565 research outputs found

    Socio-Economic Burden of Myocardial Infarction Among Cancer Patients

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    Cancer patients face a higher risk of future myocardial infarction (MI), even after completion of anticancer therapies. MI is a critical source of physical and financial stress in non-cancer patients, but its impacts associated with cancer patients also saddled with the worry (stress) of potential reoccurrence is unknown. Therefore, we aimed to quantify MI's stress and financial burden after surviving cancer and compare to those never diagnosed with cancer. Utilizing cross-sectional national survey data from 2013-2018 derived from publicly available U.S. datasets, the National Health Interview Survey (NHIS), and economic data from the National Inpatient Sample (NIS), we compared the socio-economic outcomes among those with MI by cancer-status. We adjusted for social, demographic, and clinical factors. Overall, 19,504 (10.2%) of the 189,836 NHIS survey responders reported having cancer for more than 1 year. There was an increased prevalence of MI among cancer survivors compared to non-cancer patients (8.8% vs. 3.2%, P0.05). There was no difference in annual residual family income by cancer status; however, 3 lowest deciles of residual income representing 21.1% cancer-survivor with MI had a residual income of <$9,000. Myocardial infarction continues to represent an immense source of financial and perceived stress. In conclusion, although cancer patients face a higher risk of subsequent MI, this does not appear to advance their reported stress significantly

    Percutaneous coronary intervention and in-hospital outcomes in patients with leukemia: a nationwide analysis

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    Objectives: To examine the association between current leukemia diagnosis and in-hospital clinical outcomes in patients undergoing percutaneous coronary intervention (PCI) in the US. Background: Leukemia is most common hematological malignancy and is associated with an increased risk of thrombotic and bleeding complications in patients undergoing PCI. There are limited data around clinical outcomes of leukemia patients undergoing PCI. Methods: We used the National Inpatient Sample (NIS) to investigate the outcomes of leukemia patients undergoing PCI between 2004 and 2014. Patients were then subdivided into diagnoses of acute or chronic myeloid leukemia (AML or CML) and acute or chronic lymphoid leukemia (ALL, CLL). Multiple logistic regressions were used to study the association of a leukemia diagnosis with in-hospital outcomes; mortality, bleeding, vascular and cardiac complications, and stroke. Results: There were 6,561,445 records of patients who underwent PCI during the study time, of which 15,789 patients had a diagnosis of leukemia. The most common leukemia subtype was CLL accounting for 75% of the cohort (n=10,800). After multivariable adjustment, a leukemia diagnosis was associated with significantly increased odds of in-hospital mortality (OR 1.41 (95% CI (1.11-1.79)) and bleeding (OR 1.87 (95% CI 1.56-2.09)), whereas patients with AML had a 5-fold increase of in-hospital mortality (OR 5.38 (95% CI 2.94-9.76)). Conclusion: Patients with current diagnosis of leukemia are at increased risk of procedurerelated complications following PCI. A multi-disciplinary approach is needed amongst interventional cardiologists, oncologists and hematologists to minimize procedural complications and improve outcomes in this high-risk cohort

    Brevenal Inhibits Pacific Ciguatoxin-1B-Induced Neurosecretion from Bovine Chromaffin Cells

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    Ciguatoxins and brevetoxins are neurotoxic cyclic polyether compounds produced by dinoflagellates, which are responsible for ciguatera and neurotoxic shellfish poisoning (NSP) respectively. Recently, brevenal, a natural compound was found to specifically inhibit brevetoxin action and to have a beneficial effect in NSP. Considering that brevetoxin and ciguatoxin specifically activate voltage-sensitive Na+ channels through the same binding site, brevenal has therefore a good potential for the treatment of ciguatera. Pacific ciguatoxin-1B (P-CTX-1B) activates voltage-sensitive Na+ channels and promotes an increase in neurotransmitter release believed to underpin the symptoms associated with ciguatera. However, the mechanism through which slow Na+ influx promotes neurosecretion is not fully understood. In the present study, we used chromaffin cells as a model to reconstitute the sequence of events culminating in ciguatoxin-evoked neurosecretion. We show that P-CTX-1B induces a tetrodotoxin-sensitive rise in intracellular Na+, closely followed by an increase in cytosolic Ca2+ responsible for promoting SNARE-dependent catecholamine secretion. Our results reveal that brevenal and β-naphtoyl-brevetoxin prevent P-CTX-1B secretagogue activity without affecting nicotine or barium-induced catecholamine secretion. Brevenal is therefore a potent inhibitor of ciguatoxin-induced neurotoxic effect and a potential treatment for ciguatera

    Management Strategies and Clinical Outcomes of Acute Myocardial Infarction in Leukemia Patients: Insights from Nationwide United States Hospitalizations.

