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ÂOlympic athletes best online lasix who compete despite chronic illness.â Lupus.org. ÂShannon Boxx. I want a cure.âA new method developed by Institute for Systems Biology (ISB) and University of California, Riverside provides new insights into cancer biology by allowing researchers to show how fatty acids are absorbed by single cells.Fatty acids, along with glucose and amino acids, are a major energy source for cellular growth and proliferation, and abnormal fatty acid metabolism is often seen in cancer. Dr.
Wei Wei's lab at ISB and Dr. Min Xue's lab at UC Riverside have been collaborating for years to develop a series of chemical probes and analytical approaches for quantifying cellular glucose uptake, lactate production, amino acid uptake, and other cancer-related metabolites.Unlike glucose and amino acids, however, the mechanisms underlying the uptake of fatty acids into cells have been lesser known and difficult to discern. The technical tools for measuring fatty acid uptake at the single-cell level are extremely limited."This work is the first example of profiling fatty acid uptake in conjunction with aberrant protein signaling in cancer cells at single-cell resolution and represents an important advance in the single-cell metabolic assay," said ISB Assistant Professor Dr. Wei Wei, co-corresponding author of a just-published paper in the Journal of the American Chemical Society.To profile the fatty acid uptake, the researchers chose a surrogate molecule that was structurally similar to natural fatty acids.
This similarity tricked the cells into taking up these surrogates like the native ones. Then, using a unique dendrimer molecule -- a tree-like polymer -- the researchers achieved precise quantitation of those surrogates from single cells.Applying this new single-cell tool to a brain cancer model, the researchers identified that fatty acid uptake was differentially regulated by two downstream effectors of the Mammalian Target of Rapamycin (mTOR) -- a critical regulator of cell proliferation and protein synthesis. The results revealed a compensatory activation of fatty acid metabolism upon oncogene inhibition or attenuation of glucose metabolism in these brain cancer cells and uncovered a novel combination therapy that targets this bioenergetic flexibility to synergistically block the tumor growth."This novel tool opens new avenues for studying how fatty acid metabolism affects biological systems. It has also inspired us to develop more metabolic probes for single-cell analysis," said UC Riverside Assistant Professor Dr.
Min Xue, co-corresponding author on the paper. Story Source. Materials provided by Institute for Systems Biology. Note.
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ÂFor the podcast buy lasix online with free samples associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts.Dilated cardiomyopathy (DCM) is currently defined by the presence of left ventricular (LV) or biventricular dilatation and systolic dysfunction in the absence of abnormal loading conditions, or coronary artery can lasix cause dry mouth disease sufficient to cause global systolic impairment. Research over recent decades has shed new light on the aetiology and natural history of DCM. In particular, it can lasix cause dry mouth is recognized that many patients have a long pre-clinical phase characterized by few if any symptoms and minor cardiac abnormalities that fall outside current disease definitions. It is also clear that distinct subtypes in fact share a common DCM phenotype.1,2This Focus Issue on heart failure (HF) opens with two contributions on DCM. The first contribution is a Current Opinion entitled âDilated cardiomyopathy.
So many cardiomyopathies! can lasix cause dry mouth. Â by Gianfranco Sinagra from the University of Trieste in Italy, and colleagues.3 The authors note that despite gaps in knowledge, precision medicine in cardiology is no longer a theoretical vision, but a realistic opportunity for the future treatment of patients with DCM. They also point out that the movement from symptomatic to can lasix cause dry mouth treatments targeting specific disease mechanisms represents a conceptual shift from slowing disease progression to a paradigm of disease reversal or prevention as the main objective. The authors propose that a novel approach to DCM patients, including a comprehensive evaluation, from the identification of possible environmental triggers to the identification of likely pathogenic genetic variants, should be promoted in order to apply individualized therapeutic strategies.The second contribution is a clinical research manuscript entitled âClinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy. An ESC EORP registryâ.
Karen Sliwa from the University of Cape Town in can lasix cause dry mouth South Africa and colleagues sought to describe the clinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy (PPCM) globally.4 In 2011, >100 national and affiliated member cardiac societies of the European Society of Cardiology (ESC) were contacted to contribute to a global registry on PPCM, under the auspices of the ESC EORP Programme. These societies were tasked with identifying centres who could participate in this registry. A total of 739 women were enrolled in 49 countries in can lasix cause dry mouth Europe (33%), Africa (29%), Asia-Pacific (15%), and the Middle East (22%). Mean age was 31 ± 6 years, mean left ventricular ejection fraction (LVEF) was 31 ± 10%, and 10% had a previous pregnancy complicated by PPCM. Symptom onset occurred most often within 1 month of delivery (44%).
At diagnosis, 67% of patients can lasix cause dry mouth had severe (NYHA III/IV) symptoms, 67% had an LVEF â¤35%, and 15% received bromocriptine, with significant regional variation. The 6-month mortality was 6% overall, lowest in Europe (4%), and highest in the Middle East (10%) (Figure 1). Myocardial recovery (LVEF >50%) occurred only in 46%, can lasix cause dry mouth most commonly in Asia-Pacific (62%) and least commonly in the Middle East (25%). Neonatal death occurred in 5%, with marked regional variation (Europe 2%, the Middle East 9%). Figure 1Kaplan-Meier survival curves for 6-month outcomes in women with peripartum cardiomyopathy.
(A) Death from any cause and (B) Re-hospitalization for any cause (from Sliwa K, Petrie MC, van der Meer P, Mebazaa A, Hilfiker-Kleiner D, Jackson AM, Maggioni AP, Laroche C, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, Roos-Hesselink JW, Seferovic P, Spaendonck-Zwarts Kv, Mbakwem A, Böhm M, Mouquet F, Pieske B, Johnson MR, Hamdan R, Ponikowski P, Van Veldhuisen DJ, McMurray JJV, Bauersachs J, on behalf of the EurObservational Research Programme in conjunction with the Heart Failure Association of the European Society can lasix cause dry mouth of Cardiology Study Group on Peripartum Cardiomyopathy. Clinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy. An ESC EORP can lasix cause dry mouth registry. See pages 3787â3797).Figure 1Kaplan-Meier survival curves for 6-month outcomes in women with peripartum cardiomyopathy. (A) Death from any cause and (B) Re-hospitalization for any cause (from Sliwa K, Petrie MC, van der Meer P, Mebazaa A, Hilfiker-Kleiner D, Jackson AM, Maggioni AP, Laroche C, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, Roos-Hesselink JW, Seferovic P, Spaendonck-Zwarts Kv, Mbakwem A, Böhm M, Mouquet F, Pieske B, Johnson MR, Hamdan R, Ponikowski P, Van Veldhuisen DJ, McMurray JJV, Bauersachs J, on behalf of the EurObservational Research Programme in conjunction with the Heart Failure Association of the European Society of Cardiology Study Group on Peripartum Cardiomyopathy.
Clinical presentation, management, and 6-month outcomes in women can lasix cause dry mouth with peripartum cardiomyopathy. An ESC EORP registry. See pages 3787â3797).The authors conclude that PPCM is can lasix cause dry mouth a global disease, but clinical presentation and outcomes vary by region. Just under half of women experience myocardial recovery. The manuscript is accompanied by an Editorial by Uri Elkayam and Hezzy Shmueli from the University of Southern California in Los Angeles, USA.5 The authors conclude that more research is required to determine the socioeconomic and genetic reasons for different geographical and racial characteristics of PPCM and to develop effective population-specific diagnostic and therapeutic approaches.Patients with end-stage HF have a poor quality of life, a very high mortality rate, and are potential candidates for implantation of a left ventricular assist device (LVAD).
Although cardiac transplantation can lasix cause dry mouth is associated with high 1- and 10-year survival rates, organ supply is limited. The technical improvements and proven success of implantable LVADs have made it a reasonable treatment option in these patients, either as a bridge to cardiac transplantation or as destination therapy.6 The ELEVATE Registry was designed to study long-term outcomes with the Heartmate 3 (HM3), a fully magnetically levitated centrifugal ventricular assist device, in a real-world population following CE-mark approval. In a clinical research article entitled âTwo-year can lasix cause dry mouth outcome after implantation of a full magnetically levitated left ventricular assist device. Results from the ELEVATE Registryâ, Daniel Zimpfer from the Medical University Vienna of Austria and colleagues assessed 463 patients receiving the HM3 as primary implant in Europe and in Middle East enrolled in the ELEVATE Registry.7 Data collection included demographics, survival, adverse events, quality of life assessment, and 6-min walk distance. Mean age was 55.6â±â11.7 years (89% male, 48% ischaemic cardiomyopathy).
Seventy percent of patients were in INTERMACS Profile 1â3 can lasix cause dry mouth and 12.7% were on temporary mechanical circulatory support. The survival rate was 83% after 2 years while stroke was observed in 10.2%, gastrointestinal bleedings in 9.7%, pump thrombosis in 1.5%, and outflow graft twists in 3.5%. HM3 implantation resulted in a significant and sustained improvement of functional capacity and quality of life.Zimpfer and colleagues conclude that in a real-world population cohort implanted with the HM3 LVAD, the long-term survival is good with sustained improvement of functional capacity and low rates of can lasix cause dry mouth adverse events. This manuscript is accompanied by an Editorial by Stephen James Pettit from the Royal Papworth Hospital NHS Foundation Trust in Cambridge, UK, and colleagues.8 They note that the ELEVATE Registry provides reassuring data about survival with the HM3 LVAD, demonstrates that low adverse event rates with the HM3 are achievable in the real world, but also highlights that adverse events remain problematic. Thus, we do not yet have a perfect implantable LVAD for the long-term treatment of patients with advanced heart failure.Cardiac resynchronization plays a key role in the management of chronic heart failure,9 but the identification of responders remains challenging.10 In a clinical research article entitled âImaging predictors of response to cardiac resynchronization therapy.
Left ventricular work asymmetry by echocardiography and septal viability by cardiac magnetic resonanceâ, John Aalen from the Oslo can lasix cause dry mouth University Hospital and University of Oslo in Norway, and colleagues investigated if septal and left lateral wall function measured as myocardial work, alone and combined with assessment of septal viability, identified responders to cardiac resynchronization therapy (CRT).11 In a prospective multicentre study of 200 CRT recipients, myocardial work was measured by pressureâstrain analysis and viability by cardiac magnetic resonance imaging (CMR). Before CRT, septal work was markedly lower than left lateral wall work, and the difference was largest in CRT responders. Work difference between the septum and lateral wall can lasix cause dry mouth predicted CRT response, with an area under the curve (AUC) of 0.77 (Figure 2). In patients undergoing CMR, combining work difference and septal viability significantly increased the AUC to 0.88. This was superior to the predictive power of QRS morphology, QRS duration, and the echocardiographic parameters septal flash, apical rocking, and systolic stretch index.
