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Month: August 2023
Prasugrel monotherapy after percutaneous coronary intervention (PCI) with drug-eluting stents is not superior to dual-antiplatelet therapy (DAPT) for major bleeding but is non-inferior for cardiovascular events in patients with acute coronary syndrome (ACS) or high bleeding risk (HBR), according to late breaking research presented in a Hot Line session today at ESC Congress 2023. Very short (1 to 3 months) durations of DAPT followed by P2Y12 inhibitor monotherapy has been shown to reduce bleeding events without increasing cardiovascular events compared with standard durations of DAPT after PCI using drug-eluting stents. However, the incidence of major bleeding events within the 1-month mandatory DAPT period after PCI remains high in real clinical practice, particularly in patients with ACS or HBR. In single-arm studies, aspirin-free prasugrel or ticagrelor monotherapy following successful new-generation drug-eluting stent implantation was not associated with any stent thrombosis in selected low-risk patients with or without ACS. Removing aspirin from the DAPT regimen might reduce bleeding events early after PCI without compromising the risk of cardiovascular events. However, the efficacy and safety of this strategy has not been proven in randomized trials. ESC guidelines recommend 6 months of DAPT in HBR patients with ACS and 12 months of DAPT in non-HBR patients with ACS after PCI. In patients with non-ACS, 1 to 3 months of DAPT is recommended in HBR patients after PCI. STOPDAPT-3 investigated the efficacy and safety of aspirin-free prasugrel monotherapy compared with 1-month DAPT with aspirin and prasugrel in patients with ACS or HBR undergoing PCI with cobalt-chromium everolimus-eluting stents. From January 2021 to April 2023, the study enrolled 6,002 patients with ACS or HBR from 72 centers in Japan. Just before PCI, patients were randomized in a 1:1 fashion to prasugrel (3.75 mg/day) monotherapy or to DAPT with aspirin (81-100 mg/day) and prasugrel after a loading dose of prasugrel 20 mg in both groups. There were two primary endpoints: 1) major bleeding events (defined as Bleeding Academic Research Consortium [BARC] type 3 or 5) at 1 month for superiority; and 2) cardiovascular events (a composite of cardiovascular death, myocardial infarction, definite stent thrombosis, or stroke) at 1 month for non-inferiority. The major secondary endpoint was a composite of the co-primary bleeding and cardiovascular endpoints (cardiovascular death, myocardial infarction, definite stent thrombosis, stroke, or major bleeding) at 1 month representing net clinical benefit. The full analysis set population consisted of 5,966 patients (no-aspirin group: 2,984 patients; DAPT group: 2,982 patients). The average age was 71.6 years and 23.4% were women. At 1 month, the no-aspirin strategy was not superior to DAPT for the co-primary bleeding endpoint (4.47% vs. 4.71%; hazard ratio [HR], 0.95; 95% confidence interval [CI], 0.75-1.20; p for superiority=0.66). The no-aspirin strategy was non-inferior to DAPT with a relative 50% margin for the co-primary cardiovascular endpoint (4.12% vs. 3.69%; HR, 1.12; 95% CI, 0.87-1.45; p for non-inferiority=0.01). Related Stories There was no between-group difference in the incidence of all-cause death (2.28% vs. 2.11% in the no-aspirin and DAPT groups, respectively). The major secondary endpoint occurred in 7.14% patients in the no-aspirin group and 7.38% patients in the DAPT group, with no between-group difference, indicating a similar effect on net clinical benefit for both groups. There was an excess of any coronary revascularisation (1.15% vs. 0.57%) and definite or probable stent thrombosis (0.71% vs. 0.44%) in the no-aspirin group compared with the DAPT group, while definite stent thrombosis was not different between the 2 groups (0.47% vs. 0.37%). In a subgroup analysis stratified by ACS and non-ACS, the excess risk of cardiovascular events in the no-aspirin group compared with the DAPT group was seen in patients with ACS, but not in those without ACS. The aspirin-free strategy compared with the DAPT strategy failed to reduce major bleeding within 1 month after PCI, but it was non-inferior for the co-primary cardiovascular endpoint with a relative 50% margin. Aspirin used for a limited period of 1 month after PCI as a component of DAPT might have exerted a protective effect on vulnerable coronary lesions, particularly in patients with ACS, without a large increase in major bleeding. DAPT should remain the standard strategy for PCI even in the new-generation drug-eluting stent era.” Dr. Masahiro Natsuaki, Study Author, Saga University, Japan European Society of Cardiology (ESC)
