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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.

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.

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.

There is no question that cholesterol, especially low-density lipoprotein (LDL) cholesterol, represent a major cardiovascular risk factor. The so-called lipid hypothesis has been proven by almost all epidemiologic studies, animal studies and, most importantly, by interventional studies with lipid-lowering drugs, especially statins. However, despite our better understanding of atherogenesis we cannot explain why atherosclerosis occurs most frequently and severely on coronary arteries rather than on other arteries such as those of the hands or feet. In addition, the "lipid hypothesis" is unable to explain the dramatic change in severity of a far more generalized atherosclerosis in patients suffering from diabetes mellitus.Recently, we studied the effects of fatty acids on endothelial integrity and found a dramatic increase in apoptosis under fatty acid exposition. Since it is well known that the heart depends highly on fatty acid delivery to cover its energy demand, we hypothesize that the heart becomes the victim of its energy demand. With the so-called Marburg hypothesis of atherogenesis we can explain the fact why especially the arteries of the heart show early atherosclerotic lesions, but also the fact why patients with diabetes develop more generalized atherosclerosis. Finding mechanisms to reduce the presence of fatty acids within the arterial wall might prevent plaque destabilization and could be a potential target in our fight against atherosclerosis.

The treatment of progressive and terminal heart failure follows the principle of causative therapy. Therefore, etiology and pathophysiology of the underlying disease and its hemodynamic conditions are indispensable. This applies to coronary artery disease, hypertension, valvular heart disease, the cardiomyopathies with and without inflammation, and microbial persistence similarly. The classic treatment algorithms both in heart failure with and without reduced ejection fraction are based on measures onloading the heart (angiotensin-converting enzyme inhibitors, angiotensin antagonists, beta-blockers, diuretics) and on antiarrhythmics and anticoagulation, when needed. Device therapy for cardiac resynchronization in left bundle branch block and permanent stimulation therapy may contribute to the hemodynamic benefit. ICD (implantable cardioverter defibrillator) therapy prevents sudden cardiac death, which is often associated with progressive heart failure. Heart transplantation and left ventricular assist devices are final options in the treatment repertoire of terminal heart failure.

Cardiomyopathies are an important and diverse group of heart muscle diseases in which the heart muscle itself is structurally or functionally abnormal and in which coronary artery disease, hypertension, valvular and congenital heart disease are absent or do not sufficiently explain the observed myocardial abnormality. This often results in severe heart failure accompanied by arrhythmias and/or sudden death. Clinical and morphological diversity of cardiomyopathies can reflect the broad spectrum of distinct underlying molecular causes or genetic heterogeneity. In many cases the disease is inherited and is termed familial dilated cardiomyopathy (FDC), which may account for up to 30% of dilated cardiomyopathies (DCM). FDC is principally caused by genetic mutations in FDC genes that encode for cytoskeletal, nuclear and sarcomeric proteins in the cardiac myocyte. In addition, modifying genes, lifestyle and additional factors were reported to influence onset of disease, disease progression, and prognosis. The individual patient's phenotype may reflect a summation and/or interaction of the underlying mutation(s) with other genetic or environmental factors. During the last years major advances have been made in the understanding of the molecular and genetic basis of this type of disease. Nevertheless, much more progress in the identification of underlying mutations, susceptibility genes and modifier genes is important and indispensable for the development of new etiology-orientated forms of therapy. A pivotal role for autoimmunity in a substantial proportion of patients with DCM is supported by the presence of organ-specific autoantibodies, inflammatory infiltrates and pro-inflammatory cytotoxic cytokines. Furthermore, familial occurrence of DCM goes ahead with the presence of autoantibodies and abnormal cytokine profiles in first-degree relatives with asymptomatic left ventricular enlargement. These relatives suffer from a higher risk for the development of DCM after years. This suggests the involvement of a disrupted humoral and cellular immunity early in the development of the disease. There is reasonable clinical and experimental evidence, that DCM in addition may occur as late stage of cardiac infection and inflammation. The large spectrum of clinical forms depends on several factors such as genetic determinants of the infective agent, the genetics, age and gender of the host, and the host immunocompetence. In general, infectious agents, including viruses such as entero-, cytomegalo-, and adenoviruses, bacteria such as Borrelia burgdorferi or Chlamydia pneumoniae, protozoa and even fungi can cause inflammatory heart disease leading to DCM. The infectious agents most often identified in DCM nowadays are parvovirus B19, human herpesvirus 3, and Epstein-Barr virus. Persistence of these viruses within the myocardium is associated with reduction of ejection fraction after 6 months. For patients with suspected inflammatory heart disease the immunohistochemical detection of inflammatory infiltrates is related to poor outcome. Many faces of inflammatory heart disease coexist where different phases of the disease progress simultaneously: phase 1 is dominated by viral infection itself, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation. Further investigations with regard to the etiology of structural heart diseases should include an intensive clinical investigation of the given patient. A possible family history including a pedigree should be ascertained and with regard to a possible inflammatory or viral heart disease, endomyocardial biopsies should be investigated by polymerase chain reaction and immunohistochemistry.

