. For fulminant autoreactive myocarditis, immunosuppressive treatment is beneficial; for viral myocarditis, IVIg can resolve the inflammation, reduce the viral load, and even eradicate the microbial agent. ECMO, IABP, ventricular assist devices, LifeVest, or ICD implantation can bridge to recovery or to heart transplantation.

Background Aortic wall strains are indicators of biomechanical changes of the aorta due to aging or progressing pathologies such as aortic aneurysm. We investigated the potential of time-resolved three-dimensional ultrasonography coupled with speckle-tracking algorithms and finite element analysis as a novel method for noninvasive in vivo assessment of aortic wall strain. Methods Three-dimensional volume datasets of 6 subjects without cardiovascular risk factors and 2 abdominal aortic aneurysms were acquired with a commercial real time three-dimensional echocardiography system. Longitudinal and circumferential strains were computed offline with high spatial resolution using a customized commercial speckle-tracking software and finite element analysis. Indices for spatial heterogeneity and systolic dyssynchrony were determined for healthy abdominal aortas and abdominal aneurysms. Results All examined aortic wall segments exhibited considerable heterogenous in-plane strain distributions. Higher spatial resolution of strain imaging resulted in the detection of significantly higher local peak strains ( p ≤ 0.01). In comparison with healthy abdominal aortas, aneurysms showed reduced mean strains and increased spatial heterogeneity and more pronounced temporal dyssynchrony as well as delayed systole. Conclusions Three-dimensional ultrasound speckle tracking enables the analysis of spatially highly resolved strain fields of the aortic wall and offers the potential to detect local aortic wall motion deformations and abnormalities. These data allow the definition of new indices by which the different biomechanical properties of healthy aortas and aortic aneurysms can be characterized.

Despite great advances in the pathophysiology and etiology of myocarditis, the clinical diagnosis of myocarditis in daily clinical practise remains challenging. Often the diagnosis was not clear because of the heterogeneity of clinical symptoms and the lack of guidelines for adequate diagnostic requirements and consecutive treatment options. The European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases established a working group of experts to improve the diagnosis and management of myocarditis and to provide a common consensus statement as a reference for future registries and controlled trials. The goal was to bridge the gap between clinical- and tissue-based diagnosis by formulating a concept concerning essential diagnostics and treatment of these patients that would be accepted across Europe. Only in this manner is it possible to establish a basis for national and international registries and double-blind randomized treatment trials for the etiologically differentiated treatment of myocarditis, which appear promising due to numerous studies in recent years. In this paper, two members from the expert working group summarize the most important aspects of this position paper on the etiology, diagnosis, management, and treatment of myocarditis, which were published in the July 2013 issue of European Heart Joumal.

Hypertrophic cardiomyopathy (HCM) is a cardiovascular disease with autosomal dominant inheritance caused by mutations in genes coding for sarcomeric and/or regulatory proteins expressed in cardiomyocytes. In a small cohort of HCM patients (n = 8), we searched for mutations in the two most common genes responsible for HCM and found four missense mutations in the MYH7 gene encoding cardiac β-myosin heavy chain (R204H, M493V, R719W, and R870H) and three mutations in the myosin-binding protein C3 gene ( MYBPC3 ) including one missense (A848V) and two frameshift mutations (c.3713delTG and c.702ins26bp). The c.702ins26bp insertion resulted from the duplication of a 26-bp fragment in a 54-year-old female HCM patient presenting with clinical signs of heart failure due to diastolic dysfunction. Although such large duplications (> 10 bp) in the MYBPC3 gene are very rare and have been identified only in 4 families reported so far, the identical duplication mutation was found earlier in a Dutch patient, demonstrating that it may constitute a hitherto unknown founder mutation in central European populations. This observation underscores the significance of insertions into the coding sequence of the MYBPC3 gene for the development and pathogenesis of HCM.