Rami Komrokji, MD Although the current classification systems for patients with myelodysplastic syndromes (MDS) were able to identify groups of patients with similar outcomes, further refinement is needed to create more consistent criteria, according to findings from an international dataset analysis of the 2 classification systems presented by Rami Komrokji, MD, during the 2023 EHA Congress. “It’s clear that we are moving to a new era in the classification of MDS and that we have molecularly defined groups; those patients should be thought of, treated, and enrolled in clinical trials separately,” Komrokji said. “Then we have the morphologically defined groups, but we definitely need to step up, try to harmonize those [criteria], and go back into 1 classification that hematopathologists, clinicians, and clinical trialists use as a common language rather than having 2 different classifications.” The analysis, which was conducted on behalf of the International Consortium for MDS, used datasets from Moffitt Cancer Center and the European initiative GenoMed4all:GM encompassing 7017 patients with available molecular data to validate and compare the World Health Organization (WHO) and International Consensus Classification (ICC) 2022 classification criteria. Results showed that patients with deletion 5q (del5q) in the WHO (n = 107) and ICC groups (n = 108) from the Moffitt cohort both achieved an overall survival (OS) of 75.6 months vs 82.1 months for those from GenoMed4all:GM with del5q in the WHO (n = 219) and ICC groups (n = 223), respectively. Patients with SF3B1 mutations, which represent approximately 12% of all MDS cases, had the best outcomes compared with those with del5q and TP53-mutated disease. These patients in the WHO (n = 294) and ICC groups (n = 277) from the Moffitt cohort experienced an OS of 101.8 months and 111.6 months vs 104.9 months and 101.9 months in the GenoMed4all:GM WHO (n = 654) and ICC (n = 594) groups, respectively. In an interview with OncLive®, Komrokji, the vice chair of the Malignant Hematology Department and the head of the Leukemia and MDS Section at Moffitt Cancer Center in Tampa, Florida, discussed the comparative analysis as well as the next steps being taken to develop a more harmonized classification system. OncLive: What was the rationale behind the analysis presented at the 2023 EHA Congress? Komrokji: The classification for MDS has been evolving over the years, from FAB [French American British] in the 1980s, to different iterations from the WHO, but [for] the first time, in 2022 we have 2 classification systems: the WHO and the ICC. Both of them are an attempt to improve the classification for MDS, but also it creates a dilemma in the field and controversy regarding which one to follow. There are some differences [between the classification systems]. It was important to generate data-driven evidence to hopefully guide future harmonization of those 2 classifications. People are mixing classification vs prognostic models. Risk stratification in MDS is based on [the] Revised International Prognostic Scoring System [IPSS-R]. The classification historically is pathological classification [and] it should reflect a unique biology of the disease [as well as] unique groups that have a certain clinical phenotype [where] maybe the pathogenesis of defective hematopoiesis is similar in that group. We were trying to validate those and hopefully this is the first step in trying to come up with harmonization and [return to] 1 classification [system] in MDS. How was the analysis conducted? When the [ICC 2022] classification came out we looked at our database—we have a large database with more than 2500 patients fully annotated—and then we approached our colleagues in Europe. They kindly joined us with the GenoMed4all:GM MDS database, which is the MDS database for almost the whole [of] Europe. Advertisement Together, we were able to put approximately 7000 patients with MDS [into our platform], which is a very large cohort. Hopefully [it] will be a platform not only for this project, but for several other projects down the road. We reclassified all the patients according to the WHO and ICC [criteria], included only patients with fully annotated molecular data, and we looked at the questions that we wanted to address. What were the key findings of the analysis? The 2 classifications recognize molecularly-defined categories of MDS, namely SF3B1, del5q, as well as P53. There are slight differences in the definitions between both of them. For example, we demonstrated that SF3B1 is a unique category, approximately 12% to 13% of patients with MDS have very favorable outcomes with a median OS of more than 10 years [and] low chance of [dying from] leukemia. We also looked at a subset of patients [with] MDS with ring sideroblasts, which is usually the phenotype we see with SF3B1, but [we examined patients] if they were SF3B1 wild-type. That’s a smaller subset, approximately only 4% of patients, but they did not have the same favorable outcomes. The WHO retained [classification of] MDS with ring sideroblasts, which is probably something that could go away down the road in the future based on this. However, we have to think of those models in terms of generalizing them. In countries where there is no access to SF3B1 [testing], ring sideroblasts are still a good marker for SF3B1. We also confirmed that [the patient population with] del5q is a favorable group, [constituting] approximately 5% of patients [with MDS]. Bi-allelic TP53 [is found in] approximately 10% of patients [with MDS] and unfortunately they have very poor outcomes. The ICC proposed a different group of P53, monoallelic. If the blasts were more than 10%, they would consider that MDS/AML with P53. Those patients had worse outcomes and part of it is driven by the increased blast [percentage]. In the future, that category may go away, and we’ll probably stick more to the bi-allelic [characterization of] P53. In the morphologically defined [criteria], we showed that MDS ring sideroblasts without SF3B1 [mutations] are not different. The ICC proposed that the number of lineage dysplasia, whether we have multilineage vs single lineage dysplasia, does matter [and we showed that] multilineage dysplasia did worse.