The first classifications of cardiomyopathies from 1980 and 1996 described them as heart muscle diseases, with dilated (DCM), hypertrophic (HCM), restrictive (RCM), arrhythmogenic right ventricular (ARVC), and nonclassifiable cardiomyopathies. Furthermore, the World Health Organization/International Society and Federation of Cardiology (WHO/ISFC) classification from 1996 listed among the specific cardiomyopathies inflammatory cardiomyopathy as a new and distinct entity, which was defined histologically as myocarditis in association with cardiac dysfunction. Infectious and autoimmune forms of inflammatory cardiomyopathy were recognized. Viral cardiomyopathy was defined as viral persistence in a dilated heart without ongoing inflammation. If it was accompanied by myocardial inflammation, it was termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). This entity was further elucidated in a World Heart Federation consensus meeting in 1999 by quantitative immunohistological criteria (14 infiltrating cells/mm(2)) and the etiology by molecular biological methods, e.g., polymerase chain reaction, as viral, bacterial, or autoimmune (= nonmicrobial). The development of molecular genetics, with the discovery of a genetic background in several forms of cardiomyopathies previously alluded to as "of unknown origin", was the origin of a debate on a new classification based on genomics. A genomic/postgenomic classification was postulated taking the underlying gene mutations and the cellular level of expression of encoded proteins into account, thus distinguishing cytoskeleton (cytoskeletalopathies, e.g., DCM or ARVC), sarcomeric (sarcomyopathies as in HCM and RCM) and ion channel (channelopathies, e.g., long or short QT syndrome and Brugada's syndrome) cardiomyopathies. Such a classification of cardiomyopathies was proposed in 2006 by the American Heart Association (AHA), which took the rapid evolution of molecular genetics in cardiology into account. It also introduced several recently described diseases, and is unique in that it incorporated ion channelopathies even without hemodynamic dysfunction as a "primary" cardiomyopathy. The ESC (European Society of Cardiology) Working Group on Myocardial and Pericardial Diseases has deliberately taken a different approach based on a clinically oriented classification in which heart muscle disorders were grouped according to morphology and function. This obviously remains the clinically most useful approach for the diagnosis and management of patients and families with heart muscle disease. In the ESC position statement published in 2008, cardiomyopathies were defined as myocardial disorders in which the heart muscle is structurally and functionally abnormal, and in which coronary artery disease, hypertension, valvular and congenital heart disease are absent or do not sufficiently explain the observed myocardial abnormality. The aim was to help clinicians look beyond generic diagnostic labels in order to reach more specific diagnoses. In parallel, a scientific statement on the role of endomyocardial biopsy in the management of cardiovascular disease was published at the end of 2007 making useful recommendations for clinical practice and providing an understanding for the use of endomyocardial biopsy in an individual patient. Taking the classification of cardiomyopathies and the statement on the role of endomyocardial biopsies in different clinical scenarios together, the clinician is now able to identify genetic, autoimmune and viral causative factors by using a thorough and logical approach to reach a diagnosis in patients with familial and nonfamilial forms of the underlying structural heart muscle diseases.

