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Az onko-kardiológiai gyakorlat egyik vezérelve a daganatellenes terápia szükségtelen megszakításának minimalizálása. A szakterület átfogó célja, hogy a daganatos betegek a lehető legjobb daganatellenes kezelésben részesüljenek, egyúttal minimalizálva a daganatellenes kezeléssel összefüggő esetleges kardiovaszkuláris toxicitást (CTR-CVT – cancer therapy-related cardiovascular toxicity) az onkológiai ellátás során. Jelen publikációban ismertetjük a CTR-CVT korábbi és legújabb definícióit, röviden bemutatva a mérföldkőnek számító CARDIOTOX-regisztert, valamint a 2022 nyarán publikálásra került Európai Kardiológiai Társaság első onko-kardiológiai irányelvének idevonatkozó részeit. Közleményünkben igyekszünk kitekintést nyújtani a precíziós medicina onko-kardiológiai vonatkozásaira is.

Az elmúlt 30 évben jelentős előrelépés történt a daganatellenes terápiákban. Az immunterápiák bevezetése számottevően javította az onkológiai betegek túlélését. Az immunellenőrzőpont-gátlók (ICI) az immunterápiáknak leggyakrabban alkalmazott típusát képviselik. A daganatos betegek emelkedett kardiovaszkuláris rizikóval rendelkeznek nem csupán a közös rizikófaktorok miatt, hanem bizonyos daganatellenes terápiák is jelentős kardiovaszkuláris mellékhatással járhatnak. A kardiovaszkuláris megbetegedések patomechanizmusában a gyulladás és az immunrendszer meghatározó szerepe jól ismert. Ezek alapján felmerül, hogy az ICI-terápiában részesülő daganatos betegek fokozott kardiovaszkuláris kockázattal rendelkezhetnek. Az alábbiakban rövid áttekintést adunk az ICI-terápia kardiotoxicitásának előfordulásáról, diagnózisáról, kezeléséről és szűréséről. Ezen túl ismertetjük az idén nyáron publikált Európai Kardiológus Társaság témába illő ajánlásait is.

Az onko-kardiológia napjaink egyik dinamikusan fejlődő határterületi tudománya, amelynek célja, hogy a multidiszciplináris szemlélet jegyében, optimalizálja a daganatellenes kezelések eredményességét és minimalizálja a kardiovaszkuláris szövődmények kialakulását. A személyre szabott, a kockázatbecslésen és a társszakmák szoros együttműködésen alapuló ellátásnak kiemelkedő szerepe van az onkológiai betegek kezelésének minden egyes fázisában. A sikeres daganatellenes kezelés, a hoszszú távú túlélés és a jobb életminőség biztosításának alappillére. A European Society of Cardiology (ESC) 2022-ben kiadott első onko-kardiológiai útmutatójának célja egy új szemlélet közvetítése a klinikusok és a multidiszciplináris onkológiai team számára. Fő témája az onkológiai betegek kezelés alatti és utáni kardiovaszkuláris szövődményeinek megelőzése, felismerése és kezelése. Tartalmában számos újszerű elemet hordoz. A publikáció célja az ajánlás átfogó bemutatása.