Figure 2Left ventricular work asymmetry combined with can lasix cause dry mouth septal viability identifies cardiac resynchronization therapy responders. (AâC) The panels are from the same patient and illustrate how the lateral-to-septal work difference is used in combination with viability by LGE-CMR to identify cardiac resynchronization therapy responders. Before cardiac resynchronization therapy (A) there is dominantly negative septal work, as indicated by the red-coloured pressure-strain loop area, but compensatory increase in can lasix cause dry mouth left ventricular lateral wall work, which gives a large lateral-toseptal work difference. Viable septum (B) indicates potential for recovery of septal function. After 6 months with cardiac resynchronization therapy (C), there is fine recovery of septal function.
The highly inefficient septal contractions before can lasix cause dry mouth cardiac resynchronization therapy are converted to positive work throughout systole. The improvement in septal function was accompanied by reduced workload on the lateral wall. (D) ROC curve displaying combined assessment of can lasix cause dry mouth work difference and septal viability for cardiac resynchronization therapy response prediction (n = 123). AUC, area under curve. AVC, aortic valve closure.
CI, confidence can lasix cause dry mouth interval. LGE-CMR, late gadolinium enhancement cardiac magnetic resonance. LVP, left ventricular can lasix cause dry mouth pressure. ROC, receiver operating characteristic (from Aalen JM, Donal E, Larsen CK, Duchenne J, Lederlin M, Cvijic M, Hubert A, Voros G, Leclercq C, Bogaert J, Hopp E, Fjeld JG, Penicka M, Linde C, Aalen OO, Kongsgård E, Galli E, Voigt J-U, Smiseth OA. Imaging predictors of response to cardiac resynchronization therapy.
Left ventricular work asymmetry by echocardiography and septal can lasix cause dry mouth viability by cardiac magnetic resonance. See pages 3813â3823).Figure 2Left ventricular work asymmetry combined with septal viability identifies cardiac resynchronization therapy responders. (AâC) The panels are from the same patient and illustrate how the lateral-to-septal work difference is used in combination can lasix cause dry mouth with viability by LGE-CMR to identify cardiac resynchronization therapy responders. Before cardiac resynchronization therapy (A) there is dominantly negative septal work, as indicated by the red-coloured pressure-strain loop area, but compensatory increase in left ventricular lateral wall work, which gives a large lateral-toseptal work difference. Viable septum (B) indicates potential for recovery of septal function.
After 6 can lasix cause dry mouth months with cardiac resynchronization therapy (C), there is fine recovery of septal function. The highly inefficient septal contractions before cardiac resynchronization therapy are converted to positive work throughout systole. The improvement in septal function was accompanied can lasix cause dry mouth by reduced workload on the lateral wall. (D) ROC curve displaying combined assessment of work difference and septal viability for cardiac resynchronization therapy response prediction (n = 123). AUC, area under curve.
AVC, aortic can lasix cause dry mouth valve closure. CI, confidence interval. LGE-CMR, late can lasix cause dry mouth gadolinium enhancement cardiac magnetic resonance. LVP, left ventricular pressure. ROC, receiver operating characteristic (from Aalen JM, Donal E, Larsen CK, Duchenne J, Lederlin M, Cvijic M, Hubert A, Voros G, Leclercq C, Bogaert J, Hopp E, Fjeld JG, Penicka M, Linde C, Aalen OO, Kongsgård E, Galli E, Voigt J-U, Smiseth OA.
Imaging predictors of response can lasix cause dry mouth to cardiac resynchronization therapy. Left ventricular work asymmetry by echocardiography and septal viability by cardiac magnetic resonance. See pages 3813â3823).The authors conclude that assessment of myocardial work and septal viability identifies CRT responders with can lasix cause dry mouth high accuracy. The manuscript is accompanied by an Editorial by Frits W. Prinzen and Joost Lumens from the Cardiovascular Research Institute Maastricht in the Netherlands12 who note that this study provides a strong extension of our understanding of CRT response and that it would not be a waste of work to perform a larger prospective study to prove the clinical feasibility and benefit of a meaningful measure of LV mechanical discoordination as an important additional selection criterion for CRT in the real-world setting.hypertension disease 2019 (hypertension medications) due to severe acute respiratory syndrome hypertension-2 (hypertension) has been associated with cardiovascular features of myocardial involvement including elevated serum troponin levels, acute heart failure with reduced ejection fraction, and myocarditis.13â15 In a clinical research article âPathological features of hypertension medications-associated myocardial injury.
A multicentre cardiovascular pathology studyâ Cristina Basso from the University of Padua in Italy and colleagues note that the cardiac pathological changes in these patients can lasix cause dry mouth with hypertension medications have yet to be well described.16 In an international multicentre study, cardiac tissue from the autopsies of 21 consecutive hypertension medications patients was assessed by cardiovascular pathologists. Myocarditis, as defined by the presence of multiple foci of inflammation with associated myocyte injury, was determined, and the inflammatory cell composition analysed by immunohistochemistry. Other forms of acute myocyte injury and inflammation were also described, as well as can lasix cause dry mouth coronary artery, endocardium, and pericardium involvement. Lymphocytic myocarditis was present in 3 (14%) of the cases. A mild pericarditis was present in four cases.
Acute myocyte injury in can lasix cause dry mouth the right ventricle most probably due to strain/overload was present in four cases. A non-significant trend toward higher serum troponin levels was observed in the patients with myocarditis compared with those without. The authors can lasix cause dry mouth conclude that in hypertension there are increased interstitial macrophages in a majority of the cases and multifocal lymphocytic myocarditis in a small fraction of the cases. Other forms of myocardial injury are also present in these patients. The macrophage infiltration may reflect underlying diseases rather than hypertension medications.
The manuscript can lasix cause dry mouth is accompanied by an Editorial by Nikolaos Frangogiannis from the Albert Einstein College of Medicine in the Bronx, New York, USA and colleagues.17 He notes that the findings of the current study are consistent with the notion that direct hypertension medications-mediated cardiac pathology is uncommon.The incidence of cardiogenic shock (CS) has increased remarkably over the past decade and remains a challenging condition, with mortality rates of â¼50%. CS encompasses cardiac contractile dysfunction. However, it is also a multiorgan dysfunction syndrome, often complicated by a systemic inflammatory can lasix cause dry mouth response with severe cellular and metabolic dysregulations. In a clinical review article entitled âMolecular signature of cardiogenic shockâ, Antoni Bayes-Genis from the Hospital Universitari Germans Trias i Pujol in Badalona, Spain, and colleagues sought to review the evidence on the biochemical manifestations of CS, elaborating on current gold standard biomarkers and novel candidates from molecular signatures of CS.18 Novel genomic, transcriptomic, and proteomic data are discussed, and a recently reported molecular score derived from unbiased proteomic discovery, the CS4P, which includes liver fatty acid-binding protein (L-FABP), beta-2-microglobulin (B2MG), fructose-bisphosphate aldolase B (ALDOB), and SerpinG1 (IC1), is comprehensively described.In another clinical review article entitled âWhen genetic burden reaches thresholdâ, Roddy Walsh from the University of Amsterdam in the Netherlands, and colleagues note that rare cardiac genetic diseases have generally been considered to be broadly Mendelian in nature, with clinical genetic testing for these conditions predicated on the detection of a primary causative rare pathogenic variant that will enable cascade genetic screening in families.19 Substantial variability in penetrance and disease severity among carriers of pathogenic variants, as well as the inability to detect rare Mendelian variants in considerable proportions of patients, indicates that more complex aetiologies are likely to underlie these diseases. Recent findings have suggested that genetic variants across a range of population frequencies and effect sizes may combine, along with non-genetic factors, to determine whether the threshold for expression of disease is reached and the severity of the phenotype.
The availability of increasingly large genetically characterized cohorts of patients with rare cardiac diseases is enabling the discovery can lasix cause dry mouth of common genetic variation that may underlie both variable penetrance in Mendelian diseases and the genetic aetiology of apparently non-Mendelian rare cardiac conditions. It is likely that the genetic architecture of rare cardiac diseases will vary considerably between different conditions as well as between patients with similar phenotypes, ranging from near-Mendelian disease to models more akin to common, complex disease. Uncovering the broad range of genetic factors that predispose patients to rare cardiac diseases offers the promise of improved risk prediction and more focused clinical management in patients and their families.The two primary molecular regulators of lifespan are sirtuin-1 (SIRT1) and can lasix cause dry mouth mammalian target of rapamycin complex 1 (mTORC1). In a Special Article entitled âLongevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy. Implications for understanding the effects of current and future treatments for heart failureâ, Milton Packer from the Baylor University Medical Center at Dallas in Texas, USA notes that each plays a central role in two highly interconnected pathways that modulate the balance between cellular growth and survival.20 The activation of SIRT1 [along with peroxisome proliferator-activated receptor-gamma coactivator (PGC-1a) and adenosine monophosphate-activated protein kinase (AMPK)] and the suppression of mTORC1 (along with its upstream regulator, Akt) act to prolong organismal longevity and retard cardiac ageing.
Both activation of SIRT1/PGC-1a and inhibition of mTORC1 shifts can lasix cause dry mouth the balance of cellular priorities so as to promote cardiomyocyte survival over growth, leading to cardioprotective effects in experimental models. These benefits may be related to direct actions to modulate oxidative stress, organellar function, proinflammatory pathways, and maladaptive hypertrophy. Additionally, a primary shared benefit of both SIRT1/PGC-1a/AMPK activation and Akt/mTORC1 inhibition is the enhancement of autophagy, a lysosome-dependent degradative pathway, which clears the cytosol of dysfunctional organelles and misfolded proteins that drive the ageing can lasix cause dry mouth process by increasing oxidative and endoplasmic reticulum stress. Interestingly, most treatments that have been shown to be clinically effective in the treatment of chronic heart failure with a reduced ejection fraction have been reported experimentally to activate SIRT1/PGC-1a/AMPK and/or suppress Akt/mTORC1, and, thereby, to promote autophagic flux. Therefore, the impairment of autophagy resulting from derangements in longevity gene signalling is likely to represent a seminal event in the evolution and progression of cardiomyopathy.The editors hope that readers of this issue of the European Heart Journal will find it of interest.With thanks to Amelia Meier-Batschelet, Johanna Hugger, and Martin Meyer for help with compilation of this article.
References1Elliott P, Andersson B, Arbustini E, Bilinska Z, Cecchi F, can lasix cause dry mouth Charron P, Dubourg O, Kühl U, Maisch B, McKenna WJ, Monserrat L, Pankuweit S, Rapezzi C, Seferovic P, Tavazzi L, Keren A. Classification of the cardiomyopathies. A position statement from the European can lasix cause dry mouth Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2008;29:270â276.2Pinto YM, Elliott PM, Arbustini E, Adler Y, Anastasakis A, Böhm M, Duboc D, Gimeno J, de Groote P, Imazio M, Heymans S, Klingel K, Komajda M, Limongelli G, Linhart A, Mogensen J, Moon J, Pieper PG, Seferovic PM, Schueler S, Zamorano JL, Caforio AL, Charron P. Proposal for a revised definition of dilated cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for clinical practice.