Women's greater susceptibility to autoimmune diseases has been recognized for more than 100 years. And although the basic immune response (including a more vigorous immune response and increased antibody production) has been known to differ between men and women, conclusive pathophysiological explanations for this phenomenon are still lacking. Experimental work done in animal models have revealed a profound influence of sex hormones on the susceptibility to autoimmune diseases and on clinical disease via direct and indirect signaling pathways. Apart from sex hormones additional factors seem to participate in the pathogenesis of autoimmune diseases, which remain to be elucidated ("so far, you cannot explain autoimmunity [only] with estrogen" [lockshin]).

In every year since 1984, cardiovascular disease has claimed the lives of more females than males. In the Western world more than 450,000 women succumb to heart disease annually. Despite the proportions, most women believe that heart disease is a man's disease and that they will die of breast cancer. Data on epidemiology and incidence are rare: there is only an estimated incidence of cardiac neoplasm at necropsy ranging from 0,001% to 0,3%. The majority of the primary tumors are benign. Females are affected more often than males. The most common tumor entity is benign cardiac myxoma. Malignant heart tumors are less common. Most often they are different types of sarcomas, which have a poor outcome and affect more males than females. Metastatic tumors of the heart are 100 times more common than the primary ones. They originate mainly from melanomas, leukemias, lymphomas, and cancer, especially of the lung or breast. Indeed in women breast cancer is the most common metastatic tumor associated with pericardial effusion. To prevent death from tamponade, pericardiocentesis, in addition to the systemic chemotherapy, is mandatory, best when instillation of chemotherapeutics (cisplatin or thiotepa) or radioisotopes is given into the pericardial sac to prevent recurrence of the effusion. However, more of the malignant tumors may be curable if exactly diagnosed at an earlier stage.A retrospective study was conducted of all patients with cardiac and pericardial neoplasm exactly diagnosed by endomyocardial or epicardial biopsy and pericardiocentesis, using hospital medical records and a biopsy and pericardiocentesis registry from 2000-2005 with 297 patients. Pericardial effusion and biopsy analyses included biochemistry, cytology, serology, microbiology, histology, immunohistology, and polymerase chain reaction (PCR). All patients were investigated in relation to Herzmetasgender differences to histopathologic findings, clinical presentation and outcome.In 76 cases (25.6%) a neoplasm was the reason for a pericardial effusion. 36 women suffered from the breast carcinoma (47%) and 40 males lung cancer (42%) as the firstly metastatic tumor. There was no recurrence of a relevant pericardial effusion in patients who were treated by intrapericardial instillation of cisplatin (30 mg/m2 body surface in 100 ml 0.9% NaCl).Females are more often affected by primary cardiac tumors than males with an excellent outcome. By contrast, the preventive checkup and aftercare will gain more prognostic importance, especially in case of breast cancer, to earlier recognize a secondary cardiac neoplasm by biopsy and pericardiocentesis with intrapericardial treatment of neoplastic pericarditis.

Atherosclerosis and coronary artery disease (CAD) are the main causes of death in the Western world, for both men and women. However, in premenopausal women CAD is less frequent than in men, but in elderly women (e.g.,75 years) myocardial infarction (MI) occurs even more often than in men. In summary, women suffer from CAD and MI but at a later age than men. Therefore it is important to observe and compare the cardiovascular risk factors in women and men. The typical CAD risk factors such as hyperlipidemia, smoking, arterial hypertension, diabetes mellitus, obesity, physical inactivity, and unhealthy nutrition are increasingly important for both genders. Many of these factors are comparable between men and women, but due to hormonal influences especially the lipoprotein metabolism shows some striking differences between men and women, but interestingly enough also between pre- and postmenopausal women. Therefore this paper will focus especially on the gender-specific differences in lipid metabolism as a potential target which might explain both the gender-specific and also pre- and postmenopausal differences in the occurrence of CAD.