Háttér: A szívamyloidosis egy ritkának gondolt betegség, amely kezelés nélkül gyorsan halálhoz vezet. Az utóbbi években a rohamosan fejlődő diagnosztikus módszereknek és modern terápiás lehetőségeknek köszönhetően egyre gyakrabban ismerik fel. A diagnosztikában az EKG-nak és szívultrahangnak kiemelt jelentőséget tulajdonítanak. Célkitűzés: A legfrissebb 2021-es Európai Kardiológusok Társaságának ajánlása tükrében kívántuk vizsgálni, hogy szívamyloidosisban jellemzőnek gondolt EKG-eltérések (alacsony kilengések, R-redukció), illetve a legegyszerűbb ultrahangos paraméter, mint a megnövekedett (≥12 mm) balkamra-falvastagság milyen gyakran fordulnak elő betegeink között. Szintén vizsgálni kívántuk, hogy a bal kamrai falvastagság és az EKG-n látott low voltage, illetve R-redukció előfordulása különbözik-e a háttérben álló patológiák esetén betegeinknél. Módszerek: Retrospektív vizsgálatunkba 104, 2009. január és 2022. április között szívamyloidosis miatt a Semmelweis Egyetem Belgyógyászati és Hematológiai Klinikáján megfordult beteget vontunk be. A háttérben álló patológia alapján három csoportot alkottunk: könnyűlánc-amyloidosis (AL), mutációs típusú transztiretin-amyloidosis (ATTRv) és vad típusú transztiretin-amyloidosis (ATTRwt). Leírtuk és összehasonlítottuk a legfontosabb demográfiai-, klinikai-, EKG-, szívultrahangos- és laboratóriumi paramétereket. Eredmények: Betegeink életkorának mediánja 68 (59–78) év volt, közülük. 55% férfi (n=57). AL-amyloidosisból 71, ATTRwt-csoportból 19, ATTRv-csoportból, pedig 13 beteget vizsgáltunk. Az EKG-n low voltage 54%-ban (n=56), R-hullám-redukció 56%-ban (n=58) fordult elő. Szívultrahanggal, 2D-módban mért bal kamrai szeptum és hátsó fal vastagságát átlagoltuk minden betegnél. Az így nyert értékek mediánja 16 (14–18) mm volt. A betegek 91%-ánál (n=95) megnövekedett bal kamrai falvastagságot láttunk. A fő célkitűzésünket vizsgálva szignifikánsnak adódott a különbség betegeink között mind a bal kamrai átlagos falvastagodás (nagyobb vagy egyenlő 12 mm) és low voltage, mind a bal kamrai átlagos falvastagság és EKG-n látott R-redukció jelenlétének aránya között (91% vs. 54% és 91% vs. 56%; p

A szisztémás amyloidosis ritka, progresszív, infiltratív betegség. Szívet is érintő formáit az immunglobulin könnyűláncoknak vagy a transztiretin fehérjének a mutáns vagy a vad típusú formájának a lerakódása okozza. Napjainkban incidenciája nő, az új terápiás lehetőségeknek hála a túlélés javul. A betegek kardiológiai gondozása számos speciális kérdést vet fel. A tromboembóliás szövődmények és a szívüregi thrombusok gyakorisága miatt minden pitvarfibrilláló betegnek antikoaguláns kezelést kell kapnia. Válogatott esetben sinusritmus esetén is szóba jön az alvadásgátló-terápia. Ugyanakkor a betegségre a fokozott vérzéshajlam is jellemző. Specifikus ajánlások híján terápiás döntésünket egyénre szabottan, a körülmények gondos mérlegelésével kell meghoznunk. Az antitrombotikus kezelés módja egyaránt lehet K-vitamin-antagonista vagy direkt hatású orális antikoaguláns terápia.

BACKGROUND There were gaps between guidelines and practice when surgery was the only treatment for aortic stenosis (AS). OBJECTIVES This study analyzed the decision to intervene in patients with severe AS in the EORP VHD (EURObservational Research Programme Valvular Heart Disease) II survey. METHODS Among 2,152 patients with severe AS, 1,271 patients with high-gradient AS who were symptomatic fulfilled a Class I recommendation for intervention according to the 2012 European Society of Cardiology guidelines; the primary end point was the decision for intervention. RESULTS A decision not to intervene was taken in 262 patients (20.6%). In multivariate analysis, the decision not to intervene was associated with older age (odds ratio [OR]: 1.34 per 10-year increase; 95% CI: 1.11 to 1.61; P = 0.002), New York Heart Association functional classes I and II versus III (OR: 1.63; 95% CI: 1.16 to 2.30; P = 0.005), higher age adjusted Charlson comorbidity index (OR: 1.09 per 1-point increase; 95% CI: 1.01 to 1.17; P = 0.03), and a lower transaortic mean gradient (OR: 0.81 per 10-mm Hg decrease; 95% CI: 0.71 to 0.92; P < 0.001). During the study period, 346 patients (40.2%, median age 84 years, median EuroSCORE II [European System for Cardiac Operative Risk Evaluation II] 3.1%) underwent transcatheter intervention and 515 (59.8%, median age 69 years, median EuroSCORE II 1.5%) underwent surgery. A decision not to intervene versus intervention was associated with lower 6-month survival (87.4%; 95% CI: 82.0 to 91.3 vs 94.6%; 95% CI: 92.8 to 95.9; P < 0.001). CONCLUSIONS A decision not to intervene was taken in 1 in 5 patients with severe symptomatic AS despite a Class I recommendation for intervention and the decision was particularly associated with older age and combined comorbidities. Transcatheter intervention was extensively used in octogenarians. (J Am Coll Cardiol 2021;78:2131-2143) (c) 2021 by the American College of Cardiology Foundation.