Utah State University’s Aggies have donated enough blood to win the blood drive battle against Weber State University every year for the past 19 years — and USU isn’t planning on losing this year either, according to Bridger Esplin, the Aggie Red Cross student director. The event will take place from Sept. 5-8, and students and faculty can donate blood between 9 a.m. and 9 p.m. Not only is there a competitive aspect between USU and Weber, but all registered USU clubs, including sororities and fraternities, may receive prizes. But it’s not just the fact that USU has claimed victory for several decades — both universities’ donations have saved tens of thousands of lives. In the last 19 years, the blood battles have led to over 19,355 units of blood being donated, with each unit saving multiple lives, according to Kirsten Stuart, the communications and public affairs associate with the American Red Cross. “I think service should be a huge part of any student’s experience at college, and this is just a really great opportunity for students to get involved,” said Tyson Packer, the student advocate vice president for Utah State University Student Association. While the competitive aspect is certainly enjoyable for many students, Stuart said “the blood donations are important regardless of the situation,” especially with sharp declines in summer donors. “In the summer, the blood supply does go down because people are out more, they’re out doing more things and quite frankly, some people are getting hurt more and needing blood — but the donations are down,” Stuart continued. “This specific blood battle is an amazing way to help in replenishing that supply.” Utah’s blood donations don’t just help Utahns. USU’s blood battles are crucial in helping surgery patients and those recovering from disasters from all over the country. “Utah powers a lot of the country,” Esplin said. Blood donations could especially help victims of natural disasters, from wildfires in Maui, Hawaii to Hurricane Hilary’s impact on the U.S.’s West Coast, according to Nelda Ault-Dyslin, the assistant director of community-engaged learning at the USU Center for Community Engagement. Participants can observe where their donations may travel to on the Red Cross website or app and can even receive a letter of thanks stating which hospital their blood went to, as well as how it helped save a life, Stuart said. For students that are squeamish with needles, they can either volunteer with the Red Cross professionals or at the Blood Battle itself, Esplin said. Still, donating blood is still one of the most effective ways to make a difference. Despite Esplin’s original fears when he first donated, he felt confident afterward. “It actually wasn’t nearly as bad as I thought,” he said. Packer said students who may not understand the purpose of donating blood should ask the Red Cross volunteers about what their blood will do for other people. “They’ll tell you personal stories about people who have gotten blood transfusions, about EMTs who have had to get blood transfusions or have saved lives at car accidents that they’ve been called to,” Packer said. “I just tell students to get in there, ask around, hear about those personal experiences and it’ll really open their eyes to why it’s so important.” For Stuart, donating blood is about just that. When her mother had a gastrointestinal bleed and needed a blood transfusion, she said she found herself getting emotional after seeing the American Red Cross blood donation bags. “Quite frankly, all of us at some point are going to be touched by someone who needed a blood donation,” Stuart said. “I want them (students) to really realize the huge difference that they are making in so many people’s lives with their blood donation. Whether they’re saving the lives of an infant, a child, you know, someone’s mother, grandmother — that literal act of 30 minutes to an hour of their time can mean years to somebody else that they get with a family member.” Previous Article Women’s soccer falls to Utes on late goal
TAIPEI, Taiwan (AP) — China will no longer require a negative COVID-19 test result for incoming travelers starting Wednesday, a milestone in its reopening to the rest of the world after a three-year isolation that began with the country’s borders closing in March 2020. Foreign Ministry spokesperson Wang Wenbin announced the change at a briefing in Beijing on Monday. China in January ended quarantine requirements for its own citizens traveling from abroad, and over the past few months has gradually expanded the list of countries that Chinese people can travel to and increased the number of international flights. READ MORE: Severe floods in China killed 29 and caused tens of billions of economic losses Beijing ended its tough domestic “zero COVID” policy only in December, after years of draconian curbs that at times included full-city lockdowns and lengthy quarantines for people who were infected. The restrictions slowed