Podcasts about ctni

AABP Executive Director Dr. Fred Gingrich reviews a paper published in The Bovine Practitioner with the first author Madeline Mancke from Kansas State University. The objective of this study was to determine potential associations between Cardiac Troponin I (cTnI) serum concentration of cattle at initial bovine respiratory disease (BRD) treatment with the risk of retreatment or mortality at 60 days. BRD is the most significant disease in beef cattle and is a major cause of morbidity and mortality. Developing prognostic tools may be valuable for managing individual cases. cTnI is a protein that is released into the circulatory system after myocardial damage and may be useful as a biomarker for prognostication of BRD cases. Mancke walks through the results of the paper which demonstrated that 8/318 samples had high cTnI levels and animals with high cTn1 concentrations had a significantly greater probability of not finishing the 60-day post-enrollment period. Cattle with high cardiac troponin concentrations at initial BRD treatment were more likely to have negative clinical outcomes but, in this study, very few animals had high cTnI levels. Mancke provides information about potential future research opportunities to better manage BRD cases in the feedyard.  The Bovine Practitioner is the peer-reviewed journal published by AABP. The journal publishes original research, case studies, review articles and case studies that are intended to provide information to the practicing cattle veterinarian. The journal is available open-access online and print volumes are available for purchase. There are no publication fees for authors and the peer review and submission process is managed online. Find the journal at this link.  Evaluation of cardiac troponin I as a predictor of clinical outcomes in cattle treated for bovine respiratory disease (BRD) in commercial feedyards. Bov Pract. 2025;59(1), 24-28. https://doi.org/10.21423/bpj20259053 

The JournalFeed podcast for the week of July 22-26, 2024.These are summaries from just 2 of the 5 articles we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member.Thursday Spoon Feed:The first direct comparison of the Clinical Institute Withdrawal Assessment-Alcohol Revised (CIWA-Ar) scale to a slightly modified Richmond Agitation and Sedation Scale (mRASS-AW) in a pre-post quality assurance study found mRASS-AW to not compromise length of stay or safety for the evaluation of alcohol withdrawal syndrome (AWS), while we already know it to be faster and more intuitive.Friday Spoon Feed:This RCT of U.S. patients being evaluated for acute MI using a 0/1 hour hs-cTnI protocol, compared to standard care with a 0/3 hour hs-cTnI protocol, didn't find a difference in the percentage of patients discharged from the ED nor in the rates of 30 day death or MI.

In today's VETgirl online veterinary CE podcast, we're going to review a study by Morey et al out of University of Missouri entitled “N-terminal brain natriuretic peptide, cardiac troponin-I, and point-of-care ultrasound in dogs with cardiac and noncardiac causes of nonhemorrhagic ascites.”