Depression is common in heart failure (HF) and associated with adverse outcomes. This study aimed to investigate incidence rates and predictors of depression in patients sampled from four subprojects of the German Competence Network Heart Failure.Eight hundred thirty nine symptomatic HF patients free of depression at baseline underwent repeat depression screening (Patient Health Questionnaire, PHQ-9) after 12 months. Ordered logistic regression analysis was employed to search for predictors of incident depression.Incident minor (major) depression was observed in 61 (7.3%) and 47 (5.6%) of the population. Depression was recurrent in 15 (25%) and 16 (34%), respectively. Multiple regression analysis revealed seven variables predicting minor or major depression: Previous depressive episode (odds ratio [OR] 4.04, 95% confidence interval [CI] 2.37-6.89, p ≤ 0.001), previous resuscitation (OR 2.44, CI 1.23-4.81, p=0.010), current smoking (OR 2.06, CI 1.08-3.50, p=0.008),4 visits/year to general practitioner (OR 1.67, CI 1.06-2.63, p=0.026), New York Heart Association class (OR 1.54/class, 95% CI 1.05-2.25, p=0.027), PHQ-9 baseline sum-score (OR 1.18/point, CI 1.11-1.27, p0.001), and SF-36 physical functioning (OR 1.08/-5 points, CI 1.03-1.13, p=0.002).In these HF patients initially free of depression annual incidence rates were high. Several independent predictors allowed identification of patients at particular risk. Although obtained in a selected cohort these findings call, in view of the grave prognosis of HF patients with comorbid depression, for regular depression screening and development of specific supportive strategies to improve patient care and outcomes in HF.

Pericardial diseases only affect a small proportion of patients with heart disease. But their diagnosis and differential diagnosis is, though too often neglected by cardiologists and internists, extremely important for the individual patient and of therapeutic and prognostic relevance in the differential diagnosis of cardiac symptoms [1, 2]: An excellent example for precordial pain is acute pericarditis, which should be differentiated from aortic dissection, myocardial infarction, pneumonia or pleuritis, pulmonary embolism, pneumothorax, costochondritis (Da Costa syndrome), gastroesophageal reflux or neoplasm and herpes zoster. In the spectrum of heart failure syndromes, it is pericardial constriction that causes dyspnoea and peripheral edema. Seferovic et al. particularly address these issues in their contribution, which was designed to update the 2004 guidelines of the European Society of Cardiology [3]. These guidelines are still the only guidelines worldwide on the management of pericardial diseases. Interventional pericardiologists nowadays use intrapericardial endoscopy and biopsy together with classic cytology to establish an etiologically based diagnosis [4, 5] by making use of techniques that have been accepted and applied to diagnose inflammatory cardiomyopathies [6] or tumors or rheumatic diseases since several decades. Pericardial access has become a vital interest for electrophysiologists, who now also ablate epicardial foci and reentry sites to treat malignant ventricular tachycardia [7, 8]. Pericardial access is also discussed for localized pharmacological treatment [9], even for stem cells or cocktails with growth factors [10]. Devices for locomotion on the epicardial surface have been designed and applied in preclinical settings [10, 11]. Apart from the patient’s symptoms, echocardiography remains the mainstay of imaging of acute pericardial syndromes but also of constrictive pericarditis, effusive–constrictive pericarditis, pericardial effusion, tamponade, absence of the pericardium and cysts or tumors. The remarkable progress, which has been made in echocardiography in the last years, is very well described by Veress, Feng and Oh from the Mayo-Clinic. Progress in cardiac tissue Doppler analysis, strain and strain rate imaging by speckle tracking imaging and three-dimensional echocardiography, the assessment of early diastolic annulus velocity and annulus reversus by TDI improves the differentiation of constriction from restrictive myocardial disease and is in the focus of their contribution. Threedimensional echocardiography may come up as a useful method for the precise assessment pericardial masses as it provides incremental value to 2D echocardiography by detecting anatomical and pathological structures with higher accuracy. Of particular interest are their contributions and that of others on effusive–constrictive pericarditis [12–14] and on the differential diagnosis of constrictive pericarditis to restrictive cardiomyopathy [15]. Syed and coworkers in this issue point out that effusive– constrictive pericarditis is best characterized in patients with tamponade who continue to have elevated intracardiac pressure after removal of pericardial fluid. The underlying causes are pericardial inflammation in conjunction with the presence of pericardial fluid under pressure, whereby the etiology is diverse. Alter et al. add valuable information on imaging by reviewing MRI and CT [16, 17] as well as scintigraphic Bernhard Maisch: Former Director of the University Hospital of Internal Medicine and Cardiology.