Cardiac magnetic resonance (CMR) examinations have an essential role in the differentiation of cardiac involvement of amyloidosis (CA) from hypertrophic cardiomyopathy (HCM). The CMR diagnosis is traditionally based on morphologic features and the pattern of late gadolinium enhancement (LGE). However, in patients contraindicated for contrast agent administration, the diagnosis can be challenging. Novel CMR techniques, including strain analysis, can help in the differentiation of these patients. The aim of our study was to investigate the differential diagnostic and prognostic importance of feature-tracking strain analysis in patients with left ventricular hypertrophy caused by CA or HCM. We investigated 89 HCM patients (48 males; 50±18 years) and 46 CA patients (29 males; 64±10 years) who underwent CMR examination. The left ventricular ejection fraction (LVEF), volumes (end-diastolic volume: LVEDV, end-systolic volume: LVESV, stroke volume: LVSV), mass (LVM), and the amount of LGE were quantified. Global longitudinal (GLS), circumferential (GCS) and radial (GRS) LV strain parameters, and basal, midventricular, and apical LS and CS were measured. The apex-to-base regional LS and CS ratios were calculated. The all-cause mortality of the patients was analyzed. The characteristics of groups were compared with an independent t-test or Mann-Whitney test, as appropriate. ROC curve analysis was performed to analyze the diagnostic accuracy of a parameter and to identify optimal cutoff values. The prognostic value of CMR parameters was assessed with Cox proportional hazard regression analyses. Survival probability was analyzed with Kaplan-Meier curves and compared by the log-rank test. CA patients had significantly lower LVEF (51±11 vs. 63±8%; p Our results show that CMR-based strain analysis might be a useful method for differentiating cardiac involvement of amyloidosis from HCM. Furthermore, this technique provides additional information for the assessment of prognosis in this patient population. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): National Research, Development and Innovation Office of Hungary; Ministry for Innovation and Technology in Hungary, within the framework of the Therapeutic Development and Bioimaging programmes of the Semmelweis University

Background: Variant transthyretin amyloidosis (ATTRv) is an autosomal dominant inherited disease, where the mutation of the transthyretin gene (TTR) results in the deposition of pathogenic protein fibrils in various tissues. The mutation type influences the clinical course. Until now, no data were available on the genotype, phenotype, and prevalence of Hungarian ATTRv patients. The aim of our study was to assess the prevalence, regional distribution, genotypes, and phenotypes of Hungarian patients with ATTRv. Methods: With the collaboration of Hungarian regional and university centers, we identified patients diagnosed with ATTRv. We also searched prior publications for case studies of Hungarian ATTRv patients. Results: 40 individuals in 23 families with ATTRv were identified within the borders of Hungary. At the time of the diagnosis, 24 of them were symptomatic. The two most common mutations were ATTRHis88Arg (nine families) and ATTRIle107Val (8 families). ATTRVal30Met was demonstrated in 2 families, and ATTRVal122del, ATTRPhe33Leu, ATTRIle84Ser, and ATTRAsp18Gly in one family each. The median age of the symptomatic patients at the time of clinical diagnosis was 65 years. The most common clinically significant organ involvement was restrictive cardiomyopathy, found in 24 patients. Polyneuropathy was diagnosed in 20 patients. A total of 19 patients showed a mixed phenotype. The leading symptom was heart failure in 8 cases (3 of them had only cardiac symptoms), polyneuropathy in 11 cases (all of them also had cardiac symptoms), and equally severe cardiac and neuropathy symptoms were present in 3 cases. Out of 24 symptomatic patients, 10 received targeted pharmacological therapy. The follow-up period ranged from 1 to 195 months. At the time of the retrospective analysis, 12 patients had already died, and 1 patient underwent heart transplantation. Conclusions: As TTR genotype influences the phenotype and clinical course of ATTRv, it is important to know the regional data. In Hungary, ATTRHis88Arg and ATTRIle107Val are the most common mutations in ATTRv, both presenting with mixed phenotype, but the median age at the time of the diagnosis is 9 years lower in patients with ATTRHis88Arg than in patients with ATTRIle107Val.