Our latest episode dissects three groundbreaking studies that are reshaping our understanding of the heart and its intricate connections to the body and mind.   STUDY #1: First, we explore the potential of high-sensitivity cardiac troponin I (hs-cTnI) in risk-stratifying patients with known coronary artery disease. While current guidelines don't yet recommend these tests, could there be untapped value in using troponin concentration as a preventive treatment guide? Join us as we explore the intriguing possibilities and implications presented in this study from the Journal of the American College of Cardiology. Wereski, R, Adamson, P, Daud, NSS, et al. 2023. High-sensitivity cardiac troponin for risk assessment in patients with chronic coronary artery disease. J Am Coll Cardiol. 6: 473–485. (https://doi.org/10.1016/j.jacc.2023.05.046)   STUDY #2: Next, we shift our focus to the brain-heart connection. Ever wondered about the cognitive repercussions of a myocardial infarction (MI)? This study from JAMA Neurology sheds light on the potential cognitive consequences of an MI.  Johansen, MC, Ye, W, Gross, A, et al. 2023. Association between acute myocardial infarction and cognition. JAMA Neurol. 7: 723–731. (https://doi.org/10.1001/jamaneurol.2023.1331)   STUDY #3: Third, we dive deep (pun intended!) into decompression illness. Certain divers might want to reconsider their next dive because a recent Annals of Internal Medicine study suggests a primary mechanism behind decompression illness that could change the way we perceive diving risks. What are the implications for those passionate about the deep blue? Lee, H-J, Lim, DS, Lee, J, et al. 2023. Decompression illness in divers with or without patent foramen ovale: A cohort study. Ann Intern Med. 7: 934–939. (https://doi.org/10.7326/M23-0260)   Don't miss out on these captivating discussions. Listen in to stay at the forefront of cardiology insights and to satiate your curiosity about these studies' findings. We promise, it's a heartbeat away from being your favorite episode yet! For show notes, visit us at https://www.medmastery.com/podcasts/cardiology-podcast.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.03.526715v1?rss=1 Authors: Elezaby, A., Lin, A. J., Vijayan, V., Pokhrel, S., Bechara, L. R., Ostberg, N. P., Queliconi, B. B., Campos, J. C., Ferreira, J. C., Haileselassie, B., Mochly-Rosen, D. Abstract: Cardiac troponin I (cTnI) is a sarcomeric protein critical to myocyte contraction. Unexpectedly, we found that some cTnI localized to the mitochondrial matrix in the heart, inhibited mitochondrial functions when stably expressed in non-cardiac cells and increased opening of the mitochondrial permeability transition pore under oxidative stress. Direct, specific, and saturable binding of cTnI to ATP synthase was demonstrated in vitro, using immune-captured ATP synthase, and in cells using proximity ligation assay. cTnI binding doubled F1F0 ATPase activity, whereas skeletal troponin I and several human mutant cTnI variants associated with familial hypertrophic cardiomyopathy did not. A rationally-designed ten amino acid peptide, P888, inhibited cTnI binding to ATP synthase and cTnI-induced increase in ATPase activity in vitro and reduced cardiac injury following transient ischemia in vivo. We therefore suggest that mitochondria-associated cTnI may inhibit cardiac ATP synthase under basal conditions; pharmacological agents that release this inactivating effect of cTnI and thus preventing ATP hydrolysis during cardiac ischemia may increase the reservoir of functional mitochondria to reduce cardiac injury. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this VETgirl online veterinary continuing education podcast, we discuss the cardiac biomarkers in veterinary medicine. Biomarkers have been shown to be useful in assessment of severity of disease and etiology of clinical signs in cats with cardiomyopathies. The two cardiac biomarkers most thoroughly studied to date are N-terminal pro B-type natriuretic hormone (NT-proBNP) and cardiac troponin-I (cTnI). NT-proBNP provides information regarding degree of myocardial stretch and stress, while cTnI is more specific for assessing severity of myocardial injury. Hypertrophic cardiomyopathy (HCM) is superficially thought of as a singular disease but actually encompasses a mosaic of various phenotypes dependent on location and heterogeneity of hypertrophy and presence or absence of obstructive processes. The most common obstructive process is dynamic left ventricular outflow tract obstruction (DLVOTO) in association with systolic anterior motion of the mitral valve (SAM), identified in up to 30% of cats with HCM. The presence of this finding in cats with HCM constitutes a diagnosis of hypertrophic obstructive cardiomyopathy, or HOCM. Elevations in both NTproBNP and cTnI have been documented in cats with HCM/HOCM but whether differential elevations in these markers occurs in cats with HCM vs cats with HOCM has not been thoroughly investigated. So, Seo et al out of the United Kingdom wanted to evaluate this in a study entitled Biomarker changes with systolic anterior motion of the mitral valve in cats with hypertrophic cardiomyopathy. The authors also aimed to determine what other relevant clinical factors might affect the degree of elevation of NTproBNP and/or cTnI. They hypothesized that cats with obstructive disease would have higher elevations in these biomarkers than those without.