The etiology of pericardial effusions remains unresolved in many cases because not the full spectrum of diagnostic methods including cytology, histology, immunohistology and PCR on cardiotropic agents, which are currently available, used in many institutions. After comprehensive clinical workup and use of imaging methods, such as echocardiography and cardiac MRI, pericardiocentesis and epicardial and pericardial biopsy were carried out under pericardioscopical control of the biopsy site. Biopsies and fluid were evaluated by cytological, histological, immunological and molecular (PCR) methods in 259 patients of our tertiary referral center following an identical clinical pathway, diagnostic and therapeutic algorithm in all cases. A standard clinical pathway and the same diagnostic and therapeutic algorithms were used in all cases. When all methods are applied to patients with pericardial effusions, "idiopathic" pericardial effusion is no longer a relevant diagnosis. Autoreactive and lymphocytic pericardial effusions are the leading diagnosis in 35 % of patients in the prospective Marburg registry, followed by malignant effusions in 28 % of cases. Viral genome was assessed in fluid and epi- as well as pericardial biopsies in 12 %, followed by post-traumatic/iatrogenic effusions in 15 % and purulent/bacterial effusions in only 2 %. Pericardioscopy permits the macroscopic inspection of the pulsating heart and its disease-associated macroscopic alterations. It also permits safe and targeted biopsy for further investigations of the tissue. Therapy, tailored to the individual etiology, can be selected such as intrapericardial instillation in autoreactive effusions with triamcinolone and with cisplatin or thiotepa in neoplastic effusions. With this approach the recurrence of pericardial effusion can be avoided effectively. A comprehensive approach to the diagnosis of pericardial effusions in conjunction with pericardioscopy for targeted tissue sampling is the prerequisite for an etiologically based intrapericardial and systemic treatment, which improves outcome and prognosis.

International audience; The haemoflagellate Trypanosoma cruzi is the causative agent of Chagas' disease that occurs in approximately 8 million people in Latin America. Patients infected with T. cruzi frequently suffer of cardiomegaly and may die of myocardial failure. Here we show that T. cruzi trypomastigotes (extracellular form) increased in vitro apoptosis of rat cardiomyocytes. Additionally, we demonstrated that amastigotes (intracellular form), for which a method for purification was established, were also able to induce cardiomyocyte apoptosis. Increase of apoptosis was associated with up-regulation of the apoptotic gene bax by trypomastigotes, while expression of the anti-apoptotic gene bcl-2 was down-regulated by amastigotes. The transcription factor STAT3 but not STAT1 was activated in cardiomyocytes by trypomastigotes. In addition, tlr7 gene expression was up-regulated in cardiomyocytes incubated with trypomastigotes, suggesting that this Toll-like receptor is involved in the intracellular recognition after host cell invasion by T. cruzi. Glycosylphosphatidylinositols purified from trypomastigotes did not induce cardiomyocyte apoptosis and STAT activation but down-regulated tlr7 gene expression. In conclusion, cardiomyopathy observed in Chagas' disease might be in part due to apoptosis of cardiomyocytes induced directly by the parasite.

Pericardial cysts are rare. They are often asymptomatic mediastinal abnormalities, which are usually congenital. If symptomatic differential diagnosis can pose a diagnostic challenge since it has to consider the different causes of pericardial effusion including malignant forms. In 2 symptomatic female patients (aged 51 and 58 years) pericardiocentesis, pericardioscopy and pericardial fluid analysis confirmed the diagnosis of "spring water cysts." Pericardioscopy excluded protrusions, petechial bleeding, neovascularization or inflammation. Application of contrast media into the cyst confirmed by radiological control that no communication to the true pericardial sac was present. So after aspiration of the entire fluid, subsequent instillation of 10 ml ethanol for a few minutes was carried out to prevent recurrence of the cystic formation. The aspiration of the residual fluid under moderate suction demonstrated and 24-h clinical observation at the ICU completed the short intervention. All symptoms were relieved immediately in both patients. Recurrence was not observed in the follow-up.