A position can lasix cause dry mouth statement of the ESC working group on myocardial and pericardial diseases. Eur Heart J 2016;37:1850â1858.3Sinagra G, Elliott PM, Merlo M. Dilated can lasix cause dry mouth cardiomyopathy. So many cardiomyopathies!. Eur Heart J 2020:41:3784â3786.4Sliwa K, Petrie MC, van der Meer P, Mebazaa A, Hilfiker-Kleiner D,, Jackson AM, Maggioni AP, Laroche C, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, Roos-Hesselink JW, Seferovic P, van Spaendonck-Zwarts K, Mbakwem A, Böhm M, Mouquet F, Pieske B, Johnson MR, Hamdan R, Ponikowski P, Van Veldhuisen DJ, McMurray JJV, Bauersachs J.
Clinical presentation, management, and can lasix cause dry mouth 6-month outcomes in women with peripartum cardiomyopathy. An ESC EORP registry. Eur Heart can lasix cause dry mouth J 2020:41:3787â3797.5Elkayam U, Shmueli H. Peripartum cardiomyopathy. One disease with many faces.
Eur Heart can lasix cause dry mouth J 2020:41:3798â3800.6Dickstein K, Vardas PE, Auricchio A, Daubert JC, Linde C, McMurray J, Ponikowski P, Priori SG, Sutton R, van Veldhuisen DJ. ESC Committee for Practice Guidelines (CPG). 2010 Focused Update of ESC Guidelines on device therapy in heart failure can lasix cause dry mouth. An update of the 2008 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure and the 2007 ESC guidelines for cardiac and resynchronization therapy. Developed with the special contribution of the Heart Failure Association and the European Heart Rhythm Association.
Eur Heart J 2010;31:2677â2687.7Zimpfer D, Gustafsson F, Potapov E, Pya Y, Schmitto J, Berchtold-Herz M, Morshuis M, Shaw SM, Saeed D, Laves J, can lasix cause dry mouth Heatley G, Gazzola C, Garbade J, on behalf of the ELEVATE investigators. Two-year outcome after implantation of a full magnetically levitated left ventricular assist device. Results from can lasix cause dry mouth the ELEVATE registry. Eur Heart J 2020:41:3801â3809.8Pettit SJ. HeartMate 3.
Real-world performance matches can lasix cause dry mouth pivotal trial. Eur Heart J 2020:41:3810â3812.9Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, Falk V, González-Juanatey JR, Harjola VP, Jankowska EA, Jessup M, Linde C, Nihoyannopoulos P, Parissis JT, Pieske B, Riley JP, Rosano GMC, Ruilope LM, Ruschitzka F, Rutten FH, van der Meer P. ESC Scientific can lasix cause dry mouth Document Group. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC).
Developed with can lasix cause dry mouth the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J 2016;37:2129â2200.10Daubert C, Behar N, Martins RP, Mabo P, Leclercq C. Avoiding non-responders to cardiac can lasix cause dry mouth resynchronization therapy. A practical guide. Eur Heart J 2017;38:1463â1472.11Aalen JM, Donal E, Larsen CK, Duchenne J, Lederlin M, Cvijic M, Hubert A, Voros G, Leclercq C, Bogaert J, Hopp E, Fjeld JG, Penicka M, Linde C, Aalen OO, KongsgÃ¥rd E, Galli E, Voigt JU, Smiseth OA.
Imaging predictors of response to cardiac resynchronization can lasix cause dry mouth therapy. Left ventricular work asymmetry by echocardiography and septal viability by cardiac magnetic resonance. Eur Heart J 2020:41:3813â3823.12Prinzen FW, can lasix cause dry mouth Lumens J. Investigating myocardial work as a CRT response predictor is not a waste of work. Eur Heart J 2020:41:3824â3826.13Shi S, Qin M, Cai Y, Liu T, Shen B, Yang F, Cao S, Liu X, Xiang Y, Zhao Q, Huang H, Yang B, Huang C.
Characteristics can lasix cause dry mouth and clinical significance of myocardial injury in patients with severe hypertension disease 2019. Eur Heart J 2020;41:2070â2079.14Peretto G, Sala S, Caforio ALP. Acute can lasix cause dry mouth myocardial injury, MINOCA, or myocarditis?. Improving characterization of hypertension-associated myocardial involvement. Eur Heart J 2020;41:2124â2125.15Cuomo V, Esposito R, Santoro C.
Fulminant myocarditis in the time of can lasix cause dry mouth hypertension. Eur Heart J 2020;41:2121.16Basso C, Leone O, Rizzo S, De Gaspari M, van der Wal AC, Aubry MC, Bois MC, Lin PT, Maleszewski JJ, Stone JR. Pathological features of can lasix cause dry mouth hypertension medications-associated myocardial injury. A multicentre cardiovascular pathology study. Eur Heart J 2020:41:3827â3825.17Frangogiannis NG.
The can lasix cause dry mouth significance of hypertension medications-associated myocardial injury. How overinterpretation of scientific findings can fuel media sensationalism and spread misinformation. Eur Heart J can lasix cause dry mouth 2020:41:3836â3838.18Iborra-Egea O, Rueda F, GarcÃa-GarcÃa C, Borrà s E, Sabidó E, Bayes-Genis A. Molecular signature of cardiogenic shock. Eur Heart J 2020:41:3839â3848.19Walsh R, Tadros R, Bezzina CR.
When can lasix cause dry mouth genetic burden reaches threshold. Eur Heart J 2020:41:3849â3855.20Packer M. Longevity genes, can lasix cause dry mouth cardiac ageing, and the pathogenesis of cardiomyopathy. Implications for understanding the effects of current and future treatments for heart failure. Eur Heart J 2020:41:3856â3861.
Published can lasix cause dry mouth on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020 can lasix cause dry mouth. For permissions, please email. Journals.permissions@oup.com.Dr Julius Axelrod was awarded the 1970 Nobel Prize for Physiology or Medicine with Sir Bernard Katz and Professor Ulf von Euler for their discoveries concerning âthe humoral transmitters in the nerve terminals and the mechanisms for their storage, release, and inactivation' American biochemist Julius Axelrod was an instantly recognizable figure in the scientific world.
Having lost the sight of an eye in a laboratory accident early in his career when an ammonia bottle exploded, he wore a darkened lens over his damaged left eye for the rest of his life.Yet he remained unperturbed and steadfast in his quest for scientific excellence.After graduating with a BSc in Biology, his applications to medical colleges were rejected, so he took jobs in various can lasix cause dry mouth laboratories, went to night school to achieve his Masterâs Degree, and then achieved a significant breakthrough with a role as a research associate with Bernard B. Brodie at Goldwater Memorial Hospital in New York between 1946 and 1949.The move launched his research career and set him on a path which ultimately saw him receive the 1970 Nobel Prize in Physiology or Medicine, jointly with Bernard Katz and Ulf von Euler for their discoveries concerning âthe humoral transmitters in the nerve terminals and the mechanisms for their storage, release, and inactivationâ.Whilst jointly awarded the prize, the three scientists had been working independently but together their findings led to a significant contribution toward solving principal questions concerning the neurotransmitters, their storage, release, and inactivation.The Nobel committee noted that their discoveries had advanced the understanding of the mechanism underlying the transmission between the nerve cells synapsesâand between the nerve terminals and the effector organs.While Professor von Euler had discovered that the substance noradrenaline serves as a neurotransmitter at the nerve terminals of the sympathetic nervous system, Dr Axelrodâs contribution concerned the mechanisms which regulate the formation of this transmitter in the nerve cells and the mechanisms involved in the inactivation of noradrenaline. Among other can lasix cause dry mouth things, in 1957 he showed how an excess of noradrenaline is released in response to nerve impulses and then returns to the place where it is stored after the signal is implemented. Sir Bernardâs discoveries focused on the mechanism for the release of the transmitter acetylcholine from the nerve terminals at the nerveâmuscle junction, under the influence of the nerve impulses.The Nobel committee noted that the advances were âa fundamental step in neurophysiology and neuropharmacologyâ, unlocking the pathway for advances in the search for remedies against nervous and mental disturbances, but there were also implications for advances in the neural pathophysiology of heart failure, hypertension, and some orthostatic intolerance syndromes. Indeed, Professor Guido Grassi, Professor of Internal Medicine at the Clinica Medica of the University of Milano-Bicocca, suggested.
ÂThe landmark studies performed by these three giants of neurotransmitters research represent can lasix cause dry mouth the basis of modern cardiovascular physiologyâ.Julius âJulieâ Axelrod was born on 30 May 1912, in Manhattan, New York City, the son of basket maker Isadore Axelrod and his wife Molly, who were Jewish immigrants from Poland. In 1929, he enrolled at New York University (NYU) but transferred to City College of New York (CCNY) the following year to study history, philosophy, literature, and biology, receiving his BS in biology in 1933.Having been rejected by the medical schools and seen his hopes of becoming a physician dashed, he took a job as a laboratory technician before moving to the New York City Department of Health and Mental Hygiene in 1935, testing vitamin supplements added to food. During this period, he attended night school and received his Master of Science degree in chemistry from New York University in 1941 after completing his thesis on the can lasix cause dry mouth chemical breakdown of enzymes in cancerous tumour tissues.A significant move came in 1946, to work under Bernard Brodie at Goldwater, where their work focused on analgesics. During the 1940s, users of non-aspirin analgesics were developing methaemoglobinaemia. Axelrod and Brodie discovered that acetanilide in the painkillers was to blame.
They found that one of the metabolites was can lasix cause dry mouth also an analgesic and recommended that this metabolite, acetaminophen (paracetamol, Tylenol), be used instead. It was this research that triggered Axelrodâs passion for pharmacological science.In 1949, Axelrod began work at the National Heart Instituteâforerunner of the National Heart, Lung, and Blood Institute (NHLBI)âand part of the National Institutes of Health (NIH) in Bethesda, MD, USA. Pursuing projects that built upon his earlier research, he examined the mechanisms and effects of caffeine, which led him to an interest in the sympathetic nervous system and its main neurotransmitters, epinephrine and norepinephrine.After taking a year out to achieve his PhD at George Washington University Medical School and can lasix cause dry mouth graduating in 1955, he returned to the National Institute for Mental Healthâwhere he worked until his retirement aged 72 in 1984âand began some of the key research of his career.In 1957, he focused on the activity of neurotransmitter hormones. Work which led to the development of a new class of antidepressant medications. He found that neurotransmitters do not merely stop working when they reach the post-synaptic nerve terminal but are recaptured (reuptaken) by the pre-synaptic nerve ending and used again for later transmissions.Axelrod received his Nobel Prize for his work on the release, reuptake, and storage of the neurotransmitters epinephrine and norepinephrineâalso known as adrenaline and noradrenalineâa finding that provided a new model for understanding the metabolism and regulation of neurotransmitters.