Bienvenue dans le sixième épisode Dans la Niche.  Pour ce nouvel épisode "Dans la Niche", je voulais vous parler de sport canin, histoire de se remotiver un peu. On en en plein mois de novembre, il fait froid, le soleil n'est pas souvent de sortie et on a beaucoup moins envie de sortir, avec ou sans chien d'ailleurs. Pourtant, votre chien a toujours autant besoin de bouger et vous aussi. Alors voici quelques conseils pour s'y mettre ou s'y remettre. Rester bien jusqu'au bout, je vous propose un petit challenge à faire tous ensemble à la fin de cet épisode.  Sommaire :  00:10 : Présentation de l'épisode 01:38 : Introduction 02:53 : Les multiples intérêts des sports canins 05:53 : Des sports canins pour tous les goûts 09:10 : Bien débuter en sport canin 15:00 : Challengeons-nous pour bouger plus avec nos chiens 17:07 : Soutenir le podcast On en parle dans cet épisode :  Idog : https://www.i-dog.eu/fr EP16 : http://laniche-podcast.fr/recipes/ep16-margotjeremieloxen Margot : https://www.instagram.com/margot_dvg/ Yannick Thoulon : http://www.canissimo.fr/ EP13 : http://laniche-podcast.fr/recipes/ep13-yannickcanissimo Cynotopia : https://www.cynotopia.fr/proprioception-guide-exercices EP14 : http://laniche-podcast.fr/recipes/ep14-corentinliskaoxy Corentin : https://www.cotechiens.com/ Rendre son chien heureux - Elodie Martins et Françoise Claustre EP10 : http://laniche-podcast.fr/recipes/ep10-meganeestelleqwild Qru : https://qru.pet/ Le club CTNI à Lyon pour les sports de traction : https://www.ctni-canicross.fr/ Muzo : https://www.camillenguyen.com/ DLN02 : http://laniche-podcast.fr/02-promenons-nous DLN03 : http://laniche-podcast.fr/03-libere-delivre Poursuivez votre écoute en suivant La Niche sur : Le site : http://laniche-podcast.fr/ Instagram : https://www.instagram.com/lanichepodcast/ Facebook : https://www.facebook.com/lanichepodcast YouTube : https://www.youtube.com/channel/UC8FGY3ZcycTD6AfcTVNaIKA Musique : Dolling - Cybersdf Source: https://soundcloud.com/cybersdf Licence: https://creativecommons.org/licenses/by/3.0/deed.fr Téléchargement (6MB): https://auboutdufil.com/?id=502

FDA 批准颈动脉窦压力反射刺激疗法治疗心衰Lancet 血ACE2水平与心血管疾病及死亡的关系Science子刊 一种具有几何适应性的人工心脏瓣膜BAROSTIM NEO系统BAROSTIM NEO系统包括一个植入式脉冲发生器（IPG）、一个颈动脉窦含铅套件和一个程序。医生将BAROSTIM NEO脉冲发生器植入晚期心力衰竭患者的左或右锁骨下方，并在患者的左或右颈动脉窦处放置颈动脉窦导线，然后将脉冲发生器连接到颈动脉窦导线上。医生根据病人的个人需求制定脉冲发生器程序，然后向颈动脉的压力感受器传递电脉冲。压力反射激活（BAT）疗法的目的是激活颈动脉壁的压力感受器，刺激自主神经系统的传入和传出神经，大脑接收到神经信号作出相应反应：松弛血管、降低心率、并通过改善肾功能来减少液体储留。2019年8月，FDA批准BAROSTIM NEO系统用于药物治疗无效的、不符合心脏再同步化治疗适应症的、难治性心力衰竭患者。《BeAT-HF研究：这项研究证明了压力反射刺激疗法（BAT）对射血分数降低的心力衰竭患者的安全性和有效性》Journal of American College of Cardiology，2020年7月 (1) BeAT-HF研究是一项多中心、前瞻性、随机对照研究，纳入408名射血分数降低的心力衰竭（HFrEF）患者中，入组要求：纽约心功能分级II-III级、射血分数≤35%、药物治疗方案稳定≥4周、不符合心脏再同步化治疗的I类指征。这篇报告重点汇报了D队列中、NT-proBNP

