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Aims Coronary artery disease (CAD) remains the leading cause of death worldwide. ‘Stable’ CAD is a chronic progressive condition, which recent European guidelines recommend referring to as ‘chronic coronary syndrome’ (CCS). Despite therapeutic advances, morbidity and mortality among patients with CCS remain high. Optimal secondary prevention in patients with CCS includes optimization of modifiable risk factors with behavioural changes and pharmacological therapy. The CHANGE study aims to provide evidence for optimization of secondary prevention in CCS patients by using a smartphone application (app). Methods and results The CHANGE study is designed as a prospective, randomized, controlled trial with a 1:1 allocation ratio, which is currently performed in nine centres in Germany in a parallel group design. 210 patients with CCS will be randomly allocated either to the control group (standard-of-care) or to the intervention group, who will be provided the VantisTherapy* app in addition to standard-of-care to incorporate secondary prevention into their daily life. The study will be performed in an open design. Outcomes will be assessed using objective data from three in-person visits (0, 12, and 24 weeks). Primary outcomes will involve adherence to secondary prevention recommendations and quality of life (QoL). The recruitment process started in July 2022. Conclusion The CHANGE study will investigate whether a smartphone-guided secondary prevention app, combined with a monitor function compared with standard-of-care, has beneficial effects on overall adherence to secondary prevention guidelines and QoL in patients with CCS. Trial registration The study is listed at the German study registry (DRKS) under the registered number DRKS00028081.

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): UiT The Arctic University of Norway, Northern Norway Regional Health Authority. Background/Introduction Machine learning models have been applied to magnetic resonance images of the brain to estimate brain age gap as a biomarker of biological aging. Because of its association with cognitive performance and neurological disorders, brain age gap has become an indicator of general brain health. Among others, cardiovascular risk factors are associated with brain health. Recently a novel non-invasive biomarker of vascular ageing has been proposed based on the application of a deep-learning algorithm to digitised 12-lead electrocardiograms. The difference between electrocardiogram predicted age and chronological age is defined as vascular age gap and has been shown to be associated with an adverse cardiovascular profile. However, the association of vascular age gap with cognitive health and dementias has not yet been examined. Purpose We apply a causal mediation framework to vascular age gap, brain age gap and cognitive function data obtained in the same individuals who took part in a population-based study in Norway. We hypothesise that cardiovascular risk factors encapsulated in vascular age gap can indirectly affect cognitive function by increasing the brain age gap. Methods We applied a deep learning algorithm (1) to electrocardiograms (N=7779, age 40-85 years) collected from the population-based sample in Norway (mean age 63.8 years, 45.3% men) to obtain a vascular age gap. For a subsample (N=1693) magnetic resonance images of the brain were also available and another deep neural network algorithm (2) was applied to obtain a biomarker of brain age. For 1678 participants with both vascular age gap and brain age gap available we used mediation analysis to test whether brain age gap mediates the effects of vascular age gap on cognitive function (as measured by mini mental status test, word memory test, digit–symbol coding test, tapping test) by estimating total, direct and indirect effects. Results We found a weak correlation (Pearson’s r = 0.12) between vascular age gap and brain age gap. Both age gaps were associated with cognitive scores capturing psychomotor speed, attention and mental flexibility. For a 1 standard deviation (7.3 years) increase in vascular age gap digit-symbol coding test score decreased by 0.63 (95%CI: -0.89, -0.36; p Conclusion(s) Vascular age gap was weakly associated with poorer cognitive functioning, and only 13% of this association was mediated by brain age gap. This suggests that cognitive decline linked to accumulated damage of the vascular system is not fully captured by structural changes in the brain. Further investigations of novel measures of biological aging in relation to cognitive decline are warranted as these may hold promise for improved understanding of mechanisms and clinical prediction.

Background Since kidney transplant recipients (KTRs) have a high cardiovascular disease burden, adequate risk prediction is of importance. Whether echocardiographic parameters and plasma biomarkers, natriuretic peptides [N-terminal pro-B-type natriuretic peptide (NT-proBNP)] and troponin T provide complementary or overlapping prognostic information on cardiovascular events remains uncertain. Methods The prospective Heterogeneity of Monocytes and Echocardiography Among Allograft Recipients in Nephrology (HOME ALONE) study followed 177 KTRs for 5.4 ± 1.7 years. Predefined endpoints were hospitalization for acute decompensated heart failure or all-cause death (HF/D) and major atherosclerotic cardiovascular events or all-cause death (MACE/D). At baseline, plasma NT-proBNP, plasma troponin T and echocardiographic parameters [left atrial volume index, left ventricular (LV) mass index, LV ejection fraction, and LV filling pressure] were assessed. Results Among all echocardiographic and plasma biomarkers measured, only NT-proBNP was consistently associated with HF/D in univariate and multivariate {third versus first tertile: hazard ratio [HR] 4.20 [95% confidence interval (CI) 1.02–17.27]} analysis, and only troponin T was consistently associated with MACE/D in univariate and multivariate [third versus first tertile: HR 8.15 (95% CI 2.75–24.18)] analysis. Conclusion Our data suggest that plasma biomarkers are robust and independent predictors of heart failure and atherosclerotic cardiovascular events after kidney transplantation, whereas standard echocardiographic follow-up does not add to risk prediction.

ZUSAMMENFASSUNGBei Patienten mit Vorhofflimmern besteht ein erhöhtes Risiko für thromboembolische Komplikationen und insbesondere Schlaganfall. Patienten mit chronischer Nierenerkrankung haben gehäuft Vorhofflimmern und sowohl ein erhöhtes Blutungs- wie auch Schlaganfallrisiko. Für Patienten mit einer Kreatinin-Clearance von bis zu 25–30 ml/min sind Nicht-Vitamin-K-abhängige orale Antikoagulanzien (NOAK) evidenzbasiert zur Schlaganfallprävention den Vitamin-K-Antagonisten (VKA) vorzuziehen. Darunter bzw. bei Dialysepatienten liegen keine wissenschaftlichen Daten vor; hier muss das Konzept (keine Antikoagulation vs. NOAK vs. Vorhofohrverschluss vs. VKA) individuell entschieden werden, wobei die Gabe von VKA die schlechteste Lösung zu sein scheint.

Background In patients with heart failure (HF) and reduced ejection fraction, Sacubitril/Valsartan (S/V) reduces the risk for death and hospitalisations. However, the underlying mechanism for these beneficial effects of S/V, is still lacking. Methods Consecutive patients with symptomatic HF and LV ejection fraction (EF) ≤40% who were assigned to S/V were prospectively included in this study (n=117). Non-invasive pressure volume loops were obtained from echocardiography with simultaneous arm-cuff blood pressure measurement. By this method, LV end-systolic elastance (Ees), effective arterial elastance (Ea) and ventricular-arterial coupling (Ea/Ees) were calculated. LV end-diastolic pressure was derived from the E/e' ratio. This is a prespecified interim analysis of 50 patients with completed 6 months of follow-up. The study is registered with ClinicalTrials.gov, NCT04498780. Results Mean age was 61.8±18.6 years and 12 (24%) patients were females. Ischaemic heart failure was present in 22 (44%), non-ischaemic aetiology in 24 (48%), and myocarditis in 4 (8%) patients. 34 (68%) patients were on the target dose of S/V after 6 months of treatment. At 6 months, LV end-diastolic volume (110±28 ml/m2 vs. 87±31 ml/m2, p Conclusion After 6 months of treatment with Sacubitril/Valsartan, LV remodelling and reduced LV filling pressures were observed. These changes were associated with improvements in functional capacity, natriuretic peptide levels and NYHA functional class. Thus, the study provides important mechanistic insides into the hemodynamics of angiotensin–neprilysin inhibition in heart failure which might help to individualize therapy. Funding Acknowledgement Type of funding sources: None.