He also made major contributions to the understanding of the pineal gland and how it is regulated during the sleepâwake cycle and was among the first US scientists to conduct scientific experiments on the metabolism of lysergic acid diethylamide-25.He continued can lasix cause dry mouth his research after the Nobel award, becoming acutely aware of the standing and responsibilities of a Nobel laureate, which saw him active in a political and campaigning context too. After retiring from the NIMH, he continued as an unpaid guest researcher and in 1996 was named Scientist Emeritus of the NIH.Over his career, Axelrod mentored some 70 young scientists and in 1987 the Julius Axelrod Distinguished Lecture in Neuroscience was established at CCNY. He was awarded the Gairdner Foundation International Award in 1967, elected a Foreign Member of the Royal Society in 1979, and can lasix cause dry mouth awarded the Ralph W. Gerard Prize in Neuroscience.He had married elementary school teacher Sally Taub in 1938, and they were together 53âyears until her death in 1992. On his death on 29 December 2004, aged 92 in Rockville, he was survived by two sons, Paul and Alfred, and three grandchildren, and recognized as one of the key figures of the 20th century in neurology and pharmacology.Axelrodâs co-recipient Ulf Svante von Euler was born in Stockholm on 7 February 1905, and entered the Karolinska Institute as a medical student in 1922.
Having studied abroad at various points in the 1930s, he was appointed Full Professor of Physiology at the Karolinska Institute, where he remained until 1971 and died on 9 March 1983, aged 78.Bernard Katz was born on March 26, 1911, in Leipzig, Germany, of Russian Jewish origin and studied Medicine at the University of Leipzig (1929â34) before leaving Germany in February 1935 for his can lasix cause dry mouth PhD at University College London. After moving to Australia, he returned to UCL and was later appointed Professor of Biophysics. He died on 20 April 2003.In can lasix cause dry mouth his Nobel lecture âNoradrenaline. Fate and control of its Biosynthesisâ on December 12, 1970, Axelrod opened by referring to von Eulerâs discoveries of 1946 in isolating and identifying noradrenaline in the sympathetic nervous system and how that shaped his work.âWhen I joined the National Institute of Mental Health in 1955, I began to think of an appropriate problem on which to work. In reading the literature I was surprised to learn that very little was known about the metabolism of noradrenaline and adrenalineâ.Two days earlier, when addressing the Nobel banquet, he had pointed to the privilege of receiving the honour with von Euler and Katz, and spoke about the importance of basic research.âThis award comes at a time when our young and many of our most influential people believe that basic research is irrelevant or is put to evil usesâ, he told the assembled guests.
The selection of chemical neurotransmission for a Nobel Prize this year, makes our work highly visible to the general public and gives us an opportunity to show how misinformed and mistaken they areâ.Adding that such work offers an insight in explaining such illnesses as mental depression, Parkinsonâs disease, can lasix cause dry mouth hypertension, and drug abuse, he concluded. ÂI thank the Nobel Prize Committee for bringing the adrenergic and cholinergic nervous system together again. They have been apart for too longâ can lasix cause dry mouth. Julius Axelrod legacy â Professor Murray EslerProfessor Murray Esler, a clinical cardiologist at the Alfred Hospital, Melbourne, and Adjunct Professor of Medicine, Monash University, in Australia, explained that Julius Axelrod demonstrated that the primary mechanism for terminating the neural signal in most catecholaminergic neurons was the specific transport of the neurotransmitter back into the neuron by an active transport mechanism.He said this had profound application in psychiatry (tricyclic noradrenaline uptake blockers and selective serotonin uptake blockers), but additionally in cardiovascular medicine.âSympathetic nerve scanning in the heart, and pheochromocytoma demonstration, relies on agents such as Metaiodobenzylguanidine (MIBG) which are ligands for the noradrenaline transporterâ added Professor Esler. ÂIndirect acting sympathomimetics act by releasing noradrenaline from sympathetic nerves after uptake by the noradrenaline transporter.
Noradrenaline reuptake defect is an element in the neural pathophysiology of heart failure, hypertension, can lasix cause dry mouth and some orthostatic intolerance syndromes, notably postural tachycardia syndrome (POTS)'.Professor Esler is also Head of the Human Clinical Neurotransmitters Laboratory in the Baker Heart and Diabetes Institute in Melbourne and continues to study the sympathetic nervous system in cardiovascular medicine. All Axelrod images, Courtesy. History of Medicine Division, U.S can lasix cause dry mouth. National Library of MedicineConflict of interest. None declared.
Published on behalf can lasix cause dry mouth of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email. Journals.permissions@oup.com..
ÂFor the podcast associated with best online lasix this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts.Dilated cardiomyopathy (DCM) is currently defined by the presence of http://iconographymag.com/talk-is-chic-bianca-golden/ left ventricular (LV) or biventricular dilatation and systolic dysfunction in the absence of abnormal loading conditions, or coronary artery disease sufficient to cause global systolic impairment. Research over recent decades has shed new light on the aetiology and natural history of DCM. In particular, it is recognized that many patients have a long pre-clinical phase characterized by few if any symptoms and minor cardiac abnormalities that fall best online lasix outside current disease definitions.
It is also clear that distinct subtypes in fact share a common DCM phenotype.1,2This Focus Issue on heart failure (HF) opens with two contributions on DCM. The first contribution is a Current Opinion entitled âDilated cardiomyopathy. So many cardiomyopathies! best online lasix.
 by Gianfranco Sinagra from the University of Trieste in Italy, and colleagues.3 The authors note that despite gaps in knowledge, precision medicine in cardiology is no longer a theoretical vision, but a realistic opportunity for the future treatment of patients with DCM. They also point out that the best online lasix movement from symptomatic to treatments targeting specific disease mechanisms represents a conceptual shift from slowing disease progression to a paradigm of disease reversal or prevention as the main objective. The authors propose that a novel approach to DCM patients, including a comprehensive evaluation, from the identification of possible environmental triggers to the identification of likely pathogenic genetic variants, should be promoted in order to apply individualized therapeutic strategies.The second contribution is a clinical research manuscript entitled âClinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy.
An ESC EORP registryâ. Karen Sliwa from the University of Cape Town in South Africa and colleagues sought best online lasix to describe the clinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy (PPCM) globally.4 In 2011, >100 national and affiliated member cardiac societies of the European Society of Cardiology (ESC) were contacted to contribute to a global registry on PPCM, under the auspices of the ESC EORP Programme. These societies were tasked with identifying centres who could participate in this registry.
A total of 739 women were best online lasix enrolled in 49 countries in Europe (33%), Africa (29%), Asia-Pacific (15%), and the Middle East (22%). Mean age was 31 ± 6 years, mean left ventricular ejection fraction (LVEF) was 31 ± 10%, and 10% had a previous pregnancy complicated by PPCM. Symptom onset occurred most often within 1 month of delivery (44%).
At diagnosis, 67% of patients had severe (NYHA III/IV) symptoms, 67% had an LVEF â¤35%, and best online lasix 15% received bromocriptine, with significant regional variation. The 6-month mortality was 6% overall, lowest in Europe (4%), and highest in the Middle East (10%) (Figure 1). Myocardial recovery (LVEF >50%) occurred only in 46%, most commonly in Asia-Pacific (62%) best online lasix and least commonly in the Middle East (25%).
Neonatal death occurred in 5%, with marked regional variation (Europe 2%, the Middle East 9%). Figure 1Kaplan-Meier survival curves for 6-month outcomes in women with peripartum cardiomyopathy. (A) Death from any cause and (B) Re-hospitalization for any cause (from Sliwa K, Petrie MC, van der Meer P, Mebazaa A, Hilfiker-Kleiner D, Jackson AM, Maggioni AP, Laroche C, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, Roos-Hesselink JW, Seferovic P, Spaendonck-Zwarts Kv, Mbakwem A, Böhm M, Mouquet F, Pieske B, Johnson MR, Hamdan R, Ponikowski P, Van Veldhuisen DJ, McMurray JJV, Bauersachs J, on behalf of the EurObservational Research best online lasix Programme in conjunction with the Heart Failure Association of the European Society of Cardiology Study Group on Peripartum Cardiomyopathy.
Clinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy. An ESC EORP best online lasix registry. See pages 3787â3797).Figure 1Kaplan-Meier survival curves for 6-month outcomes in women with peripartum cardiomyopathy.
(A) Death from any cause and (B) Re-hospitalization for any cause (from Sliwa K, Petrie MC, van der Meer P, Mebazaa A, Hilfiker-Kleiner D, Jackson AM, Maggioni AP, Laroche C, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, Roos-Hesselink JW, Seferovic P, Spaendonck-Zwarts Kv, Mbakwem A, Böhm M, Mouquet F, Pieske B, Johnson MR, Hamdan R, Ponikowski P, Van Veldhuisen DJ, McMurray JJV, Bauersachs J, on behalf of the EurObservational Research Programme in conjunction with the Heart Failure Association of the European Society of Cardiology Study Group on Peripartum Cardiomyopathy. Clinical presentation, best online lasix management, and 6-month outcomes in women with peripartum cardiomyopathy. An ESC EORP registry.
See pages 3787â3797).The authors conclude that PPCM is a global disease, but clinical best online lasix presentation and outcomes vary by region. Just under half of women experience myocardial recovery. The manuscript is accompanied by an Editorial by Uri Elkayam and Hezzy Shmueli from the University of Southern California in Los Angeles, USA.5 The authors conclude that more research is required to determine the socioeconomic and genetic reasons for different geographical and racial characteristics of PPCM and to develop effective population-specific diagnostic and therapeutic approaches.Patients with end-stage HF have a poor quality of life, a very high mortality rate, and are potential candidates for implantation of a left ventricular assist device (LVAD).
Although cardiac transplantation is associated with high 1- and 10-year survival rates, organ supply best online lasix is limited. The technical improvements and proven success of implantable LVADs have made it a reasonable treatment option in these patients, either as a bridge to cardiac transplantation or as destination therapy.6 The ELEVATE Registry was designed to study long-term outcomes with the Heartmate 3 (HM3), a fully magnetically levitated centrifugal ventricular assist device, in a real-world population following CE-mark approval. In a clinical research article entitled âTwo-year outcome after implantation of best online lasix a full magnetically levitated left ventricular assist device.
Results from the ELEVATE Registryâ, Daniel Zimpfer from the Medical University Vienna of Austria and colleagues assessed 463 patients receiving the HM3 as primary implant in Europe and in Middle East enrolled in the ELEVATE Registry.7 Data collection included demographics, survival, adverse events, quality of life assessment, and 6-min walk distance. Mean age was 55.6â±â11.7 years (89% male, 48% ischaemic cardiomyopathy). Seventy percent of patients were in INTERMACS best online lasix Profile 1â3 and 12.7% were on temporary mechanical circulatory support.
