Causes of elevated troponin in patients with normal coronary angiography

Troponin rise indicates myocardial cell injury. However, elevated values of troponin are not always consequence of infarction or ischemia. In this paper, aim was to elucidate diverse etiologies of elevated troponin in patients with normal coronary angiography. At KBC Zagreb in 2014 there was 976 patients identified from catheterization database who underwent coronary angiography due to suspicion of acute coronary syndrome (ACS). We identified 30 (3.1%) patients who had alternative cause for myocyte injury other than coronary artery disease (CAD), meaning that there was less than 30 % coronary arterial luminal stenosis. The elevation of cardiac troponin T (cTnT) in patients with normal coronary angiography was attributed to diverse etiologies, including hypertensive crisis, Takotsubo syndrome, severe aortic stenosis, atrial fibrillation (AF), chronic obstructive pulmonary disease (COPD) exacerbation, advanced heart failure, hypertensive cardiomyopathy, acute pulmonary embolism, malignant disease progression, and cardiogenic shock. Apart from ACS, cTnT could be elevated in a number of different conditions, which should be considered according to clinical presentation, different diagnostic procedure, and still could reflect myonecrosis, even in the absence of significant angiographic CAD

Medication related osteonecrosis of the jaw

Medikamentozna osteonekroza čeljusti, je bolest, koja nastaje upotrebom dviju vrsta lijekova: antiangiogenih lijekova te antiresorptivnih lijekova. Najpoznatiji uzročnik medikamentozne osteonekroze te lijekovi pri kojima je prvi puta otkrivena medikamentoza osteonekroza su bifosfonati koji spadaju u skupinu antiresorptivnih lijekova. Sam mehanizam nastanka medikamentozne osteonekroze nije do današnjega dana razjašnjen, ali postoje različite teorije njezinog nastanka. Postoje također različiti čimbenici, o kojima ovisi incidencija osteonekroze, kao što su način primjene lijeka, trajanje terapije, doziranje specifičnog lijeka, potentnost samoga lijeka, njegova akumulacija u tijelu te incidencija koja je ovisna o lokalnim, anatomskim te sistemskim faktorima. Medikamentoznu osteonekrozu klinički dijelimo na 4 različita stadija, s obzirom na količinu eksponirane kosti te upalu okolnoga tkiva. Stadije klasificiramo od brojke 0 do broja 3. Medikamentoznu osteonekrozu liječimo različito u različitim stadijima. Kako dijelimo osteonekrozu na četiri stadija, tako je i pristup terapiji u svakom stadiju osteonekroze različit. Prevenciju nastanka medikamentozne osteonekroze također dijelimo na preventivu koju provodimo prije početka terapije lijekovima i na preventivu koju provodimo nakon terapije lijekovima ili za vrijeme terapije.Medication-related osteonecrosis of the jaw is a disease that occurs with the use of two types of medication; antiangiogenic drugs and antiresorptive drugs. The most known cause of medication related osteonecrosis as well as medication which has been the first to detect medication-related osteonecrosis are bisphosphonates, which belong to the group of antiresorptive drugs. The mechanism for the development of medication-related osteonecrosis, is still not clarified to this day, although different theories exist explaining the development. There are also various factors that depend on the incidence of osteonecrosis, such as the mode of administration of the drug, duration of therapy, specific drug dosage, potency of the drug itself, its accumulation in the body, also incidence dependent on local, anatomic and systemic factors. Medication-related osteonecrosis is divided into 4 different stages, considering the amount of exposed bone and inflammation of the surrounding tissue. Stages are classified from 0 to 3. Medication related osteonecrosis is treated differently at different stages. Since osteonecrosis is separated into four stages, therapy at each stage of osteonecrosis is specific to the stage which has been diagnosed. Prevention of medication-related osteonecrosis is separated into two preventative measures. First line of prevention is before drug therapy begins and secondly as well as after therapy with drugs or during treatment