1. The intended fusion of the university hospitals Marburg and Giessen in the state of Hessia is "a marriage under pressure with uncalculated risk" (Spiegel 2005). In the present political and financial situation it hardly appears to be avoidable. From the point of the view of the faculty of medicine in Marburg it is difficult to understand, that the profits of this well guided university hospital with a positive yearly budget should go to the neighboring university hospital which still had a fair amount of deficit spending in the last years.2. Both medical faculties suffer from a very low budget from the state of Hessia for research and teaching. Giessen much more than Marburg, have a substantial need for investments in buildings and infrastructure. Both institutions have a similar need for investments in costly medical apparatuses. This is a problem, which many university hospitals face nowadays.3. The intended privatisation of one or both university hospitals will need sound answers to several fundamental questions and problems:a) A privatisation potentially endangers the freedom of research and teaching garanteed by the German constitution. A private company will undoubtedly influence by active or missing additional support the direction of research in the respective academic institution. An example is the priorisation of clinical in contrast to basic research.b) With the privatisation practical absurdities in the separation of research and teaching on one side and hospital care on the other will become obvious with respect to the status of the academic employees, the obligatory taxation (16%) when a transfer of labor from one institution to the other is taken into account. The use of rooms for seminars, lectures and bedside with a double function for both teaching, research and hospital care has to be clarified with a convincing solution in everyday practice.c) The potential additional acquisition of patients, which has been advocated by the Hessian state government, may be unrealistic, when the 4th biggest university hospital in Germany will be created by the merger. University hospitals recrute the patients for high end medicine beyond their region because of the specialized academic competence and advanced technical possibilities. Additional recruitment of patients for routine hospital can hardly be expected.d) A private management will have to consider primarily the "shareholder value", even when investing in infrastructure and buildings, as it can be expected for one partner. On the longterm this will not be possible without a substantial reduction of employees in both institutions. There are, however, also substantial efforts of some private hospital chains in clinical research, e. g. by Helios in Berlin and Rhön Gmbh at the Leipzig Heart Center.e) There is a yet underestimated but very substantial risk because of the taxation for the private owner when academic staff is transferred from the university to hospital care in their dual function as academic teachers and doctors. This risk also applies for the university if the transfer should come from hospital to the university. These costs would add to the financial burden, which has to be carried in addition to the DRGs.

Sudden cardiac death of suspected healthy young athletes is a rare, but deeply moving event. Usually, the affected person has been completely free of symptoms. Commonly, unrecognized inflammatory, hypertrophic or dilated cardiomyopathies are the most frequent causes. All therapeutic principles of angiotensin-converting-enzyme (ACE) inhibition, beta-blockade, and diuretics in heart failure aim to unload the heart. During physical activity increased sympathetic tonus and loading conditions for the heart point into the opposite direction. This raises the question to what extent physical activity in patients with myocarditis, dilated cardiomyopathy or heart failure in general is tolerable.Several experimental studies revealed disadvantages of physical exercise during acute myocarditis leading to an increase in mortality. On the other hand, several small trials in men demonstrate an improvement of physical fitness and quality of life attributed to controlled supervised exercise training in patients with heart failure without assessment of mortality. Dilated cardiomyopathy was diagnosed in one third of these patients. There was no biopsy confirmation of these conditions. The other two thirds of patients suffered from ischemic heart diseases.Since the borderline between inflammatory heart disease and noninflammatory or postinflammatory dilated cardiomyopathy is difficult to determine, abstention from physical training during and shortly after inflammatory heart disease is recommended, because it is known that viral persistence or autoimmune processes could last for several months.