The survival rate was 83% after 2 years while stroke was observed in 10.2%, gastrointestinal bleedings in 9.7%, pump thrombosis in 1.5%, and outflow graft twists in 3.5%. HM3 implantation resulted in a significant and sustained best online lasix improvement of functional capacity and quality of life.Zimpfer and colleagues conclude that in a real-world population cohort implanted with the HM3 LVAD, the long-term survival is good with sustained improvement of functional capacity and low rates of adverse events. This manuscript is accompanied by an Editorial by Stephen James Pettit from the Royal Papworth Hospital NHS Foundation Trust in Cambridge, UK, and colleagues.8 They note that the ELEVATE Registry provides reassuring data about survival with the HM3 LVAD, demonstrates that low adverse event rates with the HM3 are achievable in the real world, but also highlights that adverse events remain problematic.
Thus, we do not yet have a perfect implantable LVAD for the long-term treatment of patients with advanced heart failure.Cardiac resynchronization plays a key role in the management of chronic heart failure,9 but the identification of responders remains challenging.10 In a clinical research article entitled âImaging predictors of response to cardiac resynchronization therapy. Left ventricular work asymmetry by echocardiography and septal viability by cardiac magnetic resonanceâ, John Aalen from the Oslo University Hospital and University of Oslo in best online lasix Norway, and colleagues investigated if septal and left lateral wall function measured as myocardial work, alone and combined with assessment of septal viability, identified responders to cardiac resynchronization therapy (CRT).11 In a prospective multicentre study of 200 CRT recipients, myocardial work was measured by pressureâstrain analysis and viability by cardiac magnetic resonance imaging (CMR). Before CRT, septal work was markedly lower than left lateral wall work, and the difference was largest in CRT responders.
Work difference between the septum and lateral wall predicted CRT response, with best online lasix an area under the curve (AUC) of 0.77 (Figure 2). In patients undergoing CMR, combining work difference and septal viability significantly increased the AUC to 0.88. This was superior to the predictive power of QRS morphology, QRS duration, and the echocardiographic parameters septal flash, apical rocking, and systolic stretch index.
Figure 2Left ventricular work asymmetry combined with septal best online lasix viability identifies cardiac resynchronization therapy responders. (AâC) The panels are from the same patient and illustrate how the lateral-to-septal work difference is used in combination with viability by LGE-CMR to identify cardiac resynchronization therapy responders. Before cardiac resynchronization therapy (A) there is best online lasix dominantly negative septal work, as indicated by the red-coloured pressure-strain loop area, but compensatory increase in left ventricular lateral wall work, which gives a large lateral-toseptal work difference.
Viable septum (B) indicates potential for recovery of septal function. After 6 months with cardiac resynchronization therapy (C), there is fine recovery of septal function. The highly inefficient septal contractions before cardiac resynchronization therapy are converted to positive best online lasix work throughout systole.
The improvement in septal function was accompanied by reduced workload on the lateral wall. (D) ROC curve displaying combined assessment of work difference and septal viability for cardiac best online lasix resynchronization therapy response prediction (n = 123). AUC, area under curve.
AVC, aortic valve closure. CI, confidence best online lasix interval. LGE-CMR, late gadolinium enhancement cardiac magnetic resonance.
LVP, left best online lasix ventricular pressure. ROC, receiver operating characteristic (from Aalen JM, Donal E, Larsen CK, Duchenne J, Lederlin M, Cvijic M, Hubert A, Voros G, Leclercq C, Bogaert J, Hopp E, Fjeld JG, Penicka M, Linde C, Aalen OO, Kongsgård E, Galli E, Voigt J-U, Smiseth OA. Imaging predictors of response to cardiac resynchronization therapy.
Left ventricular work best online lasix asymmetry by echocardiography and septal viability by cardiac magnetic resonance. See pages 3813â3823).Figure 2Left ventricular work asymmetry combined with septal viability identifies cardiac resynchronization therapy responders. (AâC) The panels are from the same patient and illustrate how the lateral-to-septal work difference is used in combination with viability by LGE-CMR to identify cardiac best online lasix resynchronization therapy responders.
Before cardiac resynchronization therapy (A) there is dominantly negative septal work, as indicated by the red-coloured pressure-strain loop area, but compensatory increase in left ventricular lateral wall work, which gives a large lateral-toseptal work difference. Viable septum (B) indicates potential for recovery of septal function. After 6 months with cardiac resynchronization therapy best online lasix (C), there is fine recovery of septal function.
The highly inefficient septal contractions before cardiac resynchronization therapy are converted to positive work throughout systole. The improvement in septal function was accompanied by reduced workload on the best online lasix lateral wall. (D) ROC curve displaying combined assessment of work difference and septal viability for cardiac resynchronization therapy response prediction (n = 123).
AUC, area under curve. AVC, aortic best online lasix valve closure. CI, confidence interval.
LGE-CMR, late gadolinium enhancement best online lasix cardiac magnetic resonance. LVP, left ventricular pressure. ROC, receiver operating characteristic (from Aalen JM, Donal E, Larsen CK, Duchenne J, Lederlin M, Cvijic M, Hubert A, Voros G, Leclercq C, Bogaert J, Hopp E, Fjeld JG, Penicka M, Linde C, Aalen OO, Kongsgård E, Galli E, Voigt J-U, Smiseth OA.
Imaging predictors best online lasix of response to cardiac resynchronization therapy. Left ventricular work asymmetry by echocardiography and septal viability by cardiac magnetic resonance. See pages 3813â3823).The authors conclude that assessment of myocardial work best online lasix and septal viability identifies CRT responders with high accuracy.
The manuscript is accompanied by an Editorial by Frits W. Prinzen and Joost Lumens from the Cardiovascular Research Institute Maastricht in the Netherlands12 who note that this study provides a strong extension of our understanding of CRT response and that it would not be a waste of work to perform a larger prospective study to prove the clinical feasibility and benefit of a meaningful measure of LV mechanical discoordination as an important additional selection criterion for CRT in the real-world setting.hypertension disease 2019 (hypertension medications) due to severe acute respiratory syndrome hypertension-2 (hypertension) has been associated with cardiovascular features of myocardial involvement including elevated serum troponin levels, acute heart failure with reduced ejection fraction, and myocarditis.13â15 In a clinical research article âPathological features of hypertension medications-associated myocardial injury. A multicentre cardiovascular pathology studyâ Cristina Basso from the University of Padua in Italy and colleagues note that the cardiac pathological changes in these patients with hypertension medications have yet to be well described.16 In an international multicentre study, cardiac tissue from the autopsies of 21 best online lasix consecutive hypertension medications patients was assessed by cardiovascular pathologists.
Myocarditis, as defined by the presence of multiple foci of inflammation with associated myocyte injury, was determined, and the inflammatory cell composition analysed by immunohistochemistry. Other forms of acute myocyte injury and inflammation were also described, as well as coronary artery, endocardium, best online lasix and pericardium involvement. Lymphocytic myocarditis was present in 3 (14%) of the cases.
A mild pericarditis was present in four cases. Acute myocyte injury in the right ventricle most probably due to strain/overload best online lasix was present in four cases. A non-significant trend toward higher serum troponin levels was observed in the patients with myocarditis compared with those without.
The authors conclude that in best online lasix hypertension there are increased interstitial macrophages in a majority of the cases and multifocal lymphocytic myocarditis in a small fraction of the cases. Other forms of myocardial injury are also present in these patients. The macrophage infiltration may reflect underlying diseases rather than hypertension medications.
The manuscript is accompanied by an Editorial by Nikolaos Frangogiannis from the Albert Einstein College of Medicine in the Bronx, New York, USA and colleagues.17 He notes that the findings of the current study are consistent with the notion that direct hypertension medications-mediated cardiac pathology is uncommon.The incidence of cardiogenic shock (CS) has increased remarkably over the past decade and remains a challenging condition, with mortality rates of â¼50% best online lasix. CS encompasses cardiac contractile dysfunction. However, it is also a multiorgan dysfunction syndrome, often complicated best online lasix by a systemic inflammatory response with severe cellular and metabolic dysregulations.
In a clinical review article entitled âMolecular signature of cardiogenic shockâ, Antoni Bayes-Genis from the Hospital Universitari Germans Trias i Pujol in Badalona, Spain, and colleagues sought to review the evidence on the biochemical manifestations of CS, elaborating on current gold standard biomarkers and novel candidates from molecular signatures of CS.18 Novel genomic, transcriptomic, and proteomic data are discussed, and a recently reported molecular score derived from unbiased proteomic discovery, the CS4P, which includes liver fatty acid-binding protein (L-FABP), beta-2-microglobulin (B2MG), fructose-bisphosphate aldolase B (ALDOB), and SerpinG1 (IC1), is comprehensively described.In another clinical review article entitled âWhen genetic burden reaches thresholdâ, Roddy Walsh from the University of Amsterdam in the Netherlands, and colleagues note that rare cardiac genetic diseases have generally been considered to be broadly Mendelian in nature, with clinical genetic testing for these conditions predicated on the detection of a primary causative rare pathogenic variant that will enable cascade genetic screening in families.19 Substantial variability in penetrance and disease severity among carriers of pathogenic variants, as well as the inability to detect rare Mendelian variants in considerable proportions of patients, indicates that more complex aetiologies are likely to underlie these diseases. Recent findings have suggested that genetic variants across a range of population frequencies and effect sizes may combine, along with non-genetic factors, to determine whether the threshold for expression of disease is reached and the severity of the phenotype. The availability of increasingly large genetically characterized cohorts of patients with rare cardiac diseases is enabling the discovery of common genetic variation that may underlie both variable penetrance in Mendelian diseases and best online lasix the genetic aetiology of apparently non-Mendelian rare cardiac conditions.
It is likely that the genetic architecture of rare cardiac diseases will vary considerably between different conditions as well as between patients with similar phenotypes, ranging from near-Mendelian disease to models more akin to common, complex disease. Uncovering the broad range of genetic factors that predispose patients to rare cardiac diseases offers the promise of improved risk prediction and more focused clinical management in patients and their families.The two primary molecular regulators of lifespan are sirtuin-1 (SIRT1) and mammalian best online lasix target of rapamycin complex 1 (mTORC1). In a Special Article entitled âLongevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy.
Implications for understanding the effects of current and future treatments for heart failureâ, Milton Packer from the Baylor University Medical Center at Dallas in Texas, USA notes that each plays a central role in two highly interconnected pathways that modulate the balance between cellular growth and survival.20 The activation of SIRT1 [along with peroxisome proliferator-activated receptor-gamma coactivator (PGC-1a) and adenosine monophosphate-activated protein kinase (AMPK)] and the suppression of mTORC1 (along with its upstream regulator, Akt) act to prolong organismal longevity and retard cardiac ageing. Both activation best online lasix of SIRT1/PGC-1a and inhibition of mTORC1 shifts the balance of cellular priorities so as to promote cardiomyocyte survival over growth, leading to cardioprotective effects in experimental models. These benefits may be related to direct actions to modulate oxidative stress, organellar function, proinflammatory pathways, and maladaptive hypertrophy.