The aetiology of pericardial effusion has been generally assessed by clinical work-up only, which leaves a large cohort of patients with "idiopathic" effusions virtually undiagnosed. In accordance with the ESC guidelines, this contribution intends to change this attitude. After therapeutic or diagnostic pericardiocentesis of 259 patients with large to moderate pericardial effusions, pericardial fluid, epicardial and pericardial biopsies, and blood samples were analysed by PCR for cardiotropic microbial agents. Cytology, histology, immunohistology of tissue and fluids and laboratory tests were performed. Of the 259 patients, 35 % suffered from an autoreactive aetiology, 28 % suffered from a malignant and 14 % from an infectious cause. Investigating all samples by PCR, we identified viral genomes in 51 (19.7 %) patients, parvovirus B19 (B19 V) being identified in 25 and Epstein-Barr virus (EBV) in 19 cases. In patients with a sole infectious aetiology (n = 36), B19 V was detected in 21 and EBV in 10 cases. When differentiating with regard to the material investigated for the presence of cardiotropic viruses, parvovirus B19 was most often detected in the epicardium and EBV was most frequently detected in the pericardial fluid independent from the final diagnostic categorisation. Bacterial cultures including tests for tuberculosis were all negative. Molecular techniques improve sensitivity, specificity and diagnostic accuracy for the underlying aetiology in pericarditis patients with effusion. The identification of specific viral signatures will help to understand pathogenetic mechanisms in pericarditis and allow to tailor an adequate therapy beyond antiphlogistic treatment.

In inflammatory dilated cardiomyopathy and myocarditis, there is apart from heart failure and antiarrhythmic therapies no alternative to an etiologically driven specific treatment. Their prerequisites are noninvasive and invasive biomarkers including endomyocardial biopsy and PCR on cardiotropic agents. This review deals with the different etiologies of myocarditis and inflammatory cardiomyopathy including the genetic background, the predisposition for heart failure and inflammation. It analyses the epidemiologic shift in pathogenetic agents in the last 20 years, the role of innate and acquired immunity including the T cell and B cell driven immune responses. On this basis, it summarizes phases and clinical faces of myocarditis. It gives an up-to-date information on current treatment options starting with heart failure and antiarrhythmic therapy. Although inflammation can resolve spontaneously, often specific treatment directed to the causative etiology is required. For fulminant, acute and chronic autoreactive myocarditis immunosuppressive treatment is beneficial; for viral cardiomyopathy and myocarditis, IVIG can resolve inflammation and is as successful as interferon therapy in enteroviral and adenoviral myocarditis. Eradication of parvovirus B19 and HHV6 myocarditis is still a problem by anyone of these treatment options. The potential of stem cell therapy has to be tested in future trials. In perimyocardial disease, a locoregional approach with high local doses and low systemic side effects have been shown highly efficient by intrapericardial treatment of triamcinolonacetate facilitated by pericardioscopy for adequate etiopathogenetic diagnosis.

Diabetic cardiomyopathy is a controversial clinical entity that in its initial state is usually characterized by left ventricular diastolic dysfunction in patients with diabetes mellitus that cannot be explained by coronary artery disease, hypertension, or any other known cardiac disease. It was reported in up to 52-60% of well-controlled type-II diabetic subjects, but more recent studies, using standardized tissue Doppler criteria and more strict patient selection, revealed a much lower prevalence. The pathological substrate is myocardial damage, left ventricular hypertrophy, interstitial fibrosis, structural and functional changes of the small coronary vessels, metabolic disturbance, and autonomic cardiac neuropathy. Hyperglycemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function, and induce myocardial inflammation. Insulin resistance with hyperinsulinemia and decreased insulin sensitivity may also contribute to the left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy may include dyspnea, arrhythmias, atypical chest pain, and dizziness. Currently, there is no specific treatment of diabetic cardiomyopathy that targets its pathophysiological substrate, but various therapeutic options are discussed that include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), the use of ACE inhibitors, beta blockers, and calcium channel blockers. Daily physical activity and a reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles.

In the 2015 guidelines of the European Society of Cardiology (ESC) and the American Heart Association (AHA) on infective endocarditis, the diagnostics are based on the modified Duke criteria. The diagnosis can be confirmed by a combination of micro-organisms demonstrated in culture or in situ, with the detection of valvular lesions or abscess formation by an imaging modality using echocardiography, positron emission tomography computed tomography (PET/CT), cardio-CT or nuclear medical methods. The management should be further improved by an interdisciplinary endocarditis team in a specifically designated reference center. Pharmaceutical treatment is largely unchanged and based on classical antibiotics in monotherapy or as combination therapy but for staphylococcal endocarditis, gentamycin is no longer required. As cardiac surgery is needed in 50 % of the cases during the course of the disease, the urgency for surgery depends on the extent of cardiac insufficiency, the persistence of the pathogen despite antibiotic treatment and on neurological complications.