Causes of elevated troponin in patients with normal coronary angiography

Troponin rise indicates myocardial cell injury. However, elevated values of troponin are not always consequence of infarction or ischemia. In this paper, aim was to elucidate diverse etiologies of elevated troponin in patients with normal coronary angiography. At KBC Zagreb in 2014 there was 976 patients identified from catheterization database who underwent coronary angiography due to suspicion of acute coronary syndrome (ACS). We identified 30 (3.1%) patients who had alternative cause for myocyte injury other than coronary artery disease (CAD), meaning that there was less than 30 % coronary arterial luminal stenosis. The elevation of cardiac troponin T (cTnT) in patients with normal coronary angiography was attributed to diverse etiologies, including hypertensive crisis, Takotsubo syndrome, severe aortic stenosis, atrial fibrillation (AF), chronic obstructive pulmonary disease (COPD) exacerbation, advanced heart failure, hypertensive cardiomyopathy, acute pulmonary embolism, malignant disease progression, and cardiogenic shock. Apart from ACS, cTnT could be elevated in a number of different conditions, which should be considered according to clinical presentation, different diagnostic procedure, and still could reflect myonecrosis, even in the absence of significant angiographic CAD

Cyprinid herpesvirus 3 : an intersting virus for applied and fundamental research

peer reviewe

Everything in Moderation – Athlete\u27s Heart

Brojna klinička istraživanja dokazala su jasne koristi tjelesne aktivnosti za kardiovaskularno, ali i opće zdravlje svakoga čovjeka. Tjelesna aktivnost izaziva fiziološki odgovor organizma koji dovodi do različitih prilagodba pojedinih organskih sustava, a primjer jedne od njih jest i sportsko srce – benigni i reverzibilni odgovor kardiovaskularnog sustava na ponavljanu i intenzivnu tjelesnu aktivnost. Neke bolesti miokarda mogu dijeliti slične elektrokardiografske, ehokardiografske i druge karakteristike sa sportskim srcem. Pravodobno prepoznavanje takvih bolesti ključno je za zaštitu zdravlja svih koji se bave intenzivnijom tjelesnom aktivnosti rekreativno ili profesionalno.Numerous clinical studies have demonstrated obvious benefits of physical activity for cardiovascular, as well as general health of every human being. Physical activity induces a physiological response resulting in different adaptations of individual organ systems. One of such adaptations is the athlete\u27s heart representing a benign and reversible reaction of the cardiovascular system to repeated and intensive physical activity. Some of the myocardial diseases may share electrocardiographic, echocardiographic and other features similar to those of the athlete\u27s heart. Timely recognition of such diseases is crucial to the health of everyone who is engaged in a more intensive physical activity, either recreationally or professionally

Human cytokines activate JAK–STAT signaling pathway in porcine ocular tissue

Background: The JAK/STAT (Janus Tyrosine Kinase, Signal Transducers and Activators of Transcription) pathway is associated with cytokine or growth factor receptors and it is critical for growth control, developmental regulation and homeostasis. The use of porcine ocular cells as putative xenotransplants appears theoretically possible. The aim of this study was to investigate the response of various porcine ocular cells in vitro to human cytokines in regard to the activation of JAK-STAT signaling pathways. Methods: Porcine lens epithelial cells, pigmented iris epithelial cells and pigmented ciliary body cells were used in this study. These cells were isolated from freshly enucleated porcine eyes by enzymatic digestion. Cultured cells between passages 3–8 were used in all experiments. Electromobility shift assay (EMSA), proliferation assay, immunofluorescence staining and flow cytometry were used to evaluate the JAK-STAT signaling pathway in these cells. Results: JAK/STAT signaling pathways could be activated in porcine pigmented epithelial ciliary body cells, in pigmented iris epithelial cells and in lens epithelial cells in response to porcine and human interferons and cytokines. All cells showed very strong STAT1 activation upon stimulation with porcine interferon-gamma. Porcine ocular cells also respond to human cytokines; IFN-alpha induced strong activation of STAT1 in EMSA, flow cytometry and immunofluorescence experiments whereas activation of STAT3 was less strong in EMSA, but strong in flow cytometry and immunofluorescence. Human recombinant IL-6 activated STAT3 and human IL-4 activated STAT6. With the help of immunofluorescence assay and flow cytometry we observed nuclear localization of STAT proteins after activation of porcine ocular cells with cytokines and interferons. Human IFN-α had an inhibitory effect on porcine ocular cells in proliferation assays. Conclusion: Our study demonstrated that some types of human cytokines and interferon activate intracellular JAK-STAT signaling pathways in porcine ocular cells. We hypothesize that direct stimulation of the JAK-STAT pathway in porcine cells in response to human cytokines will lead to complications or failure, if pig-to-human ocular tissue xenotransplantation were to be carried out. For successful xenotransplantation among other obstacles there must be new approaches developed to regulate signaling pathways

