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Evidence in cardiovascular patient care is currently skewed to the disadvantage of women. This article provides a summary of the current state of knowledge on gender differences with a special focus on the epidemiology, pathophysiology, risk factors and treatment of the most frequent cardiovascular diseases.Evaluation and discussion of background research and expert recommendations.The necessity for a gender-specific analysis of results is a relatively recent development in clinical trials. There is increasing evidence for pathogenic mechanisms specific for women as well as pharmacodynamic and pharmacokinetic differences between women and men. Women are currently less likely to receive treatment for cardiac diseases according to medical guidelines than men.For improvement of the treatment options and effective disease prevention, it is pivotal to investigate pathogenetic mechanisms specific to women.HINTERGRUND: Es besteht ein Evidenzgefälle zwischen den Geschlechtern in der kardiovaskulären Versorgung zuungunsten der Frau. Der vorliegende Beitrag bietet eine Zusammenfassung des Wissensstands über die Geschlechterunterschiede mit besonderem Fokus auf Epidemiologie, Pathophysiologie, Risikofaktoren und Therapie der häufigsten kardialen Erkrankungen.Auswertung und Diskussion von Grundlagenarbeiten und Expertenempfehlungen.Erst jüngere Studien berücksichtigen die Notwendigkeit, die Ergebnisse geschlechtergetrennt zu analysieren. Es bestehen Hinweise sowohl auf frauenspezifische pathogenetische Mechanismen als auch auf pharmakodynamische und pharmakokinetische Unterschiede zwischen Frauen und Männern. Derzeit erhalten Frauen seltener als Männer eine leitliniengerechte Therapie ihrer Herzerkrankung.Die weitere Klärung frauenspezifischer pathogenetischer Mechanismen ist eine wichtige Grundlage für eine effektivere Prävention und eine verbesserte Behandlungsoption.

Rare diseases mostly have a genetic cause. Many rare cardiovascular diseases also have a genetic cause. For target-oriented cardiogenetic diagnostics, expert knowledge in human genetics as well as in clinical cardiology is needed. In recent years, the genetic cause of a number of heart diseases have been, at least in part, elucidated. Especially, certain arrhythmias and cardiomyopathy forms have a monogenetic cause. An early genetic diagnosis means that patients can be treated more effectively. Rare storage diseases also usually have a genetic cause and can manifest themselves in the heart; prominent examples are Fabry disease and amyloidosis. As patients with Fabry disease or amyloidosis suffer from a diverse and variable symptomatology, the correct diagnosis is often difficult.

Iron deficiency is a diagnostic and therapy-requiring comorbidity in heart failure with a negative impact on the prognosis. Even without signs of anemia, iron deficiency can lead to reduced performance with physical weakness and dyspnoea in patients with chronic heart failure.Well-known cardiologists discussed this at an expert meeting on the topic of iron deficiency in heart failure.Despite the high relevance for patients' outcome, this complication is still under-addressed, although specific diagnosis and effective therapy are possible and are also recommended in current ESC guidelines. A new evidence-tested algorithm should now help to facilitate diagnosis and therapy in everyday practice. The prerequisite is that it can be well integrated into clinical routine.

"Klug entscheiden" (Choosing Wisely) is an initiative launched by the German Society for Internal Medicine (DGIM) to boost the quality of medical indication by identifying both medical/therapeutic over- and underuse. Twelve specialist societies for internal medicine and DGIM associated societies develop corresponding recommendations which are subsequently evaluated and rejected or approved in a structured procedure by a multidisciplinary commission. Since 2016, 115 positive and negative recommendations have been developed and released for print media, radio and television. Physicians can obtain the DGIM/BDI* certificate "Klug entscheiden". First steps have been undertaken to implement "Klug entscheiden" in medical education. The wide dissemination and intense discussions give a reason to hope that positive and negative recommendations will be put into practice and that the awareness towards the relevance of the quality of medical indication will grow. And finally, specific recommendations are to be developed the implementation of which can be evaluated prospectively. * Professional organization of German specialists for internal medicine.

Cardiomyopathies often have a genetic etiology. New genetic diagnostic strategies based on next generation sequencing (NGS)-approaches will continuously increase our knowledge about the genetic basis of cardiomyopathies within the following years. Diagnostics and therapy of rare, genetically-induced cardiac diseases increasingly require special cardiac and genetic knowledge. Interestingly, mutations in the same gene or even identical gene mutations can be associated with different cardiomyopathy phenotypes and can exhibit incomplete penetrance or variable expressivity. In the future, the correct interpretation and classification of novel gene variants identified in patients with inherited cardiomyopathy forms will represent a great challenge. Genetic counselling and - if appropriate - subsequent genetic testing for cardiomyopathy patients and their asymptomatic relatives is essential for an early diagnosis of the disease, a prognostic evaluation and possibly for the start of preventive or therapeutic measures.