the world’s second-largest economy, leading to rising unemployment and occasional instances of unrest. As part of those measures, incoming travelers were required to isolate for weeks at government-designated hotels. Residents were in some cases forcibly locked into their homes in attempts to stop the virus from spreading. Protests in major cities including Beijing, Shanghai, Guangzhou and Nanjing erupted in November over the COVID curbs, in the most direct challenge to the Communist Party’s rule since the Tiananmen protests of 1989. In early December, authorities abruptly scrapped most COVID controls, ushering in a wave of infections that overwhelmed hospitals and morgues. A U.S. federally funded study this month found the rapid dismantling of the “zero COVID” policy may have led to nearly 2 million excess deaths in the following two months. That number greatly exceeds official estimates of 60,000 deaths within a month of the lifting of the curbs. During the years of “zero COVID,” local authorities occasionally imposed snap lockdowns in attempts to isolate infections, trapping people inside offices and apartment buildings. READ MORE: China’s Xi calls for measures to mitigate flooding amid economic downturn From April until June last year, the city of Shanghai locked down its 25 million residents in one of the world’s largest pandemic-related mass lockdowns. Residents were required to take frequent PCR tests and had to rely on government food supplies, often described as insufficient. Throughout the pandemic, Beijing touted its “zero COVID” policy — and the initial relatively low number of infections — as an example of the superiority of China’s political system over that of Western democracies. Since lifting the COVID curbs, the government has been contending with a sluggish economic recovery. The restrictions, coupled with diplomatic frictions with the United States and other Western democracies, have driven some foreign companies to reduce their investments in China. Associated Press news assistant Caroline Chen in Beijing contributed to this report.
image: In the panvascular system, hypoxia-inducible factors (HIFs) can lead to excessive activity of vascular smooth muscle cells (VSMCs), presenting a phenotype of proliferation and migration in atherosclerosis and pulmonary arterial hypertension. In atherosclerosis, VSMCs influenced by HIFs may also exhibit a myofibroblast-like transformation, whereas in pulmonary arterial hypertension, noteworthy electrophysiological changes occur in HIF-affected VSMCs. In the aortic aneurysm, HIFs are associated with apoptosis and vascular remodeling in VSMCs. Regarding vascular calcification, HIFs are related to osteochondral differentiation in VSMCs. view more Credit: ©Science China Press This study is led by Prof. Junbo Ge (Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases), Prof. Hua Li (Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases), and Prof. Hao Lu (Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases). As an emerging concept, panvascular diseases encompass a group of cardiovascular disorders characterized mainly by atherosclerosis, involving crucial organs such as the heart, brain, kidneys, and limbs. Hypoxia-inducible factor (HIF) plays a pivotal role as a major regulatory factor in the cardiovascular system’s response to common stressors, such as hypoxia. Meanwhile, vascular smooth muscle cells (VSMCs) serve as key cells responsible for regulating cardiovascular system pressure and oxygen delivery. The plasticity, versatility, and interaction of these two factors with panvascular diseases warrant in-depth investigation. In the pathological state of panvascular diseases, overactive VSMCs (e.g., in atherosclerosis, pulmonary arterial hypertension) or dysfunctional VSMCs (e.g., in arterial aneurysms, vascular calcification) are closely associated with HIFs. These widespread systemic diseases also underscore the interdisciplinary nature of panvascular medicine. Furthermore, considering the similarities in proliferative characteristics between VSMCs and cancer cells, as well as the delicate balance between angiogenesis and cancer progression, there is an urgent need for more precise regulatory targets or combination therapies to enhance the effectiveness of HIF-targeted treatments. Based on the above content, this review focuses on discussing the significance of the HIF signaling pathway in panvascular diseases related to VSMCs, taking into consideration the importance of balancing global and local, as well as temporal and spatial aspects. The review also explored the relevance of HIF-related drugs’ targets in panvascular diseases while weighing their pros and cons. The “-dustats” is a novel type of drug that can inhibit PHD, thus activating the HIF-EPO pathway, and its effect on increasing EPO in the body is gentle. In existing research, the drug “-dustats” has been found to improve iron metabolism while treating anemia, and it generally