Additionally, a primary shared benefit of best online lasix both SIRT1/PGC-1a/AMPK activation and Akt/mTORC1 inhibition is the enhancement of autophagy, a lysosome-dependent degradative pathway, which clears the cytosol of dysfunctional organelles and misfolded proteins that drive the ageing process by increasing oxidative and endoplasmic reticulum stress. Interestingly, most treatments that have been shown to be clinically effective in the treatment of chronic heart failure with a reduced ejection fraction have been reported experimentally to activate SIRT1/PGC-1a/AMPK and/or suppress Akt/mTORC1, and, thereby, to promote autophagic flux. Therefore, the impairment of autophagy resulting from derangements in longevity gene signalling is likely to represent a seminal event in the evolution and progression of cardiomyopathy.The editors hope that readers of this issue of the European Heart Journal will find it of interest.With thanks to Amelia Meier-Batschelet, Johanna Hugger, and Martin Meyer for help with compilation of this article.
References1Elliott P, Andersson B, Arbustini E, Bilinska Z, Cecchi F, Charron P, Dubourg O, Kühl U, Maisch B, McKenna best online lasix WJ, Monserrat L, Pankuweit S, Rapezzi C, Seferovic P, Tavazzi L, Keren A. Classification of the cardiomyopathies. A position statement best online lasix from the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.
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Eur Heart J 2020:41:3784â3786.4Sliwa K, Petrie MC, van der Meer P, Mebazaa A, Hilfiker-Kleiner D,, Jackson AM, Maggioni AP, Laroche C, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, Roos-Hesselink JW, Seferovic P, van Spaendonck-Zwarts K, Mbakwem A, Böhm M, Mouquet F, Pieske B, Johnson MR, Hamdan R, Ponikowski P, Van Veldhuisen DJ, McMurray JJV, Bauersachs J. Clinical presentation, management, and 6-month outcomes in women best online lasix with peripartum cardiomyopathy. An ESC EORP registry.
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Eur Heart J 2020:41:3798â3800.6Dickstein K, Vardas PE, Auricchio A, best online lasix Daubert JC, Linde C, McMurray J, Ponikowski P, Priori SG, Sutton R, van Veldhuisen DJ. ESC Committee for Practice Guidelines (CPG). 2010 Focused Update of ESC Guidelines on device therapy best online lasix in heart failure.
An update of the 2008 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure and the 2007 ESC guidelines for cardiac and resynchronization therapy. Developed with the special contribution of the Heart Failure Association and the European Heart Rhythm Association. Eur Heart J 2010;31:2677â2687.7Zimpfer D, Gustafsson F, Potapov E, Pya best online lasix Y, Schmitto J, Berchtold-Herz M, Morshuis M, Shaw SM, Saeed D, Laves J, Heatley G, Gazzola C, Garbade J, on behalf of the ELEVATE investigators.
Two-year outcome after implantation of a full magnetically levitated left ventricular assist device. Results from the best online lasix ELEVATE registry. Eur Heart J 2020:41:3801â3809.8Pettit SJ.
HeartMate 3. Real-world performance matches pivotal best online lasix trial. Eur Heart J 2020:41:3810â3812.9Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, Falk V, González-Juanatey JR, Harjola VP, Jankowska EA, Jessup M, Linde C, Nihoyannopoulos P, Parissis JT, Pieske B, Riley JP, Rosano GMC, Ruilope LM, Ruschitzka F, Rutten FH, van der Meer P.
ESC Scientific best online lasix Document Group. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC).
Developed with the special contribution of the Heart Failure Association best online lasix (HFA) of the ESC. Eur Heart J 2016;37:2129â2200.10Daubert C, Behar N, Martins RP, Mabo P, Leclercq C. Avoiding non-responders to best online lasix cardiac resynchronization therapy.
A practical guide. Eur Heart J 2017;38:1463â1472.11Aalen JM, Donal E, Larsen CK, Duchenne J, Lederlin M, Cvijic M, Hubert A, Voros G, Leclercq C, Bogaert J, Hopp E, Fjeld JG, Penicka M, Linde C, Aalen OO, KongsgÃ¥rd E, Galli E, Voigt JU, Smiseth OA. Imaging predictors of response to cardiac resynchronization therapy best online lasix.
Left ventricular work asymmetry by echocardiography and septal viability by cardiac magnetic resonance. Eur Heart best online lasix J 2020:41:3813â3823.12Prinzen FW, Lumens J. Investigating myocardial work as a CRT response predictor is not a waste of work.
Eur Heart J 2020:41:3824â3826.13Shi S, Qin M, Cai Y, Liu T, Shen B, Yang F, Cao S, Liu X, Xiang Y, Zhao Q, Huang H, Yang B, Huang C. Characteristics and clinical significance of myocardial best online lasix injury in patients with severe hypertension disease 2019. Eur Heart J 2020;41:2070â2079.14Peretto G, Sala S, Caforio ALP.
Acute best online lasix myocardial injury, MINOCA, or myocarditis?. Improving characterization of hypertension-associated myocardial involvement. Eur Heart J 2020;41:2124â2125.15Cuomo V, Esposito R, Santoro C.
Fulminant myocarditis best online lasix in the time of hypertension. Eur Heart J 2020;41:2121.16Basso C, Leone O, Rizzo S, De Gaspari M, van der Wal AC, Aubry MC, Bois MC, Lin PT, Maleszewski JJ, Stone JR. Pathological features of hypertension medications-associated myocardial injury best online lasix.
A multicentre cardiovascular pathology study. Eur Heart J 2020:41:3827â3825.17Frangogiannis NG. The significance of hypertension medications-associated best online lasix myocardial injury.
How overinterpretation of scientific findings can fuel media sensationalism and spread misinformation. Eur Heart J 2020:41:3836â3838.18Iborra-Egea best online lasix O, Rueda F, GarcÃa-GarcÃa C, Borrà s E, Sabidó E, Bayes-Genis A. Molecular signature of cardiogenic shock.
Eur Heart J 2020:41:3839â3848.19Walsh R, Tadros R, Bezzina CR. When genetic burden reaches threshold best online lasix. Eur Heart J 2020:41:3849â3855.20Packer M.
Longevity best online lasix genes, cardiac ageing, and the pathogenesis of cardiomyopathy. Implications for understanding the effects of current and future treatments for heart failure. Eur Heart J 2020:41:3856â3861.
Published best online lasix on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) best online lasix 2020.
For permissions, please email. Journals.permissions@oup.com.Dr Julius Axelrod was awarded the 1970 Nobel Prize for Physiology or Medicine with Sir Bernard Katz and Professor Ulf von Euler for their discoveries concerning âthe humoral transmitters in the nerve terminals and the mechanisms for their storage, release, and inactivation' American biochemist Julius Axelrod was an instantly recognizable figure in the scientific world. Having lost the sight of an eye in a laboratory accident early in his career when an ammonia bottle exploded, he wore a darkened lens over his damaged best online lasix left eye for the rest of his life.Yet he remained unperturbed and steadfast in his quest for scientific excellence.After graduating with a BSc in Biology, his applications to medical colleges were rejected, so he took jobs in various laboratories, went to night school to achieve his Masterâs Degree, and then achieved a significant breakthrough with a role as a research associate with Bernard B.
Brodie at Goldwater Memorial Hospital in New York between 1946 and 1949.The move launched his research career and set him on a path which ultimately saw him receive the 1970 Nobel Prize in Physiology or Medicine, jointly with Bernard Katz and Ulf von Euler for their discoveries concerning âthe humoral transmitters in the nerve terminals and the mechanisms for their storage, release, and inactivationâ.Whilst jointly awarded the prize, the three scientists had been working independently but together their findings led to a significant contribution toward solving principal questions concerning the neurotransmitters, their storage, release, and inactivation.The Nobel committee noted that their discoveries had advanced the understanding of the mechanism underlying the transmission between the nerve cells synapsesâand between the nerve terminals and the effector organs.While Professor von Euler had discovered that the substance noradrenaline serves as a neurotransmitter at the nerve terminals of the sympathetic nervous system, Dr Axelrodâs contribution concerned the mechanisms which regulate the formation of this transmitter in the nerve cells and the mechanisms involved in the inactivation of noradrenaline. Among other things, in 1957 he showed how an excess of noradrenaline is released in response to nerve impulses and then returns to the place where it best online lasix is stored after the signal is implemented. Sir Bernardâs discoveries focused on the mechanism for the release of the transmitter acetylcholine from the nerve terminals at the nerveâmuscle junction, under the influence of the nerve impulses.The Nobel committee noted that the advances were âa fundamental step in neurophysiology and neuropharmacologyâ, unlocking the pathway for advances in the search for remedies against nervous and mental disturbances, but there were also implications for advances in the neural pathophysiology of heart failure, hypertension, and some orthostatic intolerance syndromes.
Indeed, Professor Guido Grassi, Professor of Internal Medicine at the Clinica Medica of the University of Milano-Bicocca, suggested. ÂThe landmark studies performed by these three giants of neurotransmitters research represent the basis of modern cardiovascular physiologyâ.Julius âJulieâ Axelrod was born on 30 May 1912, in best online lasix Manhattan, New York City, the son of basket maker Isadore Axelrod and his wife Molly, who were Jewish immigrants from Poland. In 1929, he enrolled at New York University (NYU) but transferred to City College of New York (CCNY) the following year to study history, philosophy, literature, and biology, receiving his BS in biology in 1933.Having been rejected by the medical schools and seen his hopes of becoming a physician dashed, he took a job as a laboratory technician before moving to the New York City Department of Health and Mental Hygiene in 1935, testing vitamin supplements added to food.
During this period, he attended night school and received his Master of Science degree in chemistry from New York University in 1941 after completing his thesis on the chemical breakdown of enzymes in cancerous tumour tissues.A significant move came in 1946, to work under Bernard Brodie at Goldwater, where their work focused on analgesics best online lasix. During the 1940s, users of non-aspirin analgesics were developing methaemoglobinaemia. Axelrod and Brodie discovered that acetanilide in the painkillers was to blame.
They found that one of the metabolites was also an analgesic and best online lasix recommended that this metabolite, acetaminophen (paracetamol, Tylenol), be used instead. It was this research that triggered Axelrodâs passion for pharmacological science.In 1949, Axelrod began work at the National Heart Instituteâforerunner of the National Heart, Lung, and Blood Institute (NHLBI)âand part of the National Institutes of Health (NIH) in Bethesda, MD, USA. Pursuing projects that built upon his earlier research, he examined the mechanisms and effects of caffeine, which led him to an interest in the sympathetic nervous system and its main neurotransmitters, epinephrine and norepinephrine.After taking a year out best online lasix to achieve his PhD at George Washington University Medical School and graduating in 1955, he returned to the National Institute for Mental Healthâwhere he worked until his retirement aged 72 in 1984âand began some of the key research of his career.In 1957, he focused on the activity of neurotransmitter hormones.