Background Hospitalization for heart failure (HF) is associated with a high risk of in-hospital mortality, but also poor long-term outcomes. Although most hospital systems aim to admit patients with HF to cardiology departments, a significant proportion is admitted to other internal medicine departments due to shortages of beds and limited resources. The prognostic importance of being admitted to different departments is unknown. Purpose To compare the long-term mortality rate in patients admitted to hospital with a first diagnosis for HF to a cardiology department versus other internal medicine departments at a large academic hospital in Norway with a catchment area of 560,000 individuals. Methods Adult patients with a first ICD-10 diagnosis of HF (I11.0, I13.0, I13.2, I42.x, I50.x) admitted to an internal medicine department at our University Hospital between 2011 and 2019 were included. All-cause mortality was obtained from the Norwegian Cause of death registry until December 31, 2021. Results In total, we included 7,692 patients aged 76.1±13.0 years, of whom 46.0% were women, 57.4% had hypertension, 24.1% diabetes, 47.0% established coronary artery disease (CAD) and 36.0% a previous acute myocardial infarction (AMI). Of these, 50.7% were admitted to the cardiology department, 13.5% to the pulmonary department, 7.6% to the infectious disease department and the rest to other internal medicine departments. Patients admitted to the cardiology department were younger and more frequently men with established heart disease. They were more frequently examined with echocardiography during the first 30 days after admission, but had comparable levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) to those admitted to other departments (Table 1). During mean 5.9 years of follow-up, 56.6% of patients died. Patients admitted to the cardiology department had 37% lower mortality risk compared to other departments (HR 0.63 [95% CI 0.59–0.66], p Conclusion Admission to a cardiology department with HF is associated with better long-term outcomes compared to admission to other internal medicine departments. These findings support health care policy efforts to expand capacity at cardiology departments to allow best care for these vulnerable patients. Funding Acknowledgement Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): This study was in part funded by research grants from Novartis.

Understanding the (patho-)physiology of volume regulation and osmoregulation is fundamental to guide patient advice and therapy in chronic kidney disease (CKD). Volume regulation primarily impacts the amount of sodium in the body, and it mainly affects the extracellular space, while osmoregulation primarily impacts the amount of free water, and it affects both the intra- and extracellular space. The kidneys control water and sodium homeostasis both through their sensor (e. g. tubuloglomerular feedback) and regulator systems (e. g. sodium reabsorption). Many CKD patients are advised by non-nephrologists to a high fluid intake, although they often do not require a daily intake of more than 1.5 litres. Many CKD patients are hypervolemic, and sodium restriction is of key importance in patients' effort to utilize lifestyle changes as therapeutic means. Pharmacologically, (particularly loop) diuretics are the basis of therapy, increasing sodium excretion. Recent developments shift the focus towards classes of drugs ameliorating prognosis in CKD: sodium-glucose linked transporter 2 (SGLT2) inhibitors have proven beneficial in heart and renal failure - by sodium and fluid excretion, among others; additionally, a novel mineralocorticoid receptor antagonist (MRA), finerenone, was recently shown to improve prognosis in CKD.

Was ist neu? Impfstoffe Innerhalb von nur 15 Monaten nach Beginn der COVID-19-Pandemie stehen bereits mehrere SARS-CoV-2-Impfstoffe zum klinischen Einsatz bereit. Während das Zielmolekül aller prädominierenden Vakzine das Spike-Protein von SARS-CoV-2 ist, lassen sie sich anhand ihres Wirkprinzip in mRNA-basierte, Vektor-basierte und Protein-basierte Impfstoffe unterscheiden. Bedeutung für chronisch nierenkranke Menschen Das Aussprechen von Empfehlungen für chronisch nierenkranke Menschen ist aufgrund deren geringer Repräsentation in den Zulassungsstudien erschwert – wie bei anderen Patienten mit schwerer Komorbidität. Aufgrund von urämischem Immundefekt und/oder medikamentöser Immunsuppression könnte die Effektivität der Impfung im Einzelfall relativ vermindert sein. Dennoch profitieren vermutlich gerade diese Patienten von einer Impfung, da sie ein erhöhtes Risiko für einen schweren oder gar tödlichen COVID-19-Verlauf aufweisen.

Lowering of low-density lipoprotein (LDL) cholesterol represents one of the most effective interventions in cardiovascular prevention. Besides the oral treatment with statins, ezetimibe and bempedoic acid, subcutaneously administered inhibitors of proprotein convertase subtilisin-kexin type 9 (PCSK9) have been established as further cornerstones of lipid-lowering treatment. The antibodies evolocumab and alirocumab are administered subcutaneously every 2-4 weeks and lower LDL cholesterol by around 60%, independent of pre-treatment with very good tolerability. Both drugs successfully reduced cardiovascular endpoints in large outcome trials. A novel principle of PCSK9 inhibition is RNA interference, which is exploited by the novel compound inclisiran. Inclisiran is a double-stranded modified RNA molecule, which neutralizes the mRNA of PCSK9 and thus inhibits PCSK9 protein synthesis intracellularly. Inclisiran only needs to be administered every 6 months. The cardiovascular outcome trial ORION‑4 is currently ongoing. In Germany, prescription of PCSK9 inhibitors is regulated by the decision of the Federal Joint Committee. Novel strategies to inhibit PCSK9 function are under development and include orally available drugs and animal experiment concepts on gene editing, which are in different states of evaluation.Die therapeutische Senkung des LDL(„low-density lipoprotein“)-Cholesterins ist einer der effektivsten Maßnahmen in der kardiovaskulären Prävention. Neben der oralen Therapie mit Statinen, Ezetimib und Bempedoinsäure haben sich subkutan applizierte Inhibitoren der Proproteinkonvertase Subtilisin/Kexin Typ 9 (PCSK9) als weitere Säule der lipidsenkenden Therapie etabliert. Die alle 2 bis 4 Wochen subkutan zu verabreichenden Antikörper Evolocumab und Alirocumab senken das LDL-Cholesterin unabhängig von der Vorbehandlung um rund 60 % bei sehr guter Verträglichkeit. Für beide Wirkstoffe liegen positive Endpunktstudien vor. Ein neues Prinzip zur PCSK9-Inhibition ist die RNA-Interferenz, welche mit dem Wirkstoff Inclisiran genutzt wird. Bei Inclisiran handelt es sich um ein doppelsträngiges modifiziertes RNA-Molekül, welches die mRNA von PCSK9 neutralisiert und damit die PCSK9-Proteinsynthese intrazellulär hemmt. Inclisiran muss nur halbjährlich appliziert werden. Die Endpunktstudie ORION‑4 läuft gegenwärtig. Die Verschreibung von PCSK9-Hemmern ist in Deutschland durch einen Beschluss des Gemeinsamen Bundesausschusses reglementiert. Neue Strategien zur PCSK9-Hemmung sind in Entwicklung und umfassen u. a. oral verfügbare Wirkstoffe und tierexperimentelle Konzepte zur Gentherapie, welche sich in unterschiedlichen Stadien der Prüfung befinden.