Indications and diagnostic value of the most important noninvasive procedures for the diagnosis of peripheral arterial disease and diseases of the supraaortic arteries are reviewed in this article with particular emphasis on cardiologic questions.As compared to coronary artery disease, peripheral arterial disease has long been addressed as being negligible in number and importance, a view that had to be reassessed in recent years. The prevalence of claudication and critical leg ischemia has increased. Earlier diagnosis and specific therapeutic regimens will be able to prevent or at least slow progression of the disease and, thereby, major amputation. The patient's history and physical examination in addition to measurement of the ankle-brachial index (ABI; determined by dividing the systolic pressure measured by Doppler ultrasonography of the A. dorsalis pedis or A. tibialis posterior by that of the A. brachialis) usually allows for the diagnosis of peripheral arterial disease (ABI0.9). If in doubt (ABI0.9, but presence of typical claudication), a treadmill test or additional tests such as pressure-pulse recording (mechanical oscillography), toe pressure measurements, or duplex ultrasonography should be performed. When peripheral arterial disease has been diagnosed, duplex ultrasonography or treadmill testing aids in planning additional diagnostic procedures and the adequate therapeutic regimen. Transcutaneous oxymetry is of prognostic value in assessing the tendency of wound healing in distal limb ulceration and can distinguish between critical limb ischemia and complicated claudication. Thermography is used to document functional and organic peripheral arterial occlusions and capillaroscopy to directly view nail fold capillaries in order to distinguish between primary and secondary Raynaud's phenomenon. Noninvasive radiologic techniques in the diagnosis of peripheral arterial disease are also discussed in this journal.Noninvasive diagnostic procedures in assessing disease of the supraaortic arteries include history-taking, physical examination, continuous-wave-(cw-)Doppler and color-coded ultrasonography. Cw-Doppler ultrasonography is still widely used and sufficient in diagnosing moderate to severe stenosis or occlusion of the carotid artery. B-mode and color-coded ultrasonography has several advantages over cw-Doppler ultrasonography through direct visualization of the vascular membrane, perivascular structures, and intravascular blood flow. Carotid stenosis50% and plaque morphology can be assessed, inflammatory processes, aneurysms, and dissections diagnosed. Increase in intima-media thickness and echolucent plaques are associated with cerebral ischemic events and can be diagnosed via duplex sonography. These findings have great implications in the consultation of patients with atherogenic risk factors.

BACKGROUND AND THERAPY: The metabolic syndrome comprises a virulent and lethal group of atherosclerotic risk factors, including dyslipidemia, obesity, systemic hypertension and insulin resistance. The prevalence of the metabolic syndrome has continuously grown in industrialized and developing countries during the last decades, and affects tens of millions of people in Germany and Europe. Particularly prominent as a risk factor for the development of insulin resistance is central obesity, which is causally involved in the pathogenesis of insulin resistance in addition to genetic predisposition. The metabolic syndrome can easily be diagnosed in clinical practice (guidelines of the WHO and ATP III panel), and immediate treatment of the metabolic syndrome is mandatory because those patients are at increased risk to develop overt diabetes mellitus, coronary artery disease and stroke. The high risk for cardiovascular diseases is supported by findings that the risk for myocardial infarction in patients with insulin resistance is as high as the risk of patients after their first myocardial infarction. Intentional weight reduction reduces abdominal obesity and beneficially modulates all features of the metabolic syndrome, while the benefits of aerobic exercise training are discussed controversially. Thus, weight reduction causally undoes essential features of the metabolic syndrome, but effects are often not enduring. Therefore, the treatment of cardiovascular risk factors such as hypertension and dislipidemia is essential. Of note, antihypertensive treatment is more effective than tight glucose control to reduce cardiovascular events. Diuretics, ACE-inhibitors and angiotensin II type 1 receptor antagonists are suggested as first line therapeutics. However, at least two antihypertensives are usually necessary to achieve the suggested goals of blood pressure reduction. In conclusion, the prevalence of the metabolic syndrome is continuously growing. Due to its adverse impact on cardiovascular disease, early detection and aggressive treatment is mandatory to ensure longlasting benefits for affected patients.