Background Left ventricular hypertrophy and diastolic dysfunction are common echocardiographic features of both aortic valve stenosis (AS) and cardiac amyloidosis (CA). These two different entities therefore may mask each other. From recent years, there is a growing body of evidence about the relatively high incidence of wild-type transthyretin (wtTTR) amyloidosis in AS, but there are scarce data on the prevalence of AS in CA, particularly in AL-type amyloidosis. The echocardiographic approach to these patients is not obvious, and not evidence based. We aimed to study the prevalence, severity, and type of AS in patients with CA and also to evaluate the potential of echocardiography in the diagnostic process. Methods Between January 2009 and January 2019, we retrospectively analyzed the clinical and echocardiographic data, and the echocardiographic work up of 55 consecutive CA patients. Results 80% of our CA patients had AL amyloidosis. We identified 5 patients (9%) with moderate to severe AS: two with moderate AS and three with low-flow, low-grade AS (LFLG AS). Further analysis of the latter three patients with dobutamine stress echocardiography revealed pseudo-severe LFLG AS in two, and true-severe AS in one patient. Conclusion The prevalence of moderate to severe AS is 9% in our population of CA patients, the majority of whom have AL amyloidosis. Dobutamine echocardiography seems to be appropriate for the further characterization of patients with LFLG AS, even with normal ejection fraction.

Introduction - Transthyretin familial amyloid polyneuropathy is a rare autosomal dominant progressive systemic disesase of adults caused by endoneural amyloid deposition due to point mutations of the transthyretin gene. It is the most severe form among hereditary polyneuropathies, being fatal within 10 years if left untreated. The disease is underdiagnosed, the late onset forms (above the age of 50) being probably more widespread than previously thought. Early diagnosis is essential as the early introduction of causal therapy (tafamidis) slows progression and prolongs survival. Patients - We report here three non-related Hungarian cases of transthyretin familial amyloid polyneuropathy with non-Val30Met mutations (His88Arg in two cases, Phe33Leu in one case). They were all characterized by late-onset, progressive, length-dependent, axonal, sensorimotor polyneuropathy and the simultaneous presentation of severe restrictive cardiomyopathy. In all three cases, clinical and electrophysiological signs of myopathy were also present, suggesting the involvement of skeletal muscles as well. In two cases, high resolution ultrasound of the peripheral nerves was also performed, which showed segmental structural alterations (change or loss of fascicular structure) and some increase of echogenicity of the interfascicular epineurium, without substantial enlargement of the nerves. Conclusion - In Hungary, mainly the rare, non-Val30Met mutation forms of transthyretin familial amyloid polyneuropathy are encountered, as in our cases. As opposed to the Val30Met forms, these mutations are characterized by late onset and simultaneous presentation of severe cardiomyopathy. Our report highlights the importance of considering transthyretin familial amyloid polyneuropathy in the differential diagnosis of late-onset, progressive, axonal polyneuropathies of unknown etiology, particularly if associated with cardiac disease.Bevezetés - A transthyretin familiáris amyloid polyneuropathia ritka, autoszomális domináns módon öröklődő progresszív szisztémás kórkép, amelynek patológiai háttere a transthyretin gén pontmutációja következtében kialakult endoneuralis amyloid depozíció. A felnőttkori öröklődő polyneuropathiák közül a legsúlyosabb, főként a kardiológiai szövődmények miatt kezelés nélkül 10 éven belül halállal végződik. A kórkép aluldiagnosztizált, a késői kezdetű forma (50 év feletti tünetkezdet) a nem endémiás területeken valószínűleg sokkal elterjedtebb, mint korábban gondolták. Korai felismerésük lényeges a korai stádiumban adható oki kezelés (tafamidis) megkezdése miatt, amellyel a progresszió lassítható, a túlélés meghosszabbítható. Betegek - Közleményünkben három magyarországi, rokonságban nem álló, a leggyakoribb Val30Met-mutációtól eltérő mutációval (két esetben His88Arg, egy esetben Phe33Leu) járó transthyretin familiáris amyloid polyneuropathia esetet ismertetünk. Közös jellemzőjük a késői kezdetű progresszív, hosszúságfüggő, axonalis, szenzomotoros polyneuropathia, és a közel egyidejűleg induló súlyos restriktív cardiomyopathia. Mindhárom esetben a vázizom érintettségére utaló myopathia klinikai és elektrofiziológiai jelei is fennálltak. Két esetben a perifériás idegek nagy felbontású ultrahangvizsgálatát is elvégeztük, amely során szegmentális szerkezeti eltérések, illetve az interfascicularis epineurium echogenitásának fokozódása volt látható, az idegek méretének megnövekedése nélkül. Következtetés - Magyarországon a transthyretin familiáris amyloid polyneuropathia ritkább, non-Val30Met-mutációformái fordulnak elő elsősorban, ahogy eseteinknél is. Szemben a Val30Met-formákkal, ezen mutációknál jellemző a kései kezdet és az egyidejűleg induló cardiomyopathia. Közleményünkkel szeretnénk rámutatni arra, hogy idősebb korban induló ismeretlen eredetű, progresszív, axonalis polyneuropathiában - főként szívbetegség társulása esetén - gondolni kell transthyretin familiáris amyloid polyneuropathiára.