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    BACKGROUND: Patients with leukemia are at increased risk of cardiovascular events. There are limited outcomes data for patients with a history of leukemia who present with an acute myocardial infarction (AMI). METHODS: We queried the Nationwide Inpatient Sample (2004-2014) for patients with a primary discharge diagnosis of AMI, and a concomitant diagnosis of leukemia, and further stratified according to the subtype of leukemia. Multivariable logistic regression was conducted to identify the association between leukemia and major acute cardiovascular and cerebrovascular events (MACCE; composite of mortality, stroke and cardiac complications) and bleeding. RESULTS: Out of 6,750,878 AMI admissions, a total of 21,694 patients had a leukemia diagnosis. The leukemia group experienced higher rates of MACCE (11.8% vs. 7.8%), mortality (10.3% vs. 5.8%) and bleeding (5.6% vs. 5.3%). Following adjustments, leukemia was independently associated with increased odds of MACCE (OR 1.26[1.20,1.31]) and mortality (OR 1.43[1.37,1.50]) without an increased risk of bleeding (OR 0.86[0.81,0.92]). Acute myeloid leukemia (AML) was associated with approximately three-fold risk of MACCE (OR 2.81[2.51, 3.13]) and a four-fold risk of mortality (OR 3.75[3.34, 4.22]). Patients with leukemia were less likely to undergo coronary angiography (CA) (48.5% vs. 64.5%) and percutaneous coronary intervention (PCI) (28.2% vs. 42.9%) compared to those without leukemia. CONCLUSION: Patients with leukemia, especially those with AML, are associated with poor clinical outcomes after AMI, and are less likely to receive CA and PCI compared to those without leukemia. A multi-disciplinary approach between cardiologists and hematology oncologists may improve the outcomes of patients with leukemia after AMI

    Coronary stent healing in cancer patients: an optical coherence tomography perspective

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    Objective: This study assessed stent healing patterns and cardiovascular outcomes by optical coherence tomography (OCT) in cancer patients after drug-eluting stent (DES) placement.Background: Cancer treatment, owing to its cytotoxic and antiproliferative effects, could delay stent healing and increase stent thrombosis risk, especially when dual antiplatelet therapy (DAPT) is discontinued early for oncological treatment. OCT can assess stent endothelialization and other healing parameters, which may provide clinical guidance in these challenging scenarios.Methods: This single-center retrospective study enrolled all cancer patients who underwent OCT for assessment of vascular healing patterns after prior DES placement from November 2009 to November 2018. Primary study endpoints were stent healing parameters, including stent coverage, apposition, degree of expansion, neointimal hyperplasia heterogeneity, in-stent restenosis, stent thrombosis, and overall survival (OS).Results: A total of 67 patients were included in this study. Mean time between DES placement and OCT evaluation was 154 +/- 82 days. Stent healing matched published values for DES in non-cancer patients (P >= 0.063). At 1 year, the OS was 86% (95% confidence interval [CI]: 78-96%) with 0% incidence of acute coronary syndrome. Advanced cancers and active chemotherapies were associated with inferior OS (P = 0.024, hazard ratio [HR]: 3.50, 95% CI: 1.18-10.42 and P = 0.026, HR: 2.65, 95% CI: 1.13-6.22, respectively), while stent healing parameters were unassociated with OS. Forty-one patients (61%) had DAPT duration <= 6 months.Conclusions: Stent healing of contemporary DES appears similar in cancer and non-cancer patients. Cardiovascular risk of cancer patients after DES placement can be managed to facilitate timely cancer therapies, as the underlying malignancy and active chemotherapy ultimately determine survival.Cardiovascular Aspects of Radiolog

    Pulsed radiofrequency treatment in interventional pain management: mechanisms and potential indications—a review