BackgroundSince the publication of the EULAR recommendations for the management of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) in 2016, several randomised clinical trials have been published that have the potential to change clinical care and support the need for an update.MethodsUsing EULAR standardised operating procedures, the EULAR task force undertook a systematic literature review and sought opinion from 20 experts from 16 countries. We modified existing recommendations and created new recommendations.ResultsFour overarching principles and 17 recommendations were formulated. We recommend biopsies and ANCA testing to assist in establishing a diagnosis of AAV. For remission induction in life-threatening or organ-threatening AAV, we recommend a combination of high-dose glucocorticoids (GCs) in combination with either rituximab or cyclophosphamide. We recommend tapering of the GC dose to a target of 5 mg prednisolone equivalent/day within 4–5 months. Avacopan may be considered as part of a strategy to reduce exposure to GC in granulomatosis with polyangiitis (GPA) or microscopic polyangiitis (MPA). Plasma exchange may be considered in patients with rapidly progressive glomerulonephritis. For remission maintenance of GPA/MPA, we recommend rituximab. In patients with relapsing or refractory eosinophilic GPA, we recommend the use of mepolizumab. Azathioprine and methotrexate are alternatives to biologics for remission maintenance in AAV.ConclusionsIn the light of recent advancements, these recommendations provide updated guidance on AAV management. As substantial data gaps still exist, informed decision-making between physicians and patients remains of key relevance.

BackgroundThe persistence of the SARS-CoV2 pandemic, partly due to the appearance of highly infectious variants, has made booster vaccinations necessary for vulnerable groups. Questions remain as to which cohorts require SARS-CoV2 boosters. However, there is a critical lack of data on the dynamics of vaccine responses in patients with chronic inflammatory diseases (CID) undergoing immunosuppressive/disease modifying anti-rheumatic (DMARD) treatment. Here, we present the first data regarding the decline of the vaccine-induced humoral immune responses in patients with CID.Methods23 patients with CID were monitored clinically and for anti-spike IgG and IgA levels, neutralization efficacy and antigen-specific CD4+ T cell responses over the first 6 months after SARS-CoV2 vaccination. 24 healthy individuals were included as controls.ResultsWhile anti-spike IgG-levels declined in CID patients and healthy controls, patients receiving anti-TNF treatment showed significantly greater declines at 6 months post second vaccination in IgG and especially neutralizing antibodies. IgA levels were generally lower in CID patients, particularly during anti-TNF therapy. No differences in SARS-CoV2 spike-specific CD4+ T-cell frequencies were detected.ConclusionAlthough the long-term efficacy of SARS-CoV2 vaccination in CID patients undergoing disease-modifying therapy is still not known, the pronounced declines in humoral responses towards SARS-CoV2 6 months after mRNA vaccination in the context of TNF blockade should be considered when formulating booster regimens. These patients should be considered for early booster vaccinations.

Was ist neu? Übersicht und Nomenklatur Die IgG4-assoziierte Erkrankung (IgG4-RD) ist eine erst kürzlich beschriebene heterogene Krankheitsentität, der viele vorher als eigenständige Einzelorganerkrankungen interpretierte Manifestationen zugerechnet werden. Hauptsymptom ist die Schwellung oder Vergrößerung betroffener Organe. Diagnose und Klassifikation Die Diagnose wird in Zusammenschau von Anamnese, klinischem Bild, Bildgebung, Histopathologie und IgG4-spezifischen Tests in Labor und Histologie gestellt. Labor und Bildgebung Häufige Laborbefunde sind: erhöhtes Serum-IgG4, IgE und CRP, Hypergammaglobulinämie, Hypokomplementämie und Eosinophilie. Histopathologie. Das typische Bild umfasst folgende Hauptcharakteristika: dichte lymphoplasmazelluläre Infiltrate, storiforme Fibrose und obliterative Phlebitis. Ferner treten vermehrte IgG4-positive Plasmazellen auf. Differenzialdiagnostische Abgrenzung Diverse andere Krankheitsbilder können die IgG4-RD imitieren. Medikamentöse Therapie Neu sind eine Studie zu Mycophenolat-Mofetil und Daten zu Rituximab bei sonst weitgehend fehlender Evidenz aus Studien zur Behandlung der IgG4-RD. Glukokortikoide Glukokortikoide (GC) sind die Grundlage der medikamentösen Therapie. Konventionelle Immunsuppressiva Es herrscht weiterhin kein Konsens, ob konventionelle Immunsuppressiva als GC-sparende Therapie immer oder nur in besonderen Fällen Teil der medikamentösen Therapie sein sollten. Biologika Rituximab ist eine etablierte Reservetherapie. Interventionelle und chirurgische Verfahren Mechanische Obstruktionen und Kompressionen können chirurgische und interventionelle Verfahren notwendig machen.

Was ist neu? Orale Antikoagulation bei nicht dialysepflichtiger chronischer Nierenkrankheit In großen Zulassungsstudien haben sich die Nicht-Vitamin-K-abhängigen oralen Antikoagulanzien (NOAK) bei Patienten mit nicht valvulärem Vorhofflimmern als mindestens so effektiv in der Verhinderung thromboembolischer Ereignisse gezeigt wie Vitamin-K-Antagonisten (VKA). Die NOAK zeigen generell eine geringere Neigung zu schweren, lebensbedrohlichen Blutungen als die VKA. In den Zulassungsstudien wurden Patienten mit einer Kreatinin-Clearance von kleiner 30 ml/min meist nicht inkludiert, sodass für Patienten mit einer Kreatinin-Clearance von 15–30 ml/min zwar für Rivaroxaban, Apixaban und Edoxaban eine Zulassung besteht, die Datenlage zur Effektivität und Sicherheit jedoch nicht so fundiert ist wie bei Patienten mit einer Kreatinin-Clearance von > 30 ml/min. Antikoagulation bei terminaler Niereninsuffizienz Die Indikation zur Antikoagulation muss bei chronischen Dialysepatienten mit Vorhofflimmern derzeit weiterhin individualisiert gestellt werden. Es ist in diesem Kollektiv unklar, ob dialysepflichtige VHF-Patienten überhaupt von einer oralen Antikoagulation profitieren und welches hierfür eine sichere und effektive Substanz ist: Randomisiert-kontrollierte Studien zu Apixaban versus VKA werden klären, ob NOAK eine sichere und effiziente Therapiestrategie bei diesem Patientenkollektiv sind (RENAL-AF, AXADIA). Thrombozytenaggregationshemmung bei chronischer Nierenkrankheit Generell sollten Patienten auch mit schwerer CKD oder Dialysepflichtigkeit die Thrombozytenaggregationshemmung nach kardiologischer Leitlinienempfehlung erhalten. Auf dem Boden des erhöhten Blutungsrisikos in diesem Kollektiv erscheinen moderne Kombinationen aus NOAK und einer einzelnen TAH-Substanz, die das alte „Triple-Regime“, bestehend aus doppelter TAH plus VKA ersetzen, besonders interessant.