Endomyocardial fibrosis (EMF) is the most common cardiac abnormality in hyeperosinophilic syndrome (HES), sometimes complicated with mitral valve disease. Mitral valve disease without ventricular manifestation is very rare, however. Case reports link HES to prosthetic valve thrombosis (PVT), but the optimal type of prosthetic valve in HES is not known. Herein is reported the case of a young female HES patient with secondary mitral valve degeneration and severe regurgitation. A mechanical prosthetic valve was implanted six months after she was diagnosed with HES, but despite anticoagulation and antiplatelet therapy she developed PVT three months later. Partially successful thrombolysis was followed by biological prosthetic valve implantation, with no further complications during the subsequent four years. The eosinophil count and treatment for HES was basically unchanged during the follow up period, following the initiation of treatment. Based on these findings it is suggested that, in HES, the implantation of a biological prosthetic valve might be preferable over a mechanical valve.

those on twice-weekly HD (HR = 0.64). Two limitations are noted. First, this was a prospective singlecenter study with a small number of participants and limited followup. Second, we failed to randomly allocate ESRD patients to thriceweekly HD or twice-weekly HD. In conclusion, thrice-weekly HD patients may be associated with increased risk of CVD, compared with those with twice-weekly HD. Our results have important clinical implications due to the global epidemic of ESRD and the escalating financial burden of RRT. We thank all staffs in our HD center for contributing to data collection, excellent patient care, etc.

Predicting the survival of a patient with heart failure (HF) is a complex problem in clinical practice. Our previous study reported that extracellular HSP70 (HSPA1A) correlates with markers of heart function and disease severity in HF, but the predictive value of HSP70 is unclear. The goal of this study was to analyze extracellular HSP70 as predictive marker of mortality in HF. One hundred ninety-five patients with systolic heart failure were enrolled and followed up for 60 months. By the end of follow-up, 85 patients were alive (survivors) and 110 died (nonsurvivors). HSP70 (measured by ELISA in the serum) was elevated in nonsurvivors, compared with survivors (0.39 [0.27–0.59] vs. 0.30 [0.24–0.43] ng/ml, respectively, p = 0.0101). In Kaplan–Meier survival analysis higher HSP70 levels above median were associated with a significantly increased mortality. In multivariable survival models, we show that HSP70 level above the median is an age-, sex-, body mass index-, creatinine-, and NT-proBNP-independent predictor of 5-year mortality in HF. Extracellular HSP70 could prove useful for estimating survival in patients with HF.