FDA 批准颈动脉窦压力反射刺激疗法治疗心衰Lancet 血ACE2水平与心血管疾病及死亡的关系Science子刊 一种具有几何适应性的人工心脏瓣膜BAROSTIM NEO系统BAROSTIM NEO系统包括一个植入式脉冲发生器（IPG）、一个颈动脉窦含铅套件和一个程序。医生将BAROSTIM NEO脉冲发生器植入晚期心力衰竭患者的左或右锁骨下方，并在患者的左或右颈动脉窦处放置颈动脉窦导线，然后将脉冲发生器连接到颈动脉窦导线上。医生根据病人的个人需求制定脉冲发生器程序，然后向颈动脉的压力感受器传递电脉冲。压力反射激活（BAT）疗法的目的是激活颈动脉壁的压力感受器，刺激自主神经系统的传入和传出神经，大脑接收到神经信号作出相应反应：松弛血管、降低心率、并通过改善肾功能来减少液体储留。2019年8月，FDA批准BAROSTIM NEO系统用于药物治疗无效的、不符合心脏再同步化治疗适应症的、难治性心力衰竭患者。《BeAT-HF研究：这项研究证明了压力反射刺激疗法（BAT）对射血分数降低的心力衰竭患者的安全性和有效性》Journal of American College of Cardiology，2020年7月 (1) BeAT-HF研究是一项多中心、前瞻性、随机对照研究，纳入408名射血分数降低的心力衰竭（HFrEF）患者中，入组要求：纽约心功能分级II-III级、射血分数≤35%、药物治疗方案稳定≥4周、不符合心脏再同步化治疗的I类指征。这篇报告重点汇报了D队列中、NT-proBNP