Iron deficiency (ID) occurs in up to 50% of patients with heart failure (HF). Even without presence of anaemia ID contributes to more severe symptoms, increased hospitalization and mortality. A number of randomized controlled trials demonstrated the clinical benefit of replenishment of iron stores with improvement of symptoms and fewer hospitalizations. Assessment of iron status should therefore become routine assessment in newly diagnosed and in symptomatic patients with HF. ID can be identified with simple and straightforward diagnostic steps. Assessment of Ferritin (indicating iron stores) and transferrin saturation (TSAT, indication capability to mobilise internal iron stores) are sufficient to detect ID. In this review a plain diagnostic algorithm for ID is suggested. Confounding factors for diagnosis and adequate treatment of ID in HF are discussed. A regular workup for iron deficiency parameters may benefit patients with heart failure by providing symptomatic improvements and fewer hospitalizations.

The role of biomarkers in asymptomatic diastolic dysfunction (DD) has not been investigated so far. The aim of the study was to evaluate the clinical associations and the diagnostic property of different biomarkers in patients with asymptomatic DD.Within a population based observational study, healthy participants (50-85 years) with an LVEF ≥ 50 % and no cardiovascular risk factor were prospectively identified. Patients were classified as having either DD (grade ≥ 1, n = 103) or no DD (CON: n = 85). All patients underwent physical examination including medical history, six-minute-walk-testing, QoL (SF-36), comprehensive echocardiography and blood sampling to measure routine values and specified biomarkers (NTproBNP, MRproANP, GDF-15, MRproADM, CTproET1, CTproAVP).In the DD-group plasma concentration of GDF-15 (p = 0,002), MRproADM (p 0,001), and CTproAVP (p = 0,003) were significantly higher than in the CON-group. In contrast, NTproBNP (p = 0,390), MRproANP (p = 287), and CTproET1 (p = 0,393) did not differ. GDF-15, MRproADM and CTproAVP were significantly associated with the presence of DD. However, the significance of the seen associations was lost after multiple adjustments. NTproBNP, MRproANP, and MRproADM were significantly related to E / e' as a continuous measure of diastolic function. The significance of the seen associations was lost after multiple adjustments. In ROC analyses, none of the investigated biomarkers was able to relevantly improve the diagnosis of DD.In patients with asymptomatic DD plasma concentrations of GDF-15, MRproADM and CT-proAVP were significantly higher when compared with controls. In contrast, NTproBNP, MRproANP and CTproET1 did not differ. After adjustment for age, sex, BMI and renal function, no significant association between DD or E / e' and different biomarkers could be observed. Furthermore, none of the investigated biomarkers was able to substantially improve the diagnosis of DD.

The case of a 46-year-old male with progressive dyspnea on exertion and severe headache while having the head lowered is described. Clinically, the patient showed left-sided pleural effusion, jugular venous distension, and a congested liver. During cardiologic work-up, echocardiography, combined left/right heart catherization and magnetic resonance imaging established the diagnosis of constrictive pericarditis. Under conservative medical treatment, the patient again developed cardiac decompensation and, therefore, a pericardectomy was performed. Immediately after surgery, symptoms diminished and exercise tolerance increased. The patient is currently in cardiac rehabilitation.Constrictive pericarditis is a rare differential diagnosis of right heart failure. Especially in patients with congested inferior vena cava, but normal systolic left ventricular function and normal function of the cardiac valves, constrictive pericarditis should be considered as a differential diagnosis.

High doses of proton pump inhibitors like pantoprazole (PP) are used in treatment of acid-related gastrointestinal diseases. Here, we investigated the effects of pantoprazole on cardiac function.

30-50% of patients presenting with symptoms of congestive heart failure exhibit a near normal left ventricular systolic function at rest, and an impaired diastolic function of the heart may be causative. Despite a better prognosis than in systolic heart failure, frequency of hospitalizations due to diastolic heart failure is comparable with systolic heart failure. According to the criteria of Vasan and Levy diagnosis of diastolic heart failure is probable, if symptoms and signs of heart failure are accompanied in proximity (within 72 h) by objective evidence of normal left ventricular systolic function. Newer echocardiographic techniques (e. g., tissue Doppler) aid to confirm the diagnosis and to determine the severity of dysfunction and may substitute invasive demonstration of impaired left ventricular relaxation, filling, compliance or stiffness for standardized diagnosis. Incorporation of biochemical test (BNP [brain natriuretic peptide]) allows differential diagnosis and may increase the accuracy of diagnosis. Due to inconsistent diagnostic criteria, data from prospective randomized controlled trials for the treatment of diastolic heart failure are rare. Basic principles include treatment of the underlying disease, i. e., control of hypertension, diabetes, or obstructive airway disease. Angiotensin 1 antagonists (ARB) have proven effective in regression of left ventricular hypertrophy (LIFE) and may reduce morbidity, but not mortality (CHARM). Maintenance of sinus rhythm, heart rate control (beta-blockers, calcium channel blockers) and anti-ischemic therapy may be indicated in view of pathophysiological aspects. Diuretics should be administered with caution in patients with symptoms of congestion, digitalis is not useful in the treatment of isolated diastolic heart failure. The results of ongoing trials (e. g., I-Preserve) may offer new therapeutic options, and evidence-based guidelines for the so far often unsatisfactory treatment of diastolic dysfunction/heart failure are awaited.