Lower platelet count early after the heart transplantation is associated with lower rates of cellular-mediated rejection within 24 months after heart transplantation

Background: Decrease in platelet count following the induction with polyclonal anti-thymocyte globulin (ATG) is deemed as an adverse event, while decrease in lymphocyte count represents a therapeutic goal1. Still, the effect on platelets may represent an important part of ATG anti-rejection mechanisms. Patients and Methods: This was a retrospective single-center study of consecutive HTx (heart transplantation) patients (pts) from February 2010 to February 2018 in University Hospital Centre Zagreb. All pts received rATG (Thymoglobulin®) 1.5 mg/kg daily during the first 5 days. Complete blood count with differential was assessed on days 0, 7 and 14 after HTx. The incidence of cellular-mediated rejection (ACR) was monitored for two years after HTx. ACR was classified according to ISHLT classification from 1990 and expressed as ACR of grade 1B or higher (≥1B). Results: A total of 159 pts were transplanted. Median age was 55 years (IQR, 47-62 years), 76% were male. A total of 27 pts (17 %) experienced ACR ≥1B during 24 months. Pts with ACR of grade ≥1B had higher platelet count on day 7 (145 vs 104 x 103/μL, p<0.001). They also had higher the absolute lymphocyte count (ALC) on the same day, but this did not reach statistical significance (162 vs 130 x 103/μL, p=0.19) and there was no correlation between ALC and platelet counts on day 7 (Pearson’s correlation coefficient was 0.064, p=0.459). Conversely, more rejection was observed in pts with higher ALC on day 14 (326 vs 190 x 103/μL, p=0.035), with a trend towards statistical significance in the relationship with higher platelet count (210 vs 199 x 103/μL, P=0.076). In the univariate analysis, higher platelet count on day 7, younger recipient age and negative pre-transplant Cytomegalovirus (CMV) IgG serology were found as predictors of the ACR ≥1B in the first 2 years after HTx (Table 1). In multivariable model, platelet count on day 7 and pre-transplant CMV serostatus were independent predictors of rejection. ROC analysis of the aforementioned model showed a satisfying AUC of 0.75. Conclusion: Decrease in platelet count following the induction with rATG is strongly related to less graft rejection that is independent from the lymphodepleting effect. This indicates the importance of platelet involvement in anti-rejection mechanisms of ATG induction, and consequently a possible rationale for targeting platelets in future immunosuppressive regimens