Aralık 2019’da hayatımıza giren SARS-CoV-2, asemptomatik subklinik enfeksiyon tablosundan ARDS’ye kadar giden geniş bir spektrumda hastalık tablosuna yol açabilen ve kardiyovasküler etkileri açısından da başından beri tıp camiasında pek çok tartışmayı beraberinde getiren bir patojen. Halihazırda kardiyovasküler komorbiditelere sahip hastalarda mortalite ve morbidite artarken, virüsün kendisinin yol açtığı miyokardiyal hasar da beraberinde ek kardiyak komplikasyonlar getirebiliyor. Bu nedenle SARS-CoV-2’nin kardiyovasküler etkileri üzerine bir derleme yapmak istedim. COVID-19 hakkında güncel verilerin oldukça dinamik bir şekilde değiştiğini ve yazının mevcut tarihe dek olan literatürü kapsadığını hatırlatarak keyifli okumalar diliyorum. SARS-CoV-2 ve Özellikleri Kardiyak etkilerini daha iyi anlamak adına öncelikle virüsün kendisinden ve oluşturduğu tablonun patofizyolojisinden bahsedelim. Coronavirüsler, Coronaviridae familyası içinde 26 ila 32 kb uzunluğunda tek sarmallı pozitif RNA virüsleridir. SARS-CoV-2 ise bu ailenin betacoronavirüs kolundandır, enfekte hücreye S1 ucu ile bağlanırken, S2 ucu enfekte olmuş hücreye füzyonuna yardımcı olur. S1 alt birimi, N-terminal alanı ve C-terminal alanı olmak üzere iki alana bölünür. SARS-CoV ve SARS-CoV-2 (ve bir alfacoronavirüs olan HCoV-NL63), C-terminal alanı yoluyla tip II alveoler epitelyal hücreler, bağırsak epiteli, makrofajlar, perisitler ve diğer hücrelerde bulunan anjiyotensin dönüştürücü enzim 2 (ACE2) reseptörüne bağlanır. SARS-CoV-2, SARS-CoV'ye göre daha yüksek afiniteyle ACE2'ye bağlanır ve daha fazla bağlanma ve etkileşim bölgesi içerir. ​1​ Peki kardiyovasküler açıdan bunlar neden önemlidir? ACE2, perisitlerde yüksek oranda eksprese edildiğinden mikrovasküler disfonksiyon gelişimine ve dolayısıyla akut koroner sendromlar başta olmak üzere vasküler hasarlanmaya yol açabilir.​2​ Dahası, kalp yetmezliği olan hastalarda ACE2 ekspresyonu up-regüle edilir, bu da kalp yetmezlikli hastalarda virüsün yüksek enfektivitesini ve kalp yetmezliği olan hastalarda yüksek mortalite oranlarını açıklar. Ayrıca, coronavirüslerin hücreye ACE2 yoluyla girişi, vasküler instabilite ve hipotansiyona sebep olarak, bilinen hipertansiyonu olan enfekte hastalarda mortaliteyi arttırır.ACE2 inhibisyonu, immün sistem regülasyonunda bozulma, sitokin aktivitesine bağlı artan metabolik talep ve prokoagülan aktivite, COVID-19 ile ilişkili kardiyovasküler hastalığı olanlarda istenmeyen sonuçlara yol açan olası etkenler olarak görünmekte. Bir tablo ile bunları özetleyerek devam edelim.​3​ SARS-CoV-2 ve kardiyovasküler etkiler Miyokardiyal Hasar Bilindiği üzere inflamatuar miyokarditlerin en sık nedeni viral enfeksiyonlardır.​4​ Haliyle miyokard hasarı yapan ilk virüs coronavirüs değildi. Aynı aileden SARS da hastalarda kalp yetmezliği, aritmi, sistolik/diyastolik disfonksiyon ve ani ölüme sebep olabiliyordu.​5​ Ancak SARS-CoV-2 için miyokard hasarını gösteren belirteçler, diğer Coronavirüslere göre daha somut şekilde ortaya konmuş durumdadır. Özellikle COVID-19 kritik hastalarında miyokardiyal hasar ve inflamasyonun belirteçleri olan yüksek NT-proBNP, yüksek cTnI, yüksek hs-CRP gibi faktörler ve ileri yaş, erkek cinsiyet, bilinen hipertansiyon ve koroner kalp hastalığı varlığı gibi risk faktörleri, yoğun bakım gereksiniminde ve mortalitede artış ile ilişkili bulunmuştur.​6​ ​7​ ​8​ Ek olarak, SARS-CoV-2 nedeniyle takip edilen 150 hastanın dahil edildiği ve 68 hastanın hayatını kaybetmesi sonucu mortalite verilerinin incelendiği bir çalışmada, ölen hastaların 5'inde ölüm nedeni olarak dolaşım yetmezliğine yol açan miyokard hasarı ve 22’sinde miyokard hasarının eşlik ettiği solunum yetmezliği görülmüştür.​9​ Ölen hasta grubundaki kardiyak troponin ve miyoglobin düzeyleri iyileşen gruba göre anlamlı derecede yüksek bulunmuş ve ölen hastaların bazılarında fulminan miyokardit gelişmiş olabileceğinden şüphelenilmiştir. Miyokard hasarı ve miyokardit spesifik olmayan ST segment-T dalga anorma...

Commentary by Dr. Valentin Fuster

Assista também em vídeo: https://youtu.be/UNeLgN2nt-E Este é o PodCast diálogo com os espíritos, a versão em áudio dos vídeos disponíveis em www.youtube.com/jeffersonviscardi. Não conhece o projeto diálogo com os espíritos? Visite a página do youtube ou o nosso website: www.dialogocomosespiritos.com.br e tenha sempre acesso aos diálogos mais recentes.

Assista também em vídeo: https://youtu.be/UNeLgN2nt-E Este é o PodCast diálogo com os espíritos, a versão em áudio dos vídeos disponíveis em www.youtube.com/jeffersonviscardi. Não conhece o projeto diálogo com os espíritos? Visite a página do youtube ou o nosso website: www.dialogocomosespiritos.com.br e tenha sempre acesso aos diálogos mais recentes.