does not exhibit significant cardiovascular side effects or promote cancer occurrence. Furthermore, more precise and targeted HIF pathway-activating drugs require either more specific indirect activation of HIF (e.g., inhibitors targeting specific PHD1-3 or FIH) or more effective direct activation targeting the specific HIF isoforms. Additionally, the issue of drug resistance also needs to be addressed. Collectively, there are three key points in advancing the transformation of HIF-related treatment strategies for VSMC in panvascular medicine: (1) focusing on the commonality and specificity of HIFs in panvascular disease; (2) the overall consideration of targeting HIF-related pathways, and (3) the development of precise drugs targeting HIF-related pathways. Overall, the clinical transformation of HIFs-related therapies requires that doctors pay more attention to individual differences (eg, place of residence, gender, and disease) in diagnosis and treatment to identify underlying problems; researchers explore and clarify the different roles and interactions of HIFs in different organs/systems or different stages of the disease; and pharmaceutical experts or engineers strive to industrialize the production of personalized targeted drugs with superior pharmacodynamics and pharmacokinetics. Therefore, based on the principle of “from doctors, by engineers/researchers, for patients”, the substantial clinical transformation of HIFs-related treatment in panvascular medicine can be realized. Journal Science Bulletin Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
In iron-deficient patients with heart failure and reduced or mildly reduced left ventricular ejection fraction, intravenous ferric carboxymaltose (FCM) is associated with a reduced risk of the composite outcome of total cardiovascular hospitalization and cardiovascular death through 52 weeks compared with placebo, according to late-breaking research presented in a Hot Line session today at ESC Congress 2023. Iron deficiency is common in heart failure, with a prevalence of 30-80%, and is associated with increased mortality and hospitalization. Randomised controlled trials of intravenous iron in iron-deficient patients with heart failure have shown improvements in symptoms, functional capacity and quality of life, but the effect on clinical events has been unclear. The current meta-analysis evaluated the effects of FCM therapy on hospitalizations and mortality in iron-deficient patients with heart failure and reduced or mildly reduced left ventricular ejection fraction. The meta-analysis pooled individual participant data from three randomized, placebo-controlled trials of FCM in adult patients with heart failure and iron deficiency with at least 52 weeks of follow up: CONFIRM-HF, AFFIRM-AHF and HEART-FID. There were two primary efficacy endpoints: 1) composite of total cardiovascular hospitalizations and cardiovascular death and 2) composite of total heart failure hospitalizations and cardiovascular death. Both endpoints were examined through 52 weeks of follow up. Key secondary endpoints included individual components of the composite endpoints. In the three trials, a total of 4,501 patients with heart failure and reduced or mildly reduced left ventricular ejection fraction and iron deficiency were randomly assigned to FCM (n=2,251) or placebo (n=2,250). The mean age of the total population was 69 years, 63% were men, and the mean left ventricular ejection fraction was 32%. FCM therapy significantly reduced the co-primary composite endpoint of total cardiovascular hospitalizations and cardiovascular death compared with placebo, with a rate ratio (RR) of 0.86 (95% confidence interval [CI] 0.75 to 0.98; p=0.029). There was a trend towards reduction of the co-primary composite endpoint of total heart failure hospitalizations and cardiovascular death but it failed to reach statistical significance (RR 0.87; 95% CI 0.75 to 1.01; p=0.076). FCM therapy was associated with a 17% relative rate reduction in total cardiovascular hospitalizations (RR 0.83; 95% CI 0.73 to 0.96; p=0.009) and a 16% relative rate reduction in total heart failure hospitalizations (RR 0.84; 95% CI 0.71 to 0.98; p=0.025). There was no effect of FCM administration on mortality. In subgroup analyses, patients in the lowest transferrin saturation (TSAT) tertile (<15%) derived greater benefit from FCM on the composite endpoint of total cardiovascular hospitalizations or cardiovascular death than those with higher baseline TSAT (interaction p=0.019). Treatment with FCM appeared to be safe and well-tolerated. This was the largest and most up-to-date analysis of the effect of FCM in iron-deficient heart failure patients with reduced or mildly reduced ejection fraction. FCM was associated with a reduction in the composite endpoint of total cardiovascular hospitalizations and cardiovascular death compared with placebo, and with significantly reduced risks of hospitalization due to heart failure or cardiovascular causes, with no effect on survival. The findings indicate that intravenous FCM should be considered in iron-deficient patients with heart failure and reduced or mildly reduced ejection fraction to reduce the risk of hospitalization due to heart failure and cardiovascular causes.” Piotr Ponikowski, Principal Investigator, Professor, Wroclaw Medical University, Poland European Society of Cardiology (ESC)