Work which led to the development of a new class of antidepressant medications. He found that neurotransmitters do not merely stop working when they reach the post-synaptic nerve terminal but are recaptured (reuptaken) by the pre-synaptic nerve ending and used again for later transmissions.Axelrod received his Nobel Prize for his work on the release, reuptake, and storage of the neurotransmitters epinephrine and norepinephrineâalso known as adrenaline and noradrenalineâa finding that provided a new model for understanding the metabolism and regulation of neurotransmitters. He also made major contributions to the understanding of the pineal gland and how it is regulated during the sleepâwake cycle and was among the first best online lasix US scientists to conduct scientific experiments on the metabolism of lysergic acid diethylamide-25.He continued his research after the Nobel award, becoming acutely aware of the standing and responsibilities of a Nobel laureate, which saw him active in a political and campaigning context too.
After retiring from the NIMH, he continued as an unpaid guest researcher and in 1996 was named Scientist Emeritus of the NIH.Over his career, Axelrod mentored some 70 young scientists and in 1987 the Julius Axelrod Distinguished Lecture in Neuroscience was established at CCNY. He was awarded the Gairdner Foundation International best online lasix Award in 1967, elected a Foreign Member of the Royal Society in 1979, and awarded the Ralph W. Gerard Prize in Neuroscience.He had married elementary school teacher Sally Taub in 1938, and they were together 53âyears until her death in 1992.
On his death on 29 December 2004, aged 92 in Rockville, he was survived by two sons, Paul and Alfred, and three grandchildren, and recognized as one of the key figures of the 20th century in neurology and pharmacology.Axelrodâs co-recipient Ulf Svante von Euler was born in Stockholm on 7 February 1905, and entered the Karolinska Institute as a medical student in 1922. Having studied abroad at various points in the 1930s, he was appointed Full Professor of Physiology at the Karolinska Institute, where he remained until 1971 and died on 9 March 1983, aged 78.Bernard Katz was born on March 26, 1911, in Leipzig, Germany, of Russian Jewish origin and studied best online lasix Medicine at the University of Leipzig (1929â34) before leaving Germany in February 1935 for his PhD at University College London. After moving to Australia, he returned to UCL and was later appointed Professor of Biophysics.
He died on 20 April 2003.In his Nobel lecture best online lasix âNoradrenaline. Fate and control of its Biosynthesisâ on December 12, 1970, Axelrod opened by referring to von Eulerâs discoveries of 1946 in isolating and identifying noradrenaline in the sympathetic nervous system and how that shaped his work.âWhen I joined the National Institute of Mental Health in 1955, I began to think of an appropriate problem on which to work. In reading the literature I was surprised to learn that very little was known about the metabolism of noradrenaline and adrenalineâ.Two days earlier, when addressing the Nobel banquet, he had pointed to the privilege of receiving the honour with von Euler and Katz, and spoke about the importance of basic research.âThis award comes at a time when our young and many of our most influential people believe that basic research is irrelevant or is put to evil usesâ, he told the assembled guests.
The selection of chemical neurotransmission for a Nobel Prize this year, makes our work highly visible to the general public and gives us an opportunity to show how misinformed and mistaken they areâ.Adding that such work offers an insight in explaining such illnesses as mental depression, Parkinsonâs disease, hypertension, and drug abuse, he concluded. ÂI thank the Nobel Prize Committee for bringing the adrenergic and cholinergic nervous system together again. They have been apart for too longâ.
Julius Axelrod legacy â Professor Murray EslerProfessor Murray Esler, a clinical cardiologist at the Alfred Hospital, Melbourne, and Adjunct Professor of Medicine, Monash University, in Australia, explained that Julius Axelrod demonstrated that the primary mechanism for terminating the neural signal in most catecholaminergic neurons was the specific transport of the neurotransmitter back into the neuron by an active transport mechanism.He said this had profound application in psychiatry (tricyclic noradrenaline uptake blockers and selective serotonin uptake blockers), but additionally in cardiovascular medicine.âSympathetic nerve scanning in the heart, and pheochromocytoma demonstration, relies on agents such as Metaiodobenzylguanidine (MIBG) which are ligands for the noradrenaline transporterâ added Professor Esler. ÂIndirect acting sympathomimetics act by releasing noradrenaline from sympathetic nerves after uptake by the noradrenaline transporter. Noradrenaline reuptake defect is an element in the neural pathophysiology of heart failure, hypertension, and some orthostatic intolerance syndromes, notably postural tachycardia syndrome (POTS)'.Professor Esler is also Head of the Human Clinical Neurotransmitters Laboratory in the Baker Heart and Diabetes Institute in Melbourne and continues to study the sympathetic nervous system in cardiovascular medicine.
All Axelrod images, Courtesy. History of Medicine Division, U.S. National Library of MedicineConflict of interest.
None declared. Published on behalf of the European Society of Cardiology. All rights reserved.
© The Author(s) 2020. For permissions, please email. Journals.permissions@oup.com..
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This programme firstly explored the experience of patients, families and staff who have been involved in a serious incident and/or investigation in acute and mental health settings, and the process of further litigation. These findings have been helping us to co-design â with patients and families, staff and other stakeholders â new processes and guidance for involving patients and families in serious incident investigations. From Autumn 2021 we will begin evaluating these processes and guidance in a small number of investigations across mental health settings, acute care settings and nationally, within the Healthcare Safety Investigation Branch. We seek an enthusiastic, organised researcher with experience of qualitative research to cover a period of maternity leave.
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This programme firstly explored the experience of patients, families and staff who have been best online lasix involved in a serious incident and/or investigation in acute and mental health settings, and the process of further litigation. These findings have been helping us to co-design â with patients and families, staff and other stakeholders â new processes and guidance for involving patients and families in serious incident investigations. From Autumn 2021 we will begin evaluating these processes and guidance in a small number of investigations across mental health settings, acute care settings and nationally, best online lasix within the Healthcare Safety Investigation Branch. We seek an enthusiastic, organised researcher with experience of qualitative research to cover a period of maternity leave.
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This research programme also sits within the NIHR Yorkshire and Humber Patient Safety Translational Research Centre, contributing to a theme of work (led by Jane OâHara) around patient involvement in patient safety. If you would like to know more about this role, the YQSR Group and YH PSTRC, please contact. Professor Jane OâHara, jane.oâhara@bthft.nhs.uk or Dr Ruth Simms-Ellis r.simms-ellis@leeds.ac.uk We can offer staff gymnasiums on both hospital sites, excellent pension scheme and advice on childcare. Closing Date.
29.08.21 (This date may change dependent on the response) Interview Date. 10.09.21 Apply on-line at. www.jobs.nhs.uk/in/btht quoting post ref 389-A-21-49316Job Type. Fixed term contract 18 monthsOverviewWe're looking for a passionate, values-driven Health Research Lead to support Imperial College Health Partners in delivering complex change by bringing a breadth of economic, statistical, and analytical skills.
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Cases of special info Myocarditis Table 1 metolazone with lasix. Table 1 metolazone with lasix. Reported Myocarditis Cases, According to Timing of First or Second treatment Dose.
Table 2 metolazone with lasix. Table 2. Classification of Myocarditis Cases Reported to metolazone with lasix the Ministry of Health.
Among 9,289,765 Israeli residents who were included during the surveillance period, 5,442,696 received a first treatment dose and 5,125,635 received two doses (Table 1 and Fig. S2). A total of 304 cases of myocarditis (as defined by the ICD-9 codes for myocarditis) were reported to the Ministry of Health (Table 2).
These cases were diagnosed in 196 persons who had received two doses of the treatment. 151 persons within 21 days after the first dose and 30 days after the second dose and 45 persons in the period after 21 days and 30 days, respectively. (Persons in whom myocarditis developed 22 days or more after the first dose of treatment or more than 30 days after the second dose were considered to have myocarditis that was not in temporal proximity to the treatment.) After a detailed review of the case histories, we ruled out 21 cases because of reasonable alternative diagnoses.
Thus, the diagnosis of myocarditis was affirmed for 283 cases. These cases included 142 among vaccinated persons within 21 days after the first dose and 30 days after the second dose, 40 among vaccinated persons not in proximity to vaccination, and 101 among unvaccinated persons. Among the unvaccinated persons, 29 cases of myocarditis were diagnosed in those with confirmed hypertension medications and 72 in those without a confirmed diagnosis.
Of the 142 persons in whom myocarditis developed within 21 days after the first dose of treatment or within 30 days after the second dose, 136 received a diagnosis of definite or probable myocarditis, 1 received a diagnosis of possible myocarditis, and 5 had insufficient data. Classification of cases according to the definition of myocarditis used by the CDC 4-6 is provided in Table S1. Endomyocardial biopsy samples that were obtained from 2 persons showed foci of endointerstitial edema and neutrophils, along with mononuclear-cell infiates (monocytes or macrophages and lymphocytes) with no giant cells.
No other patients underwent endomyocardial biopsy. The clinical features of myocarditis after vaccination are provided in Table S3. In the 136 cases of definite or probable myocarditis, the clinical presentation in 129 was generally mild, with resolution of myocarditis in most cases, as judged by clinical symptoms and inflammatory markers and troponin elevation, electrocardiographic and echocardiographic normalization, and a relatively short length of hospital stay.
However, one person with fulminant myocarditis died. The ejection fraction was normal or mildly reduced in most persons and severely reduced in 4 persons. Magnetic resonance imaging that was performed in 48 persons showed findings that were consistent with myocarditis on the basis of at least one positive T2-based sequence and one positive T1-based sequence (including T2-weighted images, T1 and T2 parametric mapping, and late gadolinium enhancement).
Follow-up data regarding the status of cases after hospital discharge and consistent measures of cardiac function were not available. Figure 1. Figure 1.
Timing and Distribution of Myocarditis after Receipt of the BNT162b2 treatment. Shown is the timing of the diagnosis of myocarditis among recipients of the first dose of treatment (Panel A) and the second dose (Panel B), according to sex, and the distribution of cases among recipients according to both age and sex after the first dose (Panel C) and after the second dose (Panel D). Cases of myocarditis were reported within 21 days after the first dose and within 30 days after the second dose.The peak number of cases with proximity to vaccination occurred in February and March 2021.
The associations with vaccination status, age, and sex are provided in Table 1 and Figure 1. Of 136 persons with definite or probable myocarditis, 19 presented after the first dose of treatment and 117 after the second dose. In the 21 days after the first dose, 19 persons with myocarditis were hospitalized, and hospital admission dates were approximately equally distributed over time.
A total of 95 of 117 persons (81%) who presented after the second dose were hospitalized within 7 days after vaccination. Among 95 persons for whom data regarding age and sex were available, 86 (91%) were male and 72 (76%) were under the age of 30 years. Comparison of Risks According to First or Second Dose Table 3.
Table 3. Risk of Myocarditis within 21 Days after the First or Second Dose of treatment, According to Age and Sex. A comparison of risks over equal time periods of 21 days after the first and second doses according to age and sex is provided in Table 3.