A 24-year-old woman in her 13th gestational was admitted to our department with acute retrosternal and epigastric pain. She had been transferred from the gynecologic department where she was treated for vaginal bleeding because of abortus imminens. A cardiac cause was excluded by ECG and echo. Clinical chemistry and abdominal ultrasound confirmed the diagnosis of acute pancreatitis. The woman was known in our outpatient department for hyperchylomicronemia and had already had an earlier episode of acute pancreatitis under oral contraception years ago. At current admission, triglycerides were 11,500 mg/dl. To reduce plasma triglycerides, selective lipid apheresis was performed. Apheresis was well tolerated, and the patient became free of pain within the first 30 min of treatment. Triglycerides decreased to 6,600 mg/dl at this session. Keeping to a low-fat diet (30 g fat per day), the patient remained healthy and completed pregnancy with the delivery of a healthy girl in her 39th week of pregnancy.Selective lipid apheresis is a safe and effective option in the treatment of hyperlipidemic pancreatitis, even in pregnant patients.

This overview on the topic of cardiomyopathy and gestation comprises the diagnostic and therapeutic options of patients with preexistent cardiomyopathies (dilated, hypertrophic, inflammatory, and others) and with cardiomyopathies which have been discovered during or in the 6 months following delivery. CARDIOMYOPATHIES PREEXISTENT BEFORE GESTATION: If cardiomyopathy is present before an intended gestation, the couple should be advised against pregnancy because of the high risk of deterioration both during gestation and peripartum. If pregnancy occurs, according to ESC (European Society of Cardiology) recommendations termination should be advised if the ejection fraction is50% and/or the LV dimensions are definitely above normal. If termination is refused, the patient must be checked regularly by both gynecologist and cardiologist, by the latter to perform regular echocardiograms. Termination is not recommended for the hypertrophic (nonobstructive) cardiomyopathies. If atrial fibrillation occurs, anticoagulation with low molecular weight heparin and digoxin and/or Betablockers are recommended for rhythm and rate control. PERIPARTUM CARDIOMYOPATHIES: In peripartum cardiomyopathies, which are discovered clinically postpartum, inflammation of the myocardium sometimes associated with pericarditis is frequently found. For those patients, we recommend heart catheterization with endomyocardial biopsy to allow for the exact diagnosis of the underlying cardiac process (inflammatory and/or viral vs autoreactive myocarditis or noninflammatory or nonviral [= idiopathic] forms). This diagnostic algorithm, which we recommend for any form of dilated cardiomyopathy, bears impact on treatment options beyond the mere heart failure therapy that should be instigated anyhow.

Drugs for counteracting the neuroendocrine activation in heart failure can reduce the adverse remodelling of the extracellular matrix of the heart. Progression of heart failure can, however, often not be prevented and the question arises whether important pharmacological targets remain unidentified. Promising are drugs targeted at ventricular diastolic dysfunction which is a marker of early progression of heart failure.Left ventricular dysfunction is characteristic of overloaded hypertrophied hearts with molecular structures that are not adapted to the increased Ca2+ diffusion distances. Thus, the Ca(2+)-pump (SERCA2) of sarcoplasmic reticulum is inadequately expressed leading to a reduced force development and relaxation of hypertrophied cardiomyocytes.Drugs in development (CPT-1 inhibitor/PPARalpha activator) that increase glucose oxidation can enhance SERCA2 expression. The lead compound etomoxir had a selective influence on the contraction and relaxation rate of pressure-overloaded hearts. The functional parameters were correlated with the proportion of alpha-myosin heavy chains. Since viral or inflammatory injury of the heart can also induce a fetal phenotype, metabolic modulators such as etomoxir represent a promising therapeutic approach also for cardiomyopathies with inadequate SERCA2 expression.