Abstract: Background: Myocardial injury can be detected by cardiac troponin I (cTnI) concentrations, which appears to be a predictor of short-term death in critically ill patients. It is unknown if the best prognostic indicator of short-term survival is cTnI measurement at admission or at later time points. Hypothesis/Objectives: Measuring cTnI with a high-sensitivity (hs) test at different time points after admission may be a better short-term prognostic indicator than a single cTnI measurement at admission in dogs with systemic inflammatory response syndrome (SIRS). Animals: Prospective, observational clinical study of 60 dogs with SIRS. Methods: Cardiac troponin I concentration was measured in 133 serum samples, collected at days 1, 2, 3 and 5. Additionally, the acute patient physiologic and laboratory evaluation (APPLE) fast score was evaluated at admission. Prognostic capabilities of cTnI measurement and APPLE fast score for 28-day mortality were assessed by receiver operating characteristic (ROC) curve analysis. Results: Forty-one dogs with SIRS that survived 28 days had significantly lower serum cTnI concentrations at admission (median, 0.09 ng/mL; p = 0.004) and at the peak time point (median, 0.23 ng/mL; p = 0.01) compared to 19 non-survivors (median at admission, 0.63 ng/mL; median at peak, 1.22 ng/mL). Area under the curve (AUC) to predict survival, using cTnI was similar at admission (0.732) and at peak (0.708), and was 0.754 for the APPLE fast score. Conclusions: Increased cTnI concentration in dogs with SIRS is associated with poor outcome. Daily follow-up measurement of cTnI concentration provides no additional prognostic information for short-term mortality.

Hintergrund Klinisches Standardverfahren zur Überwachung der linksventrikulären Funktion unter potenziell kardiotoxischer antineoplastischer Therapie ist die transthorakale Echokardiographie. Ziel dieser Studie war die Evaluation des USCOM® und der Laborparameter BNP, NT-proBNP und cTnI in der Überwachung der Herzfunktion unter potenziell kardiotoxischer antineoplastischer Therapie. Patienten und Methoden Bei insgesamt 68 Patienten [Anthrazykline (A) n=21, Trastuzumab (T) n=10, Bevaci-zumab (B) n=19, Cetuximab (C) n=18] wurde vor (T0) und nach (T1) der Infusion des potenziell kardiotoxischen Agens, nach einer Woche (T2) und nach drei Monaten (T3) eine Untersuchung mit dem USCOM® durchgeführt und die Laborspiegel bestimmt. Parallel dazu erfolgte eine echokardiographische Untersuchung vor und drei Monate nach Therapiebeginn. Die Ergebnisse von USCOM® (SVUSCOM), Echokardio-graphie (EFEcho) und die Laborspiegel wurden zu den jeweiligen Zeitpunkten korreliert. Ergebnisse Kein Patient entwickelte klinische Zeichen einer Herzinsuffizienz. Innerhalb der Patientengruppen korrelierten die in der Echokardiographie erhobenen Befunde (EFEcho) direkt mit den im USCOM® erhobenen Parametern (SVUSCOM) und indirekt mit den Spiegeln der natriuretschen Peptide. Der zeitliche Aufwand einer USCOM®-Untersuchung betrug dabei weniger als eine Minute. Zusammenfassung Das Doppler-basierte USCOM®-Verfahren ist ein nahezu risikofreies Verfahren zur schnellen, nicht-invasiven Analyse des HMV in Echtzeit und scheint zur Überwachung der kardialen Funktion unter potenziell kardiotoxischer antiproliferativer Therapie geeignet zu sein. Die Methode ist nach eine kurzen Lernphase leicht durchzuführen und kosteneffizient. Für die Anthrazyklintherapie scheinen die natriuretischen Peptide Marker früher myokardialer Schädigung zu sein. Zur weiteren Evaluation beider Verfahren sind umfangreichere Studien innerhalb definierter Patientengruppen notwendig und bereits initiiert.