Epidemiological and clinical studies have shown a relevant association between heart rate and cardiovascular mortality. Experimental studies identified vascular effects of heart rate reduction with the If channel inhibitor ivabradine. Therefore, the effects of heart rate reduction on endothelial function and indices of arterial stiffness were examined in patients with stable coronary artery disease in a prospective, placebo-controlled clinical crossover study.Twenty-three patients (18 men and 5 women) with a resting heart rate (HR) of at least 70 beats per minute (bpm) and stable coronary artery disease were enrolled in this study. In a cross-over design, all patients were treated with ivabradine (Iva, 7.5 mg b.i.d.) and placebo for 6 months each. Iva reduced heart rate by 11.4 bpm (Iva 58.8 ± 8.2 bpm vs. placebo 70.2 ± 8.3 bpm, P 0.0001). Augmentation index (AIx75), carotid-femoral pulse wave velocity (cfPWV) and central aortic blood pressure were measured using applanation tonometry (SphygmoCor). HRR by Iva increased AIx75 by 12.4% (Iva 24.3 ± 10.5% vs. placebo 21.3 ± 10.1%, P 0.05) and reduced cfPWV by 14.1% (Iva 6.3 ± 1.7 m/s vs. placebo 7.3 ± 1.4 m/s, P 0.01). Iva increased mean central blood pressure by 7.8% (Iva 107.5 ± 15.4 mmHg vs. placebo 99.1 ± 12.2 mmHg, P 0.001). Endothelial function was determined measuring the flow-mediated vasodilation (FMD) of the brachial artery. HRR by Iva increased FMD by 18.5% (Iva 7.3 ± 2.2% vs. placebo 6.0 ± 2.0%, P 0.001). Aortic distensibility was characterized by MRI. HRR by Iva increased aortic distensibility by 33.3% (Iva 0.003 ± 0.001/mmHg vs. placebo 0.002 ± 0.010/mmHg, P 0.01) and circumferential cyclic strain by 37.1% (Iva 0.062 ± 0.027 vs. placebo 0.039 ± 0.018, P 0.0001).Heart rate reduction with Iva increased endothelium-dependent vasodilation and reduced arterial stiffness in patients with stable CAD. These findings corroborate and expand the results collected in experimental studies and indicate the importance of heart rate as a determinant of vascular function.

Among the eosinophilic diseases treated by rheumatologists other than eosinophilic granulomatosis with polyangiitis, there are further organ-related and systemic diseases with hypereosinophilia. Only the exact differential diagnostic demarcation of the diseases enables a pathogenetic oriented treatment. This article focuses on the hypereosinophilic syndromes. The potential differential diagnoses of Ig(immunoglobulin)G4-related disease, eosinophilic fasciitis and drug-induced vasculitis as well as eosinophilia-myalgia syndrome and toxic oil syndrome as historic drug-induced inflammatory rheumatic diseases are described and the clinical manifestations and treatment are summarized.

Only fifteen months after the beginning of the COVID-19 pandemic, several vaccines are already available for clinical use. While the spike protein of SARS-CoV-2 constitutes the main target of all predominant SARS-CoV-2 vaccines, they work by different mechanisms (mRNA-based vaccines vs. vector-based vaccines vs. protein-based vaccines).Though there are slight differences regarding the level of protection against mild COVID-19, all five vaccines that have been through phase 3 trials were nearly 100 % effective in preventing severe or fatal cases of COVID-19. The side effects were of short duration.Patients with chronic kidney disease (or other significant comorbidities) were largely excluded from Phase 3 trials, which makes definite recommendations concerning their vaccination difficult. The vaccine's effectiveness may be reduced in that population due to a uremic immune defect and/or immunosuppressive medication. However, these patients have an increased risk for severe or fatal COVID-19, so that they may particularly benefit from the vaccine. Innerhalb von nur 15 Monaten nach Beginn der COVID-19-Pandemie stehen bereits mehrere SARS-CoV-2-Impfstoffe zum klinischen Einsatz bereit. Während das Zielmolekül aller prädominierenden Vakzine das Spike-Protein von SARS-CoV-2 ist, lassen sie sich anhand ihres Wirkprinzip in mRNA-basierte, Vektor-basierte und Protein-basierte Impfstoffe unterscheiden. BEDEUTUNG FüR CHRONISCH NIERENKRANKE MENSCHEN: Das Aussprechen von Empfehlungen für chronisch nierenkranke Menschen ist aufgrund deren geringer Repräsentation in den Zulassungsstudien erschwert – wie bei anderen Patienten mit schwerer Komorbidität. Aufgrund von urämischem Immundefekt und/oder medikamentöser Immunsuppression könnte die Effektivität der Impfung im Einzelfall relativ vermindert sein. Dennoch profitieren vermutlich gerade diese Patienten von einer Impfung, da sie ein erhöhtes Risiko für einen schweren oder gar tödlichen COVID-19-Verlauf aufweisen.

Objectives We sought to assess central hemodynamic effects in 23 patients (18 male, 5 female) with a resting heart rate (HR) of ≥70 beats per minute (bpm) and chronic coronary syndrome after long-term ivabradine therapy (6 months) by cardiac magnetic resonance (CMR). Methods and results In a cross-over design, all patients were treated with ivabradine (Iva, 7.5 mg bid) and placebo for 6 months each. CMR was performed three times (at baseline, after 6 and 12 months) to determine left ventricular (LV) function parameters, including end-diastolic and end-systolic volumes (EDVi, ESVi), stroke volume (SVi) and ejection fraction (EF) as well as volume-time curve (VTC) parameters, including peak ejection rate (PER), peak ejection time (PET), peak filling rate (PFR), peak filling time from ES (PFT), peak ejection rate normalized to EDV (PER/EDV) and peak filling rate normalized to EDV (PFR/EDV) for global LV function (systolic and diastolic) assessment. Flow measurements of the ascending aorta were performed with phase-contrast velocity imaging. Treatment with Iva led to a HR reduction of 11.4 bpm (Iva 58.8±8.2 bpm vs placebo 70.2±8.3 bpm, p Conclusion Systolic LV function was unaffected by treatment with Iva, while the filling during diastole was significantly improved. While medium and maximum aortic flow were not affected by Iva, mean velocity was significantly reduced. Aortic distensibility as surrogate parameter for arterial stiffness was significantly correlated to aortic mean velocity. This study confirms the underlying physiological principle of the If-current inhibitor Ivabradine. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): This work was supported by the Deutsche Herzstiftung (German Heart Foundation) (F/14/11 to F.C.) and the Deutsche Forschungsgemeinschaft (DFG KFO 196 to U.L., S.H.S and M.B. and SFB TTR 219, S-01 to M.B.). The Saarland University Medical Center has received an unrestricted grant from Servier (France).