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    Item does not contain fulltextBACKGROUND: The objective of this review is to evaluate the efficacy of Pulsed Radiofrequency (PRF) treatment in chronic pain management in randomized clinical trials (RCTs) and well-designed observational studies. The physics, mechanisms of action, and biological effects are discussed to provide the scientific basis for this promising modality. METHODS: We systematically searched for clinical studies on PRF. We searched the MEDLINE (PubMed) and EMBASE database, using the free text terms: pulsed radiofrequency, radio frequency, radiation, isothermal radiofrequency, and combination of these. We classified the information in two tables, one focusing only on RCTs, and another, containing prospective studies. Date of last electronic search was 30 May 2010. The methodological quality of the presented reports was scored using the original criteria proposed by Jadad et al. FINDINGS: We found six RCTs that evaluated the efficacy of PRF, one against corticosteroid injection, one against sham intervention, and the rest against conventional RF thermocoagulation. Two trials were conducted in patients with lower back pain due to lumbar zygapophyseal joint pain, one in cervical radicular pain, one in lumbosacral radicular pain, one in trigeminal neuralgia, and another in chronic shoulder pain. CONCLUSION: From the available evidence, the use of PRF to the dorsal root ganglion in cervical radicular pain is compelling. With regards to its lumbosacral counterpart, the use of PRF cannot be similarly advocated in view of the methodological quality of the included study. PRF application to the supracapular nerve was found to be as efficacious as intra-articular corticosteroid in patients with chronic shoulder pain. The use of PRF in lumbar facet arthropathy and trigeminal neuralgia was found to be less effective than conventional RF thermocoagulation techniques

    Anti–miR-93-5p therapy prolongs sepsis survival by restoring the peripheral immune response

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    Sepsis remains a leading cause of death for humans and currently has no pathogenesis-specific therapy. Hampered progress is partly due to a lack of insight into deep mechanistic processes. In the past decade, deciphering the functions of small noncoding miRNAs in sepsis pathogenesis became a dynamic research topic. To screen for new miRNA targets for sepsis therapeutics, we used samples for miRNA array analysis of PBMCs from patients with sepsis and control individuals, blood samples from 2 cohorts of patients with sepsis, and multiple animal models: mouse cecum ligation puncture–induced (CLP-induced) sepsis, mouse viral miRNA challenge, and baboon Gram+ and Gram– sepsis models. miR-93-5p met the criteria for a therapeutic target, as it was overexpressed in baboons that died early after induction of sepsis, was downregulated in patients who survived after sepsis, and correlated with negative clinical prognosticators for sepsis. Therapeutically, inhibition of miR-93-5p prolonged the overall survival of mice with CLP-induced sepsis, with a stronger effect in older mice. Mechanistically, anti–miR-93-5p therapy reduced inflammatory monocytes and increased circulating effector memory T cells, especially the CD4+ subset. AGO2 IP in miR-93–KO T cells identified important regulatory receptors, such as CD28, as direct miR-93-5p target genes. In conclusion, miR-93-5p is a potential therapeutic target in sepsis through the regulation of both innate and adaptive immunity, with possibly a greater benefit for elderly patients than for young patients

    Immune Evasion by Yersinia enterocolitica: Differential Targeting of Dendritic Cell Subpopulations In Vivo

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    CD4+ T cells are essential for the control of Yersinia enterocolitica (Ye) infection in mice. Ye can inhibit dendritic cell (DC) antigen uptake and degradation, maturation and subsequently T-cell activation in vitro. Here we investigated the effects of Ye infection on splenic DCs and T-cell proliferation in an experimental mouse infection model. We found that OVA-specific CD4+ T cells had a reduced potential to proliferate when stimulated with OVA after infection with Ye compared to control mice. Additionally, proliferation of OVA-specific CD4+ T cells was markedly reduced when cultured with splenic CD8α+ DCs from Ye infected mice in the presence of OVA. In contrast, T-cell proliferation was not impaired in cultures with CD4+ or CD4−CD8α− DCs isolated from Ye infected mice. However, OVA uptake and degradation as well as cytokine production were impaired in CD8α+ DCs, but not in CD4+ and CD4−CD8α− DCs after Ye infection. Pathogenicity factors (Yops) from Ye were most frequently injected into CD8α+ DCs, resulting in less MHC class II and CD86 expression than on non-injected CD8α+ DCs. Three days post infection with Ye the number of splenic CD8α+ and CD4+ DCs was reduced by 50% and 90%, respectively. The decreased number of DC subsets, which was dependent on TLR4 and TRIF signaling, was the result of a faster proliferation and suppressed de novo DC generation. Together, we show that Ye infection negatively regulates the stimulatory capacity of some but not all splenic DC subpopulations in vivo. This leads to differential antigen uptake and degradation, cytokine production, cell loss, and cell death rates in various DC subpopulations. The data suggest that these effects might be caused directly by injection of Yops into DCs and indirectly by affecting the homeostasis of CD4+ and CD8α+ DCs. These events may contribute to reduced T-cell proliferation and immune evasion of Ye
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