All forms of chronic heart failure (high-output and low-output failure) are accompanied by an "arterial underfilling" inducing the activation of various neurohumoral systems (renin-angiotensin-aldosterone system, sympathic nervous system, non-osmotic stimulation of vasopressin). Elevated levels of those neurohormones detrimentally modulate renal function. Subsequently, renal salt and volume retention occurs leading to the main symptoms of heart failure, edema formation and dyspnea.Diuretics, which have been discovered more than 40 years ago, beneficially influence renal salt- and volume retention by their effects on tubular sodium reabsorption. While thiazides are recommended in mild forms, loop diuretics are used in severe stages of congestive heart failure. The clinician has to consider the changed pharmacokinetic and -dynamic properties during the application of diuretics in patients with chronic heart failure. In addition, increased sodium reabsorption occurs immediately after cessation of diuretic action often nullifying the preceding diuresis. Thus, salt- and volume restriction should be guaranteed, and a regular application of loop diuretics during the day should be preferred due to the short-acting nature of currently available loop diuretics. Sometimes, diuresis does not longer occur during the treatment with one substance (diuretic resistance), although the therapeutic goals of water excretion have not been achieved. After ruling out factors reducing the actions of diuretics (non-compliance, hyponatremia, etc.), a sequential nephron blockade should be initiated (combination of loop diuretics and a thiazide or an aldosterone-receptor antagonist) to increase diuresis and to elevate symptoms of volume overload.Loop diuretics and thiazides often induce mild hypokalemia, which has been demonstrated to be not as benign as thought before. Chronic treatment with oral potassium supplements has several drawbacks, as urine excretion of potassium is subsequently increased and supplementation is not as effective as believed. Diuretic-induced hypokalemia seems to be aldosterone dependent. As aldosterone levels increase during diuretic therapy even during chronic treatment with an angiotensin-converting enzyme (aldosterone-escape) a combined treatment including an aldosterone-receptor antagonist has been suggested. Beneficial effects of aldosterone-receptor blockade on mortality (RALES trial) appear to be mediated be extrarenal and renal mechanisms. The suggested beneficial renal mechanisms of aldosterone receptor blockade are discussed in detail in the review.In conclusion, diuretic therapy of patients with congestive heart failure is effective to relieve symptoms and, presumably, to prolong life. As renal function and pharmacokinetics and -dynamics of diuretics are changed in heart failure, diuretic treatment has to be adapted to provide optimal treatment. Increased levels of aldosterone appear to play an important role in diuretic-induced hypokalemia, and in the progression of heart and renal failure. Thus, aldosterone receptor antagonists should be used in the treatment of heart failure more frequently.

Artificial bradycardias due to tape-running alterations of old long-term ECG recorders were observed with increasing frequency in the last 2 years at our hospital. To document the extent of this problem, 115 consecutive 24-hour long-term ECG recordings of 10 still used tape recorders with an age of 12 +/- 4 years were examined. Analysis of the tapes with a new analysis system revealed artificial bradycardias with rates of 10 to 40/min in 22 of 115 long-term ECG recordings (19%). These artificial bradycardias were observed in 4 out of 10 examined tape recorders (40%). Three of 4 concerned recorders were 14 years old at the time of examination, and one recorder was only 5 years old. Artificial bradycardias were caused by extensive alterations of tape-running speed in all cases. Diagnostic proof of artificial bradycardias due to tape running alterations on long-term ECG are simultaneous with prolonged RR-intervals occurring increases in all ECG times including P-width. PQ-time, QRS-width and QT-duration with otherwise unchanged ECG morphology. To avoid prolonged hospital stays or therapeutic mistakes like unnecessary pacemaker implantation, especially older long-term ECG-tape recorders should be checked regularly and, if necessary, be replaced by new devices.

Isolation of microorgaisms from blood cultures is the classic diagnostic value of infective endocarditis.The rates of positive blood cultures has dercreased in the past few decades.Premature antibiotic treatment is responsible for the inability to isolate microorganisms from blood cultures.Therefore,the course of proinflammatory cytokines IL-6 and IL-2 receptor was analyzed during treatment of 55 Patients with infective endocarditis., Die infektiöse Endokarditis ist eine Erkrankung des Herzens,die trotz des Fortschritts in der Diagnostik und Therapie immer noch eine ernste Prognose hat.Da der Anteil der positiven Blutkulturen in den letzten Jahren zurückgegangen ist,sind zusätzliche Kriterien sowohl in der Diagnostik als auch in der Therapie notwendig.In der vorliegenden Arbeit wurden neben den üblichen Entzündungsparameter,wie Leukozyten und CRP,die Cytokine IL-6 und IL-2 Rezeptor bestimmt.