European Society of Cardiology Cardiovascular disease (CVD) cost the EU an estimated €282 billion in 2021, according to late breaking research presented at ESC Congress 2023.1 Health and long-term care accounted for €155 billion (55%) of these costs, equalling 11% of EU health expenditure. The analysis was a collaborative effort by the European Society of Cardiology (ESC) and the University of Oxford, UK. Study author Dr. Ramon Luengo-Fernandez of the University of Oxford said: “CVD had a significant impact on the EU27 economy, costing a total of €282 billion in 2021. That’s equivalent to 2% of Europe’s GDP and is significantly more than the entire EU budget2 itself, used to fund research, agriculture, infrastructure and energy across the Union.” This was the most comprehensive and up-to-date analysis of the economic costs of CVD to society in the EU since 2006. It is the first study to use Europe-wide patient registries and surveys rather than relying on assumptions and, unlike previous reports, includes the costs of long-term social care. The current analysis provides estimates of the societal economic costs of CVD for the 27 members states of the EU in 2021, including 1) health and social care; 2) informal care; and 3) productivity losses. The breakdown includes:3 €130 billion for healthcare (46%) €25 billion for social care (9%) €79 billion for informal care (28%) €15 billion in productivity losses due to illness/disability (5%) €32 billion in productivity losses due to premature death (12%). The total cost equated to €630 per EU citizen, ranging from €381 in Cyprus to €903 in Germany.4 CVD cost health and social care systems approximately €155 billion in 2021, accounting for 11% of total healthcare expenditure. There was wide variation between countries in the proportion of healthcare budgets spent on CVD, from 6% in Denmark to 19% in Hungary. Healthcare included primary care, emergency care, hospital care, outpatient care and medications, while social care included long-term institutionalised care, and care at home. The main contributor was hospital care, which cost €79 billion, representing 51% of CVD-related care costs. CVD medications accounted for €31 billion (20%) of care costs, followed by residential nursing care homes at €15 billion (9%). Informal care costs included the work or leisure time, valued in monetary terms, that relatives and friends gave up to provide unpaid care. Relatives and friends provided 7.5 billion hours of unpaid care for patients with CVD, amounting to €79 billion across the EU. Productivity losses included lost earnings due to illness/disability (early retirement/absenteeism) or premature death. In 2021, 256 million working-days were lost in the EU because of CVD illness/disability, at a cost of €15 billion. That same year, 1.7 million people died due to CVD across the EU, representing 1.3 million working-years lost, and generating productivity losses of €32 billion. ESC Board member and study author Professor Victor Aboyans of Limoges University, France said: “This study underscores the urgent need to act collectively on the European scale to better combat the cardiovascular risk of European citizens, in particular through regulations for better cardiovascular prevention and investment in research. By choosing not to invest in cardiovascular disease we are simply deferring the cost. These data force us to ask the question: do we invest in cardiovascular health today or be forced to pay more at a later stage?” Professor Panos Vardas, chief strategy officer of the European Heart Agency, the ESC’s office in Brussels, said: “Today’s presentation provides a clear understanding of the overall economic burden of cardiovascular disease across different EU countries, offering the opportunity to draw valuable conclusions that are useful for those responsible for designing healthcare plans. It is evident that there is significant fragmentation among EU countries in terms of cardiovascular disease healthcare expenditures. This necessitates a re-evaluation by the EU as a whole, and the 27 EU countries individually, to better address the outstanding needs and invest more effectively in supporting those suffering from cardiovascular disease.” /Public Release. This material from the originating organization/author(s) might be of the point-in-time nature, and edited for clarity, style and length. Mirage.News does not take institutional positions or sides, and all views, positions, and conclusions expressed herein are solely those of the author(s).View in full here.