Causes of Elevated Troponin in Patients with Normal Coronary Angiography

Porast troponina u većini slučajeva upućuje na oštećenje stanica miokarda, no povišene vrijednosti troponina nisu uvijek posljedica infarkta ili ishemije. Svrha je ovog istraživanja bila osvijetliti različite uzroke povišenoga troponina u bolesnika s normalnim nalazom koronarografije. U Kliničkom bolničkom centru Zagreb 2014. godine izdvojeno je 947 bolesnika iz baze podataka Laboratorija za invazivnu kardiologiju, u kojih je učinjena koronarografija radi postavljanja dijagnoze akutnoga koronarnog sindroma (ACS). Trideset dva bolesnika (3,38 %) nisu imala uzrok oštećenja miocita od koronarne bolesti srca (CAD), definiranoj kao stenoza lumena koronarnih arterija veća od 30 %. Porast miokardnoga troponina T (cTnT) u bolesnika s normalnim koronarnim arterijama rezultat su različitih uzroka, uključujući hipertenzivnu bolest srca, Takotsubo sindrom, supraventrikulsku tahikardiju, miokarditis i dilatativnu kardiomiopatiju, da spomenemo samo neke. Osim u ACS-u, cTnT može biti povišen u nizu različitih stanja, o čemu treba razmišljati kada se razmatra klinička slika, i to može biti odraz nekroze miokarda i u odsutnosti značajne CAD.Troponin elevation usually indicates myocardial cell injury. However, elevated values of troponin are not always a consequence of infarction or ischemia. The aim of this study was to elucidate the diverse etiologies of elevated troponin in patients with normal coronary angiography. There were 947 patients at the Zagreb University Hospital Centre identified from the catheterization database who underwent coronary angiography in 2014 due to suspected acute coronary syndrome. We identified 32 (3.38%) patients who had an alternative cause for myocyte injury other than coronary artery disease, defined as coronary artery lumen stenosis above 30%. The elevation of cardiac troponin T (cTnT) in patients with normal coronary angiography was found to be the consequence of diverse etiologies, including hypertensive heart disease, Takotsubo syndrome, supraventricular tachycardia, myocarditis, and dilated cardiomyopathy, to name a few. Apart from acute coronary syndrome, cTnT can be elevated in a number of different conditions, which should be considered according to clinical presentation, and that could still reflect myocardial necrosis even in the absence of significant coronary artery disease

Myelodysplastic syndrome in a patient with untreated chronic lymphoproliferative neoplasm

U bolesnika s kroničnom limfoproliferativnom bolesti (LPB) veća je učestalost nastanka sekundarnih neoplazma. Istodobna pojava limfoproliferativne neoplazme (LPN) i mijelodisplastičnog sindroma (MDS) vrlo je rijetka. Druga hematološka neoplazma dijagnosticira se slučajno tijekom kontrola ili pri dodatnim analizama zbog nesukladnih kliničkih ili laboratorijskih nalaza. Prikazujemo dijagnostički postupak, tijek bolesti i liječenje 65-godišnje bolesnice s kroničnom limfoproliferativnom neoplazmom i MDS-om sa suviškom blasta tipa 2 (MDS-EB2). Vodeći nalaz bila je neutropenija, a tek su citološkim analizama koštane srži i periferne krvi dijagnosticirane navedene neoplazme. Liječenje jedne i druge hematološke neoplazme nije dalo zadovoljavajuće rezultate i MDS je progredirao u akutnu mijeloičnu leukemiju. U bolesnika s limfoproliferativnom neoplazmom i citopenijom valja tragati za mogućim drugim uzrocima takvih aberantnih nalaza. Pri liječenju tih bolesnika razumno je liječiti dominantnu bolest.High frequency of second malignancies is observed in chronic lymphoproliferative disease (LPD) patients. The simultaneous occurrence of myelodysplastic syndrome (MDS) with untreated LPD is extremely rare. Second haematological neoplasms are usually diagnosed incidentally during a routine clinical check-up, or due to discordant clinical or laboratory findings. We are reporting diagnostic procedures, clinical course, and treatment of a 65-year-old woman with chronic lymphoproliferative neoplasm and MDS with excess of blasts type 2 (MDSEB2). Neutropenia was the most aberrant finding. A diagnosis of two malignant haematological neoplasms was done by cytological analysis and immunophenotyping of bone marrow and peripheral blood cells. In spite of treating both neoplasms no satisfactory results were achieved and MDS progressed to acute myeloid leukaemia. In patients with lymphoproliferative neoplasms and cytopenias it is important to find out other causes of these laboratory findings. In such patients the dominant disease should be treated. A concomitant MDS should be suspected and examined