BACKGROUND: Inflammatory mechanisms involving complement activation has been shown to take part in the pathophysiology of congestive heart failure, but the initiating mechanisms are unknown. We hypothesized that the main initiator molecules of the lectin complement pathway mannose-binding lectin (MBL), ficolin-2 and ficolin-3 were related to disease severity and outcome in chronic heart failure. METHODS AND RESULTS: MBL, ficolin-2 and ficolin-3 plasma concentrations were determined in two consecutive cohorts comprising 190 patients from Hungary and 183 patients from Norway as well as controls. Disease severity and clinical parameters were determined at baseline, and all-cause mortality was registered after 5-years follow-up. In univariate analysis a low level of ficolin-3, but not that of MBL or ficolin-2, was significantly associated with advanced heart failure (New York Heart Association Class IV, p

Caseous calcification is a rare form of mitral annular calcification. Echocardiography reveals an echodense mass in the inferior mitral annulus with smooth borders and an echolucent inner core. We present a case where caseous calcification of the mitral annulus caused severe mitral regurgitation, atrial fibrillation and heart failure. Transthoracic echocardiography, transesophageal echocardiography, cardiac mag- netic resonance and computed tomography were performed and ensured the diagnosis. The mass was surgically removed and a prosthetic valve was implanted. We conclude that caseous calcification of the mitral annulus should be considered not only in the differential diagnosis of cardiac masses but also in the background of mitral regurgitation, atrial fibrillation and heart failure. This case also represents the usefulness of multimodal imaging in identifying cardiac masses.

Neuroendocrine activation with endothelial dysfunction is a key pathophysiological process in chronic heart failure (CHF). Although increased soluble E-selectin (sE-selectin) levels predict adverse events in several forms of cardiovascular disease, there are only scarce data on its predictive value in CHF. The aim of our study was to investigate whether sE-selectin is a useful predictor of mortality in CHF patients and whether its predictive power is additive to that of NT-proBNP.Plasma levels of sE-selectin were measured by ELISA in 192 CHF patients with clinical systolic heart failure. The study population was followed up for 14.9 months on average; 46 patients died during this period.Levels of sE-selectin were significantly higher in non-surviving patients than in survivors (p = 0.005) and significantly correlated with the following inflammatory markers: CRP (r = 0.242, p = 0.001), TNF-α (r = 0.201, p = 0.005), TNF-RII (r = 0.207, p = 0.004), and IL-6 (r = 0.339, p 0.0001). According to Cox regression analysis of the prediction power of sE-selectin for all-cause mortality, high sE-selectin levels independently and significantly predicted short-term mortality in CHF (HR 1.47, 95% CI 1.103-1.956). Furthermore, sE-selectin predicted mortality in CHF patients with concomitant diabetes mellitus, as well as simultaneously elevated sE-selectin and NT-proBNP levels additively predicted mortality.This study demonstrated a weak correlation of sE-selectin level with inflammatory markers and prediction of short-term mortality in diabetic CHF patients. Elevated serum sE-selectin levels and concomitantly increased NT-proBNP concentrations have additive predictive power in CHF. This suggests that parallel activation of various pathophysiological pathways confers increased risk of adverse outcome in CHF.

SummaryDecreased activity of ADAMTS13, the von Willebrand factor (VWF) cleaving protease, was recently reported in cardiovascular diseases and in hepatic failure. Chronic heart failure (CHF) is characterised by abnormalities of left ventricular function accompanied by the failure of the liver and dysregulation of endothelial activation. Therefore, the aim of our study was to measure ADAMTS13 activity in CHF, and determine the prognostic value of VWF and ADAMTS13 on major clinical events in CHF.ADAMTS13 activity (measured by FRETS-VWF73 substrate) was decreased in CHF (n = 152, left ventricular ejection fraction Decreased activity of ADAMTS13 with concomitant high VWF:Ag levels is a significant independent predictor of clinical events in CHF. The levels of the two molecules may integrate the impaired synthetic capacity of the liver and the disturbed endothelial regulation and can therefore be a useful tool to predict clinical events in CHF.