Einleitung: Die Riesenzellarteriitis (RZA) und Takayasu – Arteriitis (TAK) sind Großgefäßvaskulitiden (GGV), die zu schweren Komplikationen wie Erblindung, Organ- und Extremitätenischämien und bei einem Teil der Erkrankten zum Tod führen können. Glukokortikoid-assoziierte[zum vollständigen Text gelangen Sie über die oben angegebene URL], Deutscher Rheumatologiekongress 2020, 48. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 34. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh)

Die antithrombotische Therapie bei Vorhofflimmern und koronarer Herzkrankheit erfahrt einen Wandel. Neuere Studien zeigen eine Sicherheits-Uberlegenheit der dualen Therapie aus Antikoagulans (NOAK) und P2Y12-Hemmer, meist Clopidogrel, ohne Aspirin nach Stentimplantation ohne Inkaufnahme relevanter Effektivitatseinbusen. Bis 2019 sollten Daten zu allen NOAK vorliegen.

We aimed to explore whether interventional closure of patent foramen ovale (PFO) results in reduction of composite outcome [stroke/transitory ischemic attack (TIA), death, and thrombolysis in myocardial infarction—TIMI bleeding], stroke and stroke/TIA compared to medical treatment in patients with cryptogenic stroke. Searching the PUBMED and Cochrane library database, we performed meta-analysis from all randomized controlled studies that compared effects of interventional PFO closure with medical treatment on stroke prevention. 3560 patients from six randomized trials were included. Interventional PFO closure reduced composite outcome (RR of 0.47, 0.26–0.85, p = 0.01), stroke (RR of 0.38, 0.18–0.82, p = 0.01) and stroke/TIA (RR of 0.56, 0.43–0.74, p

Secondary mitral regurgitation (MR) results from left ventricular dilatation and dysfunction. Quantification of secondary MR is challenging because of the underlying myocardial disease. Clinical and echocardiographic evaluation requires a multi-parametric approach. Severe secondary MR occurs in up to one-fourth of patients with heart failure with reduced ejection fraction, which is associated with a mortality rate of 40% to 50% in 3 years. Percutaneous edge-to-edge mitral valve repair (MitraClip) has emerged as an alternative to surgical valve repair to improve symptoms, functional capacity, heart failure hospitalizations, and cardiac haemodynamics. Further new transcatheter strategies addressing MR are evolving. The Carillion, Cardioband, and Mitralign devices were designed to reduce the annulus dilatation, which is a frequent and important determinant of secondary MR. Several transcatheter mitral valve replacement systems (Tendyne, CardiAQ-Edwards, Neovasc, Tiara, Intrepid, Caisson, HighLife, MValve System, and NCSI NaviGate Mitral) are emerging because valve replacement might be more durable compared with valve repair. In small studies, these interventional therapies demonstrated feasibility and efficiency to reduce MR and to improve heart failure symptoms. However, neither transcatheter nor surgical mitral valve repair or replacement has been proven to impact on the prognosis of heart failure patients with severe MR, which remains high with a mortality rate of 14-20% at 1 year. To date, the primary indication for treatment of secondary severe MR is the amelioration of symptoms, reinforcing the value of a Heart Team discussion. Randomized studies to investigate the treatment effect and long-term outcome for any transcatheter or surgical mitral valve intervention compared with optimized medical treatment are urgently needed and underway.

Aufgrund der hohen extrarenalen Komorbiditat von chronisch nierenkranken Menschen mit haufigem Auftreten von Herz-Kreislauf-Erkrankung ist ein Grundverstandnis der Diagnostik von kardiovaskularen Erkrankungen fur Nephrologen unabdingbar. Neben der Elektrokardiographie spielt die Echokardiographie eine zentrale Rolle in der kardiovaskularen Basisdiagnostik. Rezente epidemiologische Untersuchungen zeigen auf, dass nichtdialysepflichtige und dialysepflichtige chronisch nierenkranke Menschen sehr haufig pathologische echokardiographische Befunde aufweisen, insbesondere eine linksventrikulare Hypertrophie, eine linksatriale Dilatation sowie diastolische und systolische linksventrikulare Dysfunktionen. Trotz dieser hohen Komorbiditat ist bislang weitgehend ungeklart, inwieweit der Nachweis pathologischer echokardiographischer Befunde in spezifischen pharmakologischen Interventionen munden sollte.

Background and purpose Oral anticoagulation prevents thromboembolism in atrial fibrillation. Factor Xa inhibitors, like edoxaban, are known to reduce inflammation and proliferation of smooth muscle cells, while vitamin K antagonism can cause vascular calcific damage. The influence of edoxaban compared to warfarin on vascular remodeling, atherosclerosis and arteriogenesis is unknown. Experimental approach Apolipoprotein E knockout (ApoE −/−) mice were fed cholesterol-rich diet alone (control, co), with warfarin+vitamin K1 (warf) or with edoxaban (Edo) for 8 weeks. After 6 weeks, femoral artery ligation was performed. Key results There was no difference in hind-limb perfusion restoration between the three groups after 14 days (Co 0.36 ± 0.05 vs. Warf 0.39 ± 0.09 (p = .39), Co vs. Edo 0.51 ± 0.06 (p = .089), Warf vs. Edo (p = .83)) after ligation. Immuno-histologically, there was no difference in smooth muscle cell count in both hindlimbs between the three groups or in the amount of perivascular macrophages in collateral-bearing hindlimb tissue. Edoxaban showed the lowest amount of plaque tissue in the aortic sinus tissue (Co 74 ± 11% vs. Edo 62 ± 12% (p = .024), Co vs. Warf 69 ± 14% (p = .30), Edo vs. Warf (p = .14)) as well as the least amount of fibrosis (Co 3.1 ± 0.9% vs. Edo 1.7 ± 0.6% (p = .027), Co vs. Warf 4.1 ± 0.7% (p = .081), Edo vs. Warf (p Conclusion and implications These data suggest that treatment with edoxaban unlike warfarin prevents vascular maladaptive remodeling, which may be clinically important.

IgG4-related disease (IgG4-RD) is an entity first described less than 20 years ago, characterized by tumorous swelling of affected organs. Differentiation from malignant disease, systemic infections and other systemic autoimmune diseases can be challenging. Typical histopathologic findings facilitate a diagnosis in a compatible clinical context. Because nearly every organ system can be affected, management of IgG4-RD is a challenging task requiring multidisciplinary work-up and treatment. Medical treatment usually consists of glucocorticoids, which may be combined with other immunosuppressives. Surgical or interventional treatment may be necessary if complications arise. Since high-quality evidence is lacking for most aspects of the management of IgG4-RD, international collaborative studies are urgently needed.ÜBERSICHT UND NOMENKLATUR: Die IgG4-assoziierte Erkrankung (IgG4-RD) ist eine erst kürzlich beschriebene heterogene Krankheitsentität, der viele vorher als eigenständige Einzelorganerkrankungen interpretierte Manifestationen zugerechnet werden. Hauptsymptom ist die Schwellung oder Vergrößerung betroffener Organe.Die Diagnose wird in Zusammenschau von Anamnese, klinischem Bild, Bildgebung, Histopathologie und IgG4-spezifischen Tests in Labor und Histologie gestellt.Häufige Laborbefunde sind: erhöhtes Serum-IgG4, IgE und CRP, Hypergammaglobulinämie, Hypokomplementämie und Eosinophilie.Das typische Bild umfasst folgende Hauptcharakteristika: dichte lymphoplasmazelluläre Infiltrate, storiforme Fibrose und obliterative Phlebitis. Ferner treten vermehrte IgG4-positive Plasmazellen auf.Diverse andere Krankheitsbilder können die IgG4-RD imitieren. MEDIKAMENTöSE THERAPIE: Neu sind eine Studie zu Mycophenolat-Mofetil und Daten zu Rituximab bei sonst weitgehend fehlender Evidenz aus Studien zur Behandlung der IgG4-RD.Glukokortikoide (GC) sind die Grundlage der medikamentösen Therapie.Es herrscht weiterhin kein Konsens, ob konventionelle Immunsuppressiva als GC-sparende Therapie immer oder nur in besonderen Fällen Teil der medikamentösen Therapie sein sollten.Rituximab ist eine etablierte Reservetherapie.Mechanische Obstruktionen und Kompressionen können chirurgische und interventionelle Verfahren notwendig machen.