Researchers at Ohio State University (OSU) have found that white-tailed deer are reservoirs for SARS-CoV-2 viruses. The experts report that a significant number of white-tailed deer across Ohio have been infected with SARS-Cov-2 and that viral variants evolve about three times faster in deer than in humans. Focus of the study Between November 2021 and March 2022, the researchers collected 1,522 nasal swaps from free-ranging deer in 83 of Ohio’s 88 counties and tested them for the virus causing COVID-19. What the researchers discovered The analysis revealed that over 10 percent of the samples were positive, and at least one positive case was found in 59 percent of the counties in which testing was conducted. Surprisingly, genomic analysis showed that at least 30 infections in deer have spilled over from humans. Interspecies transmission “We generally talk about interspecies transmission as a rare event, but this wasn’t a huge sampling, and we’re able to document 30 spillovers. It seems to be moving between people and animals quite easily,” said study co-senior author Andrew Bowman, an associate professor of Veterinary Preventive Medicine at OSU. “And the evidence is growing that humans can get it from deer – which isn’t radically surprising. It’s probably not a one-way pipeline.” These findings suggest that white-tailed deer are a reservoir for SARS-CoV-2 which enables continuing mutation, and that the virus’s widespread circulation in deer could potentially lead to its spread to other wildlife and livestock. Not just a localized problem In December 2021, Bowman and his colleagues first reported the detection of the virus in white-tailed deer in nine locations in Ohio. In the current study, they expanded monitoring in a variety of other locations. “We expanded across Ohio to see if this was a localized problem – and we find it in lots of places, so it’s not just a localized event,” Bowman explained. “Some of the thought back then was that maybe it’s just in urban deer because they’re in closer contact with people. But in rural parts of the state, we’re finding plenty of positive deer.” Besides detecting active infections, the scientists also found a significant number of blood samples containing antibodies, suggesting that an estimated 23.5 percent of deer in Ohio had already been infected with the coronavirus. Spillover events Among the 80 whole-genome sequences obtained from the samples, the researchers identified the highly contagious and virulent delta variant (the predominant human strain in the United States in the early fall of 2021), which accounted for nearly 90 percent of the sequences, and alpha, the first variant of concern that was identified in humans in the spring of 2021. The investigation revealed that the genetic composition of delta variants in deer closely matched the dominant lineages found in humans during the same time period, pointing to several spillover events, and suggesting that deer-to-deer transmission followed in clusters, some of them spanning multiple counties. “There’s probably a timing component to what we found – we were near the end of a delta peak in humans, and then we see a lot of delta in deer. But we were well past the last alpha detection in humans. So the idea that deer are holding onto lineages that have since gone extinct in humans is something we were worried about,” Bowman said. According to the experts, vaccination is likely to protect people against severe diseases in case the virus will spill back into humans. For instance, an investigation of the effects of deer variants on Siberian hamsters (an animal model widely used in COVID-19 studies) provided clear evidence that vaccinated hamsters did not get as sick after infection as unvaccinated ones. Study implications Unfortunately, the variants circulating in deer are expected to continue to change at a faster rate than that seen in humans. “Not only are deer getting infected with and maintaining SARS-CoV-2, but the rate of change is accelerated in deer – potentially away from what has infected humans,” Bowman reported. Further research is needed to clarify how the virus is transmitted from humans to white-tailed deer and assess the likelihood of mutated variants to spill back into humans. Although no substantial outbreaks of deer-origin strains have occurred in humans until now, circulation among animals remains very likely. Moreover, since about 70 percent of free-ranging deer in Ohio have not been exposed to the virus yet, there is a large number of immunologically-naïve animals that the virus could spread through uninhibited. “Having that animal host in play creates things we need to watch out for. If this trajectory continues for years and we have a virus that becomes deer-adapted, then does that become the pathway into other animal hosts, wildlife or domestic? We just don’t know,” Bowman concluded. The study is published in the journal Nature Communications. — By Andrei Ionescu, Earth.com Staff Writer Check us out on EarthSnap, a free app brought to you by Eric Ralls and Earth.com. .