Cases were clustered during the first few days after the second dose of treatment, according to visual inspection of the data (Figure 1B and 1D). The overall risk difference between the first and second doses was 1.76 per 100,000 persons (95% confidence interval [CI], 1.33 to 2.19). The overall risk difference was 3.19 (95% CI, 2.37 to 4.02) among male recipients and 0.39 (95% CI, 0.10 to 0.68) among female recipients.
The highest difference was observed among male recipients between the ages of 16 and 19 years. 13.73 per 100,000 persons (95% CI, 8.11 to 19.46). In this age group, the percent attributable risk to the second dose was 91%.
The difference in the risk among female recipients between the first and second doses in the same age group was 1.00 per 100,000 persons (95% CI, â0.63 to 2.72). Repeating these analyses with a shorter follow-up of 7 days owing to the presence of a cluster that was noted after the second treatment dose disclosed similar differences in male recipients between the ages of 16 and 19 years (risk difference, 13.62 per 100,000 persons. 95% CI, 8.31 to 19.03).
These findings pointed to the first week after the second treatment dose as the main risk window. Observed versus Expected Incidence Table 4. Table 4.
Standardized Incidence Ratios for 151 Cases of Myocarditis, According to treatment Dose, Age, and Sex. Table 4 shows the standardized incidence ratios for myocarditis according to treatment dose, age group, and sex, as projected from the incidence during the prelasix period from 2017 through 2019. Myocarditis after the second dose of treatment had a standardized incidence ratio of 5.34 (95% CI, 4.48 to 6.40), which was driven mostly by the diagnosis of myocarditis in younger male recipients.
Among boys and men, the standardized incidence ratio was 13.60 (95% CI, 9.30 to 19.20) for those 16 to 19 years of age, 8.53 (95% CI, 5.57 to 12.50) for those 20 to 24 years, 6.96 (95% CI, 4.25 to 10.75) for those 25 to 29 years, and 2.90 (95% CI, 1.98 to 4.09) for those 30 years of age or older. These substantially increased findings were not observed after the first dose. A sensitivity analysis showed that for male recipients between the ages of 16 and 24 years who had received a second treatment dose, the observed standardized incidence ratios would have required overreporting of myocarditis by a factor of 4 to 5 on the assumption that the true incidence would not have differed from the expected incidence (Table S4).
Rate Ratio between Vaccinated and Unvaccinated Persons Table 5. Table 5. Rate Ratios for a Diagnosis of Myocarditis within 30 Days after the Second Dose of treatment, as Compared with Unvaccinated Persons (January 11 to May 31, 2021).
Within 30 days after receipt of the second treatment dose in the general population, the rate ratio for the comparison of the incidence of myocarditis between vaccinated and unvaccinated persons was 2.35 (95% CI, 1.10 to 5.02) according to the Brighton Collaboration classification of definite and probable cases and after adjustment for age and sex. This result was driven mainly by the findings for males in younger age groups, with a rate ratio of 8.96 (95% CI, 4.50 to 17.83) for those between the ages of 16 and 19 years, 6.13 (95% CI, 3.16 to 11.88) for those 20 to 24 years, and 3.58 (95% CI, 1.82 to 7.01) for those 25 to 29 years (Table 5). When follow-up was restricted to 7 days after the second treatment dose, the analysis results for male recipients between the ages of 16 and 19 years were even stronger than the findings within 30 days (rate ratio, 31.90.
95% CI, 15.88 to 64.08). Concordance of our findings with the Bradford Hill causality criteria is shown in Table S5..
Cases of Myocarditis Table 1 best online lasix http://blog.hiddenblessings.com/2010/09/21/hello-world/. Table 1 best online lasix. Reported Myocarditis Cases, According to Timing of First or Second treatment Dose. Table 2 best online lasix. Table 2.
Classification of Myocarditis Cases Reported to best online lasix the Ministry of Health. Among 9,289,765 Israeli residents who were included during the surveillance period, 5,442,696 received a first treatment dose and 5,125,635 received two doses (Table 1 and Fig. S2). A total of 304 cases of myocarditis (as defined by the ICD-9 codes for myocarditis) were reported to the Ministry of Health (Table 2). These cases were diagnosed in 196 persons who had received two doses of the treatment.
151 persons within 21 days after the first dose and 30 days after the second dose and 45 persons in the period after 21 days and 30 days, respectively. (Persons in whom myocarditis developed 22 days or more after the first dose of treatment or more than 30 days after the second dose were considered to have myocarditis that was not in temporal proximity to the treatment.) After a detailed review of the case histories, we ruled out 21 cases because of reasonable alternative diagnoses. Thus, the diagnosis of myocarditis was affirmed for 283 cases. These cases included 142 among vaccinated persons within 21 days after the first dose and 30 days after the second dose, 40 among vaccinated persons not in proximity to vaccination, and 101 among unvaccinated persons. Among the unvaccinated persons, 29 cases of myocarditis were diagnosed in those with confirmed hypertension medications and 72 in those without a confirmed diagnosis.
Of the 142 persons in whom myocarditis developed within 21 days after the first dose of treatment or within 30 days after the second dose, 136 received a diagnosis of definite or probable myocarditis, 1 received a diagnosis of possible myocarditis, and 5 had insufficient data. Classification of cases according to the definition of myocarditis used by the CDC 4-6 is provided in Table S1. Endomyocardial biopsy samples that were obtained from 2 persons showed foci of endointerstitial edema and neutrophils, along with mononuclear-cell infiates (monocytes or macrophages and lymphocytes) with no giant cells. No other patients underwent endomyocardial biopsy. The clinical features of myocarditis after vaccination are provided in Table S3.
In the 136 cases of definite or probable myocarditis, the clinical presentation in 129 was generally mild, with resolution of myocarditis in most cases, as judged by clinical symptoms and inflammatory markers and troponin elevation, electrocardiographic and echocardiographic normalization, and a relatively short length of hospital stay. However, one person with fulminant myocarditis died. The ejection fraction was normal or mildly reduced in most persons and severely reduced in 4 persons. Magnetic resonance imaging that was performed in 48 persons showed findings that were consistent with myocarditis on the basis of at least one positive T2-based sequence and one positive T1-based sequence (including T2-weighted images, T1 and T2 parametric mapping, and late gadolinium enhancement). Follow-up data regarding the status of cases after hospital discharge and consistent measures of cardiac function were not available.
Figure 1. Figure 1. Timing and Distribution of Myocarditis after Receipt of the BNT162b2 treatment. Shown is the timing of the diagnosis of myocarditis among recipients of the first dose of treatment (Panel A) and the second dose (Panel B), according to sex, and the distribution of cases among recipients according to both age and sex after the first dose (Panel C) and after the second dose (Panel D). Cases of myocarditis were reported within 21 days after the first dose and within 30 days after the second dose.The peak number of cases with proximity to vaccination occurred in February and March 2021.
The associations with vaccination status, age, and sex are provided in Table 1 and Figure 1. Of 136 persons with definite or probable myocarditis, 19 presented after the first dose of treatment and 117 after the second dose. In the 21 days after http://exploringtheusbyrv.com/2011/07/19/highlights-from-the-walker-art-park/ the first dose, 19 persons with myocarditis were hospitalized, and hospital admission dates were approximately equally distributed over time. A total of 95 of 117 persons (81%) who presented after the second dose were hospitalized within 7 days after vaccination. Among 95 persons for whom data regarding age and sex were available, 86 (91%) were male and 72 (76%) were under the age of 30 years.
Comparison of Risks According to First or Second Dose Table 3. Table 3. Risk of Myocarditis within 21 Days after the First or Second Dose of treatment, According to Age and Sex. A comparison of risks over equal time periods of 21 days after the first and second doses according to age and sex is provided in Table 3. Cases were clustered during the first few days after the second dose of treatment, according to visual inspection of the data (Figure 1B and 1D).
The overall risk difference between the first and second doses was 1.76 per 100,000 persons (95% confidence interval [CI], 1.33 to 2.19). The overall risk difference was 3.19 (95% CI, 2.37 to 4.02) among male recipients and 0.39 (95% CI, 0.10 to 0.68) among female recipients. The highest difference was observed among male recipients between the ages of 16 and 19 years. 13.73 per 100,000 persons (95% CI, 8.11 to 19.46). In this age group, the percent attributable risk to the second dose was 91%.
The difference in the risk among female recipients between the first and second doses in the same age group was 1.00 per 100,000 persons (95% CI, â0.63 to 2.72). Repeating these analyses with a shorter follow-up of 7 days owing to the presence of a cluster that was noted after the second treatment dose disclosed similar differences in male recipients between the ages of 16 and 19 years (risk difference, 13.62 per 100,000 persons. 95% CI, 8.31 to 19.03). These findings pointed to the first week after the second treatment dose as the main risk window. Observed versus Expected Incidence Table 4.
Table 4. Standardized Incidence Ratios for 151 Cases of Myocarditis, According to treatment Dose, Age, and Sex. Table 4 shows the standardized incidence ratios for myocarditis according to treatment dose, age group, and sex, as projected from the incidence during the prelasix period from 2017 through 2019. Myocarditis after the second dose of treatment had a standardized incidence ratio of 5.34 (95% CI, 4.48 to 6.40), which was driven mostly by the diagnosis of myocarditis in younger male recipients. Among boys and men, the standardized incidence ratio was 13.60 (95% CI, 9.30 to 19.20) for those 16 to 19 years of age, 8.53 (95% CI, 5.57 to 12.50) for those 20 to 24 years, 6.96 (95% CI, 4.25 to 10.75) for those 25 to 29 years, and 2.90 (95% CI, 1.98 to 4.09) for those 30 years of age or older.
These substantially increased findings were not observed after the first dose. A sensitivity analysis showed that for male recipients between the ages of 16 and 24 years who had received a second treatment dose, the observed standardized incidence ratios would have required overreporting of myocarditis by a factor of 4 to 5 on the assumption that the true incidence would not have differed from the expected incidence (Table S4). Rate Ratio between Vaccinated and Unvaccinated Persons Table 5. Table 5. Rate Ratios for a Diagnosis of Myocarditis within 30 Days after the Second Dose of treatment, as Compared with Unvaccinated Persons (January 11 to May 31, 2021).
Within 30 days after receipt of the second treatment dose in the general population, the rate ratio for the comparison of the incidence of myocarditis between vaccinated and unvaccinated persons was 2.35 (95% CI, 1.10 to 5.02) according to the Brighton Collaboration classification of definite and probable cases and after adjustment for age and sex. This result was driven mainly by the findings for males in younger age groups, with a rate ratio of 8.96 (95% CI, 4.50 to 17.83) for those between the ages of 16 and 19 years, 6.13 (95% CI, 3.16 to 11.88) for those 20 to 24 years, and 3.58 (95% CI, 1.82 to 7.01) for those 25 to 29 years (Table 5). When follow-up was restricted to 7 days after the second treatment dose, the analysis results for male recipients between the ages of 16 and 19 years were even stronger than the findings within 30 days (rate ratio, 31.90. 95% CI, 15.88 to 64.08). Concordance of our findings with the Bradford Hill causality criteria is shown in Table S5..
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