Due to a high rate of cardiovascular events and the high-incidence of atrial fibrillation, many patients with chronic kidney disease (CKD) need to be anticoagulated and/or be subjected to anti platelet therapy (APT). As most studies historically excluded patients with CKD and a creatinine-clearance below 30 ml/min, guidelines for this patient group are only slowly being renewed depending on emerging study data.In patients with CKD stage 1-3, any non-vitamin K dependent oral anticoagulant (NOAC) should be preferentially used over vitamin K antagonists (VKA). In CKD stage 4, dabigatran should be avoided.The decision to anticoagulate a maintenance dialysis patient with atrial fibrillation has to be made on an individual basis considering their thrombosis and bleeding risk. Currently, in Europe all oral anticoagulants can be used only on an off-label basis in these patients. Randomized controlled trials investigating the efficacy and safety of apixaban versus VKA are currently underway. Alternative treatment options (e. g. left appendage occlusion) should be considered.Study data on APT in moderate to advanced CKD are similarly scarce. Despite APT not being renally eliminated, bleeding risk is increased due to uremic platelet dysfunction. When combining APT with NOAC, dose reduction of the latter needs to be addressed.ORALE ANTIKOAGULATION BEI NICHT DIALYSEPFLICHTIGER CHRONISCHER NIERENKRANKHEIT: In großen Zulassungsstudien haben sich die Nicht-Vitamin-K-abhängigen oralen Antikoagulanzien (NOAK) bei Patienten mit nicht valvulärem Vorhofflimmern als mindestens so effektiv in der Verhinderung thromboembolischer Ereignisse gezeigt wie Vitamin-K-Antagonisten (VKA). Die NOAK zeigen generell eine geringere Neigung zu schweren, lebensbedrohlichen Blutungen als die VKA. In den Zulassungsstudien wurden Patienten mit einer Kreatinin-Clearance von kleiner 30 ml/min meist nicht inkludiert, sodass für Patienten mit einer Kreatinin-Clearance von 15–30 ml/min zwar für Rivaroxaban, Apixaban und Edoxaban eine Zulassung besteht, die Datenlage zur Effektivität und Sicherheit jedoch nicht so fundiert ist wie bei Patienten mit einer Kreatinin-Clearance von 30 ml/min. ANTIKOAGULATION BEI TERMINALER NIERENINSUFFIZIENZ: Die Indikation zur Antikoagulation muss bei chronischen Dialysepatienten mit Vorhofflimmern derzeit weiterhin individualisiert gestellt werden. Es ist in diesem Kollektiv unklar, ob dialysepflichtige VHF-Patienten überhaupt von einer oralen Antikoagulation profitieren und welches hierfür eine sichere und effektive Substanz ist: Randomisiert-kontrollierte Studien zu Apixaban versus VKA werden klären, ob NOAK eine sichere und effiziente Therapiestrategie bei diesem Patientenkollektiv sind (RENAL-AF, AXADIA). THROMBOZYTENAGGREGATIONSHEMMUNG BEI CHRONISCHER NIERENKRANKHEIT: Generell sollten Patienten auch mit schwerer CKD oder Dialysepflichtigkeit die Thrombozytenaggregationshemmung nach kardiologischer Leitlinienempfehlung erhalten. Auf dem Boden des erhöhten Blutungsrisikos in diesem Kollektiv erscheinen moderne Kombinationen aus NOAK und einer einzelnen TAH-Substanz, die das alte „Triple-Regime“, bestehend aus doppelter TAH plus VKA ersetzen, besonders interessant.

Background Pressure overload dependent cardiac remodeling is characterized by a continuous functional loss of cardiomyocytes, cardiomyocyte hypertrophy, cell death and fibrosis. The relevance of the MyD88- and NFκB-independent inflammatory TRIF (TIR-domain-containing adapter protein inducing IFN-β) signaling pathway in myocardial hypertrophy is incompletely understood. Methods and results The murine model of afterload induced myocardial hypertrophy (trans-aortic constriction, TAC) was used to investigate the time dependent chemokine expression in C57Bl/6J Wild type (WT) mice after intervention. Myd88- as well as TRIF-dependent chemokines reached their expression maximum at d7 post intervention. This time point was determined for further investigations on TRIF knockout-mice (TRIF−/−) compared to WT mice. While left ventricular (LV) mRNA-expression of TNFalpha and IL6 was upregulated in TRIF−/− mice, CXCL10, CXCL11, RANTES and pathway molecule IRF3 remained unchanged. In the stage of established hypertrophy (35 days after TAC) cytokine levels returned to baseline in WT as well as in TRIF−/− mice. Cellular hypertrophy (increase in cardiomyocyte size) as well as echocardiographic determined increase of LV mass was similar in TRIF−/− and WT mice at d7 as well as at d35 after TAC. Additionally at d7 and d35 the fractional shortening function didn't show any differences between the groups after TAC. On the other hand LV interstitial fibrosis (determined by collagen content) was significantly less distinct in TRIF−/− mice (1.4±0.2%) than in WT mice (2.3±0.3%, (p Conclusion In afterload induced hypertrophy TRIF-dependent signaling doesn't influence cardiomyocyte hypertrophy. But TRIF plays an important role in the regulation of fibrosis in pressure overload dependent remodeling. Through the modulation of the TGF-beta signaling pathway and antifibrotic microRNAs TRIF signaling is involved in the development of interstitial fibrosis. Especially in the early stage of the cardiac remodeling. Acknowledgement/Funding KFO196

Objectives: We assessed left ventricular (LV) function and central hemodynamic effects in patients with a heart rate (HR) at rest of ≥70 beats per minute (bpm) and chronic coronary syndrome (CCS) after long-term treatment with ivabradine compared to placebo by cardiac magnetic resonance (CMR) imaging. Methods and results: In a randomized, double-blinded, prospective cross-over design, 23 patients (18 male, 5 female) were treated with ivabradine (7.5 mg bid) or placebo for 6 months. CMR imaging was performed at baseline and after 6 and 12 months to determine LV functional parameters.Mean resting HR on treatment with ivabradine was 58 ± 8.2 bpm and 70.2 ± 8.3 bpm during placebo (p