For patients with myeloproliferative neoplasms (MPNs) — blood cancers that cause the bone marrow to overproduce red or white blood cells or platelets — being able to engage in educated and productive conversations with their care team can be crucial. “There are so many variables in cancer from not only the diagnoses, but ‘how do we treat it?’ to what the prognosis is, and that’s always evolving (so) that it’s hard for providers to keep up with that, let alone patients,” said Charina Toste, a nurse practitioner specializing in oncology and hematology at OptumCare Cancer Care and a professor at Chamberlain College of Nursing, both located in Las Vegas, Nevada. When it comes to the vast category of MPNS (which includes a range of diseases such as myelofibrosis, essential thrombocythemia, and polycythemia vera) patients don’t know what they don’t know. “(Patients) don’t always know, what is the treatment that’s out there? What are the clinical trials that are out there? Oh, and then let’s talk about symptom management, how is my life going to change? How is this going to affect me? How is this going to affect my family? These are questions patients don’t even know to ask. And they trust their health care provider to have the three or four hours it takes to educate them at an appointment that usually is only 15 to 30 minutes.” Toste spoke with CUREⓇ about the importance of education for patients with MPNs in order to empower themselves to have informed conversations with their care team. CUREⓇ: In general, why is it so important for patients to educate themselves, and be prepared to have informed conversations with their care team as they’re going through their cancer journey? Patients with myeloproliferative neoplams should learn about their disease to ensure that they know what questions to ask, a nurse practitioner said. Toste: I think because with any type of diagnosis, there’s kind of the shock factor. And once you get over the shock factor, it’s a different language that patients are learning, it’s a different lifestyle that they’re learning, they have to learn to adjust their entire life for it. And many patients don’t know what to ask because they don’t know what they don’t know. So, I think it’s important to at least have a solid basis of information about your disease, your cancer diagnosis, so you know what to ask. There are so many variables in cancer, from not only the diagnoses, but how we treat it to what the prognosis is, and that’s always evolving (so) that it’s hard for providers to keep up with that, let alone patients. Advertisement What sorts of questions should patients be prioritizing, especially if they are early on in the experience? ‘What is their current diagnoses?’ specifically, so that they understand their diagnoses. Quite honestly, they hear the words and they don’t understand what those words mean; if they see myeloproliferative neoplasms, that’s all they might look up and not know their specific diagnoses (or) that there are different types underneath there. As we well know, there are so many different hematological malignancies. And when you say the word leukemia, there are 200 different types of leukemia. So, you have to know exactly what you have. And what does that mean to you? What does that mean, as far as prognosis? What can I expect now? And what can I expect in the future? So they can adjust their life. Because if anything, after a world pandemic has happened, we realize we can’t always predict the future and we have to enjoy what we have to the best (of our) abilities. So, does this mean I have to quit my job? Does this mean I need to adjust my family lifestyle? Should I move to where I have family and support? Will I be OK here on my own? I think those are the questions that they need to ask: how is it going to impact them personally now and in the future so they can prepare? What are some specific challenges or roadblocks related to MPNs that make it a particularly disease type for patients to inform themselves on? Not always but usually, most of these diagnoses are based in an elderly population. So, with the myelofibrosis and the polycythemia vera, you’re usually looking around the 60s or 70s age group. And for a lot of these patients, they don’t always have the best support, so they don’t always know how to go to Dr. Google and look everything up. They don’t always know what the latest clinical trials are, they don’t always know how to ask those questions. And they aren’t always surrounded by family members, their children are grown, they have their own lives. So, they don’t always have that support that others would have. Sometimes they’re on their own, and they don’t have transportation. They’re wondering about the basics: economics, transportation, those kinds of things. So that’s how it affects them. And those can be some of the obstacles going forward for these patients in obtaining information. And then (for) some of these patients, some are working, some aren’t some are active and family, some aren’t. Some are socially active. And I also think in an elderly population, what are some of the symptoms, when you look at a patient and they go, ‘Well, yes, I’m tired. Yes, I have bone pain, but I’m 80. How do I know that this is disease related?’ So, I think those are also some of the obstacles. Whereas if you’re 20 or 30 years old, and you’re saying, ‘Wow, I have a lot of bone pain, I have a lot of fatigue, I have memory loss,’ that’s going to seem unusual at that age versus if you’re older, a lot of times you just take it as the age and the sands of time moving forward. First, is this actual disease might be progressing. Say there is a patient who is kind