Objectives The goal of this study was to independently validate the recent observations on the predictive role of red cell distribution width (RDW) for outcomes in chronic heart failure and to provide epidemiologic data on the biological correlates of RDW in heart failure (HF). Understanding the mechanism underlying this observation is unclear, largely hampered by the lack of epidemiologic studies demonstrating factors that are associated with anisocytosis in cardiovascular diseases. Methods One hundred ninety-five patients (145 men, 50 women) with systolic HF were enrolled and followed up for a median of 14.5 months. Primary end points were all-cause mortality and hospital readmission due to worsening HF symptoms. A total of 19 clinical chemistry, hematology, and biochemical variables were considered for analysis together with clinical parameters in Cox proportional hazards and multiple regression models. Results Red cell distribution width was found to be an N-terminal pro–brain natriuretic peptide independent predictor of all-cause mortality (adjusted HR 1.61 per 1 SD increase) in our study. Multiple correlations between biomarkers of ineffective erythropoiesis (serum iron, ferritin, and soluble transferrin receptor levels), inflammation and acute-phase reaction (interleukin-6, soluble tumor necrosis factor (TNF) receptor I and soluble TNF receptor II, C-reactive protein, and prealbumin concentrations), undernutrition (total cholesterol and albumin levels), and renal function were observed. In the multiple regression model, the strongest relationship for RDW was obtained with soluble transferrin receptor, soluble TNF receptor I, soluble TNF receptor II, and total cholesterol. Conclusions Here we validate the strong, independent prediction of morbidity and mortality in HF by RDW. The described correlations between RDW and inflammation, ineffective erythropoiesis, undernutrition, and impaired renal function may facilitate the understanding why this marker is associated with adverse outcomes in HF.

Adrenomedullin (ADM) and endothelin-1 (ET-1) are novel promising peptide biomarkers in chronic heart failure (CHF). According to recent studies among their pleiotropic effect they play roles in the regulation of inflammation. The aim of the study was to measure the above mentioned two vasoactive peptides in parallel in a well characterized population of patients with CHF, and study their associations with inflammatory markers.A total of 186 patients (138 male, 48 female) with45% left ventricular ejection fraction (LVEF), and without acute inflammatory disease, were enrolled. Plasma midregional-proADM (MR-proADM) and C-terminal-proET-1 (CT-proET-1) were determined by a novel sandwich immunoluminometric assay.Increased MR-proADM and CT-proET-1 plasma levels were measured in patients with severe CHF (NYHA III-IV) as compared to the group of NYHA I-II (p0.0001). MR-proADM and CT-proET-1 levels showed significant negative correlation with serum albumin and prealbumin levels (por=0.0001), while positive correlations were found with levels of CRP, TNF-alpha, soluble TNF receptors and IL-6 (por=0.0001). In multiple linear regression models after adjustments for several potential confounders (disease severity [LV-EF, NYHA classes, NT-proBNP], ion and water homeostasis [sodium and presence of peripheral oedema], renal function [serum creatine]) the relationship between ADM and albumin, CRP, soluble TNF receptors and between ET-1 and CRP, TNF receptors and IL-6 remained significant.Vasoregulation and inflammation may be connected in heart failure patients independently of the disease severity. The observed link may contribute to the understanding of the complex pathomechanism in CHF.

A primer cardialis tumorok ritka kórképek, amelyek sokszor sokáig tünetmentesek maradhatnak. Az áttétet még nem adó tumor kuratív terápiája a reszekció és a kombinált célzott kemoterápiás kezelés. A legtöbb olyan esetben azonban, amikor a terime már nem reszekálható, szükséges lehet a biopszia elvégzése a pontos szövettani diagnózis felállításához, valamint a terápiás terv kidolgozásához. A következőkben egy 56 éves nőbeteg esetét ismertetjük, akinél ismétlődő pericardialis fluidum kivizsgálása során derült fény az intracardialis tumormassza jelenlétére. Az elváltozás nonreszekábilisnak bizonyult, így biopsziát és célzott kemoterápiás kezelést terveztünk. A beteg kisebb megterhelése érdekében a tumormassza-biopsziát nem thoracotomiából, hanem percutan katéteres módszerrel végeztük el. A biopszia pontosságát egy új módszer, az intracardialis ultrahang biztosította. Esetünk jól mutatja, hogy az intracardialis ultrahang vezérelte biopszia hatékony, biztonságos módszer, amely segíti a pontos mintavételt, és a beavatkozás biztonságosságát is növelheti.

Circulating heat shock protein 70 (Hsp70) is present in the circulation of healthy individuals and in patients with various disorders, including chronic heart failure (CHF). However, the source and routes of release of Hsp70 is only partially characterised in clinical samples. The purpose of this study was to study the clinical and biological correlates of Hsp70 in a CHF population and, for the first time, to investigate the association of HspA1B (also known as Hsp70-2) +1267 alleles with serum Hsp70 levels. A total of 167 patients (123 men, 44 women) with