Moderate consumption of red wine is associated with fewer cardiovascular events. We investigated whether red wine consumption counteracts the adverse vascular effects of cigarette smoking.Participants smoked 3 cigarettes alone or after drinking a titrated volume of red wine. Clinical chemistry, blood counts, plasma cytokine enzyme-linked immunosorbent assays, immunomagnetic separation of CD14Compared with baseline, leukocytosis (P = .019), neutrophilia (P.001), lymphopenia (P .001), and eosinopenia (P = .008) were observed after only smoking. Endothelial and platelet-, monocyte-, and leukocyte-derived microparticles (P.001 each) were elevated. In monocytes, messenger RNA expression of interleukin (IL)-6 (2.6- ± 0.57-fold), tumor necrosis factor alpha (2.2- ± 0.62-fold), and IL-1b (2.3- ± 0.44-fold) were upregulated, as was IL-6 (1.2 ± 0.12-fold) protein concentration in plasma. Smoking acutely inhibited mononuclear cell telomerase activity. Markers of endothelial damage, inflammation, and cellular aging were completely attenuated by red wine consumption.Cigarette smoke results in acute endothelial damage, vascular and systemic inflammation, and indicators of the cellular aging processes in otherwise healthy nonsmokers. Pretreatment with red wine was preventive. The findings underscore the magnitude of acute damage exerted by cigarette smoking in "occasional lifestyle smokers" and demonstrate the potential of red wine as a protective strategy to avert markers of vascular injury.

Mitral regurgitation represents a volume load on the left ventricle leading to congestion and symptoms of heart failure. The aim of this study was to characterize early hemodynamic adaptions after percutaneous mitral valve (MV) repair.Forty-six consecutive patients with symptomatic high-grade MV insufficiency (mean age, 72 years; 54% men) were prospectively included in the study and examined before and after successful catheter-based clip implantation. Seventy percent of patients had secondary mitral regurgitation. Noninvasive pressure-volume loops were reconstructed from echocardiography with simultaneous blood pressure measurements.MV repair reduced left ventricular end-diastolic volume index from 87 ± 41 to 80 ± 40 mL/m(2) (P .0001). End-systolic volume index was 55 ± 37 mL/m(2) before versus 54 ± 37 mL/m(2) after repair (P = .52). Hence, total stroke volume decreased from 60 ± 23 to 49 ± 16 mL (P .0001), as did total ejection fraction (from 41 ± 14% to 37 ± 13%, P = .002) and global longitudinal strain (from -11 ± 4.9% to -9.1 ± 4.4%, P = .0001). Forward stroke volume, forward ejection fraction, and forward cardiac output remained constant (43 ± 12 mL vs 42 ± 11 mL, 33 ± 17% vs 35 ± 18%, and 3.2 ± 0.9 L/min vs 3.4 ± 0.8 L/min, respectively). Parameters of left ventricular contractility (end-systolic elastance and peak power index) and measurements of afterload (arterial elastance, end-systolic wall stress, and total peripheral resistance) were similar before and after MV repair. Forward ejection fraction correlated more strongly with end-systolic elastance (r = 0.61, P .0001) than did total ejection fraction (r = 0.35, P = .0007) or global longitudinal strain (r = -0.38, P = .0002). Total mechanical energy (pressure-volume area) decreased from 10,903 ± 4,410 to 9,124 ± 2,968 mm Hg × mL (P = .0007) because of reduced stroke work (5,546 ± 2,241 mm Hg × mL vs 4,414 ± 1,412 mm Hg × mL, P .0001). At 3 months, symptom status had improved (76% of patients in New York Heart Association classes I and II), and 97% of patients had mitral regurgitation grade ≤2+.Left ventricular contractility and forward cardiac output remained unchanged after percutaneous MV repair despite decreases in total ejection fraction and global longitudinal strain. The left ventricle was unloaded through reduced end-diastolic volume. Thus, MV repair is associated with an improved hemodynamic state in noninvasive pressure-volume analysis.

Rheumatologist should be familiar with the concept of IgG4-related disease (IgG4-RD). Due to the clinical spectrum IgG4-RD can fall directly within the scope of rheumatology and are often diagnosed primarily by rheumatologists. Furthermore, IgG4RD are relevant differential diagnoses for many other rheumatic conditions. Finally, there are an increasing amount of data suggesting an important role of immunological processes observed in IgG4-RD for other rheumatic diseases.

Objective Obesity is a risk factor for cardiovascular disease and venous thrombosis. Previous studies have shown that in late pregnancy a compression of the inferior vena cava (VCI) leads to a hypotensive syndrome. The objective of this study was to explore the correlation between obesity and an elevated pressure in the VCI simulating obesity-induced vena cava compression syndrome. Methods A left and right heart catheterization was performed in 29 patients. After right atrial pressure measurement, the catheter was pulled back through the VCI, and the pressure gradient between the thoracic and abdominal vena cava was measured. We determined the correlation between the BMI and the pressure gradient. Results In 29 patients, a high BMI was associated with an increased pressure gradient between the thoracic and abdominal vena cava (r = 0.66). This correlation was particularly close in patients with a BMI >30 kg/m2 (P = 0.0008). Two patients had complications such as recurrent thrombosis, with one of them having the highest pressure gradient of 16 mm Hg. Conclusions Because mechanical obstruction of the VCI leads to an increased risk for venous thrombosis in patients with obesity, this finding needs to be considered in the decision-making for interventional treatments like bariatric surgery.

Background:IgG4-related disease (IgG4-RD) is a polymorphic autoimmune disease leading to tumourous swelling and/or fibrosis of affected organs. Riedel’s thyroiditis is – besides chronic periaortitis, Mikulicz Syndrome and many others – an organ manifestation of IgG4-RD that has been thought to be an independent disease for a long time. About 40% of patients have single organ IgG4-RD while the others suffer from multisystemic disease [1].Objectives:Glucocorticoids, sometimes combined with other immunosuppressives are the standard treatment of IgG4-RD, in some situations (e.g. mechanical complications or suspected malignancy) surgery may be necessary but little is known about the management of fully resected single-organ IgG4-RD [1].Methods:We report a case of single-organ IgG4-RD (Riedel’s thyroiditis) after complete resection and perform a brief review of the literature to guide clinical management in this situation.Results:A woman (51 y) with pre-existing Hashimoto’s thyroiditis (thyroid peroxidase antibody positive) developed a rapidly growing struma with very firm consistency (not allowing fine needle biopsy). Besides slightly increased C-reactive protein (5,3 mg/l) there was no laboratory sign suggestive for IgG4-RD (normal serum IgG4, complement, eosinophils and IgE). Within 4 months the patient suffered from hoarseness and progredient dyspnea. Surgical thyroidectomy was performed and histopathology revealed IgG4-related Riedel’s thyroiditis with extensive (storiform) fibrosis, a dense lymphoplasmacytic infiltrate, obliterative phlebitis, eosinophilia and 13 IgG4-positive plasma cells per high power field.After referral to our department a comprehensive work-up showed no signs of other manifestations of IgG4-RD. Treatment with glucocorticoids is clearly recommended for patients with symptomatic IgG4-RD in an international consensus statement, whereas “watchful waiting” may be appropriate in some cases of asymptomatic or mild disease. While some highly fibrotic lesions may not respond well to glucocorticoids and may require surgical intervention, no clear guidance is available for the management of fully resected single organ IgG4-RD [2].A brief review of the literature revealed that few cases of single-organ IgG4-RD remaining in remission after resection without medical treatment have been reported e.g. IgG4-related cholecystitis, autoimmune-pancreatitis, tumours of the intestinal tract, lung, thymus, meninges, paravertebral space and others [3–9].After discussion of the options with the patient no systemic immunosuppression was given under close follow up without signs of relapse in clinical examinations, laboratory or imaging during the first 6 months.Conclusion:Limited evidence from case reports suggests that a “watchful waiting” strategy without systemic immunosuppressive treatment may be reasonable in some cases of single-organ IgG4-RD after the affected organ was completely resected (e.g. due to mechanical complications or suspected malignoma). However, close follow-up monitoring should be applied due to the risk of relapse or development of new organ manifestations.References:[1]Brito-Zerón et al.Best Pract. Res. Clin. Rheumatol.2016[2]Khosroshahi et al.Arthritis Rheumatol.2015[3]Takahashi et al.Surg. Case Rep.2015[4]Akbari et al.ACG Case Rep. J.2018[5]Oda et al.Thorac. Cancer2019[6]Nambirajan et al.Childs Nerv. Syst. ChNS Off. J. Int. Soc. Pediatr. Neurosurg.2019[7]Uchida et al.Asian J. Endosc. Surg.2018[8]Hart et al.Mod. Pathol. Off. J. U. S. Can. Acad. Pathol. Inc2015[9]Kim et al.Tuberc. Respir. Dis.2014Disclosure of Interests:Jan Schirmer: None declared, Marcus Seeger: None declared, Dominik Schulte Paid instructor for: Ferring, Speakers bureau: Amgen, Astra Zeneca, Braun, Fresenius, Ipsen, Johnson & Johnson, Lilly, MSD, Novartis, Novo Nordisk, Sanofi, Matthias Laudes Speakers bureau: Roche, Sanofi, Chugai, Stefan Schreiber Consultant of: AbbVie, Arena, BMS, Biogen, Celltrion, Celgene, IMAB, Gilead, MSD, Mylan, Pfizer, Fresenius, Janssen, Takeda, Theravance, provention Bio, Protagonist and Falk, Bimba F. Hoyer: None declared

Die Polyarteriitis nodosa (PAN) ist eine nekrotisierende Arteriitis mittelgroser Gefase, die unbehandelt oftmals letal verlauft. Sie manifestiert sich haufig an der Haut (Noduli oder Ulzera), am peripheren Nervensystem (Mononeuritis multiplex) und durch Stenosen und Mikroaneurysmen der viszeralen Gefase. Die Diagnose erfordert eine komplexe diagnostische Aufarbeitung zur Abgrenzung von infektiosen, malignen, medikamenteninduzierten und anderen inflammatorischen Erkrankungen. Die PAN kann in weitere Varianten unterteilt werden (idiopathisch, Hepatitis-B-assoziiert, mit hereditaren inflammatorischen Syndromen assoziiert und eine isoliert kutane Verlaufsform). Wahrend idiopathische und hereditar inflammatorische Formen einer immunsuppressiven Therapie bedurfen, wird die Hepatitis-B-assoziierte Variante mit Virostatika und Plasmapherese behandelt. Die Prognose der isoliert kutanen Form ist gut und bedarf selten hochpotenter Immunsuppression.

BACKGROUND Cardiological societies recommend, in their guidelines, that patients with atrial fibrillation and an intermediate (or higher) risk of stroke and systemic embolization should be treated with oral anticoagulant drugs. For patients who do not have mitral valve stenosis or a mechanical valve prosthesis, non-vitamin-K dependent oral anticoagulants (NOAC) are preferred over vitamin K antagonists (VKA) for this purpose. It is unclear, however, whether patients with chronic kidney disease and atrial fibrillation benefit from oral anticoagulation to the same extent as those with normal kidney function. It is also unclear which of the two types of anti - coagulant drug is preferable for patients with chronic kidney disease; NOAC are, in part, renally eliminated. METHODS This review is based on pertinent publications retrieved by a selective literature search, and on international guidelines. RESULTS Current evidence suggests that patients with atrial fibrillation who have chronic kidney disease with a glomerular filtration rate (GFR) above 15 mL/ min/1.73 m² should be treated with an oral anticoagulant drug if they have an at least intermediate risk of embolization, as assessed with the CHA2DS2-VASc score. For patients with advanced chronic kidney disease (GFR from 15 to 29 mL/ min/1.73 m²), however, this recommendation is based only on registry studies. For dialysis patients with atrial fibrillation, decisions whether to give oral anticoagulant drugs should be taken on an individual basis, in view of the elevated risk of hemorrhage and the unclear efficacy of such drugs in these patients. The subgroup analyses of the NOAC approval studies show that, for patients with atrial fibrillation and chronic kidney disease with a creatinine clearance of >25-30 mL/min, NOAC should be given in preference to VKA, as long as the patient does not have mitral valve stenosis or a mechanical valve prosthesis. For those whose creatinine clearance is less than 25 mL/min, the relative merits of NOAC versus VKA are still debated. CONCLUSION The cardiological societies' recommendation that patients with atrial fibrillation should be given oral anticoagulant drugs applies to the majority of such patients who also have chronic kidney disease.

Afferent and efferent sympathetic nerves of the kidney located in the adventitia of the renal artery are involved in the regulation of blood pressure and play a pathophysiological role in the progression and maintenance of hypertension. Renal sympathetic denervation is a potent and safe catheter-based therapeutic approach for the treatment of patients with resistant hypertension. Clinical trials of renal sympathetic denervation have shown significant reduction in blood pressure, which was associated with a reduction in local renal norepinephrine spillover as well as a reduction of whole body sympathetic activation in resistant hypertensive patients.

Background Correction of mitral regurgitation (MR) alters the load on the left ventricle. There are few data on the long-term hemodynamic adaptations of the cardiovascular system after transcatheter mitral valve repair (TMVR). The aim of this study was to determine a comprehensive hemodynamic status using noninvasive pressure-volume analysis. Methods Pressure-volume parameters were calculated from echocardiography with simultaneous arm-cuff blood pressure measurements at baseline before TMVR and 12 months after TMVR. Eighty-eight consecutive patients undergoing edge-to-edge mitral clip implantation because of grade 3+ or 4+, symptomatic (79.5% in New York Heart Association functional class ≥III) MR were prospectively enrolled. The mean left ventricular (LV) ejection fraction was 42 ± 14%. Sixty-seven percent of the patients had secondary MR. Results Twelve months after TMVR, 17.7% of patients had died, and 19.0% were rehospitalized because of decompensated heart failure. MR grade was ≤2+ in 90% of surviving patients, and 77% were in New York Heart Association functional class ≤II. LV end-diastolic volume index decreased from 87 ± 38 to 77 ± 40 mL/m2 (P Conclusions One year after TMVR, patients showed reverse remodeling and improved LV performance that was associated with improved symptom status. This hemodynamic improvement supports TMVR as long-term effective therapy for patients with symptomatic MR.