Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Venous thromboembolism (VTE), which consists of deep vein thrombosis (DVT) and pulmonary embolism, is a potentially fatal disease. The existing Asian literature has shown a wide variation in the prevalence of VTE, with very limited data from India. In the present study, the risk factors for VTE in Indian patients were compared with Caucasians and Blacks. We used data prospectively collected from total of 1396 Indian patients (716 males, 680 females) enrolled over a decade and compared with White (n = 2002) and Black (n = 395) patients objectively diagnosed with VTE. When compared with females, males had significantly higher episodes of pulmonary embolism and VTE (P = 0.0001). Amongst the known thrombophilia markers, only homocysteine was found to be significantly higher in males as compared with females (P = 0.006). Males had a higher proportion of rheumatic heart disease (RHD) and ischaemic heart disease (IHD) as compared with females. The prevalence of DVT amongst Indians was significantly higher as compared with Whites and Blacks. However, the rate of pulmonary embolism and VTE was lower in Indians as compared with both the races. Amongst the baseline characteristics identified as risk factors for VTE, Indians had a higher prevalence of infection as compared to both Whites and Blacks, but lower HIV infection as compared to Blacks. As compared to Whites, Indians had lower prevalence of idiopathic VTE (but similar to blacks) and had higher prevalence of idiopathic pulmonary embolism (P < 0.0001). This can be explained by different inherited and environment risk factors between these three populations.
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PMID:Cause of deep venous thrombosis and pulmonary embolism in young patients from India as compared with other ethnic groups. 2249 80

Neutrophil extracellular traps (NETs) contribute to innate immunity as well as numerous diseases processes such as deep vein thrombosis, myocardial ischemia, and autoimmune disease. To date, most knowledge on NETs formation has been gathered via the qualitative microscopic examination of individual neutrophils in vitro, or aggregate structures in vivo. Here we describe a novel flow cytometry (FLOW)-based assay to identify and quantify NETs using antibodies against key NETs constituents, specifically DNA, modified histones, and granular enzymes. This method is applicable to both murine and human samples for the assessment of induced NETs in vitro, or detection of NETosis in vivo in blood samples. This FLOW-based method was validated by comparison with the well-established microscopy assay using two genetic mouse models previously demonstrated to show defective NETosis. It was then used on healthy human neutrophils for detection of ex vivo induced NETs and on blood samples from patients with sepsis for direct assessment of in vivo NET-forming neutrophils. This new methodology allows rapid and robust assessment of several thousand cells per sample and is independent of potential observer-bias, the two main limitations of the microscopic quantification. Using this new technology facilitates the direct detection of in vivo circulating NETs in blood samples and purification of NETting neutrophils by fluorescence-activated cell sorting (FACS) for further analysis.
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PMID:Flow cytometric assay for direct quantification of neutrophil extracellular traps in blood samples. 2674 59

The paper proposes a pathophysiologic framework to explain the well-established epidemiological association between exposure to ambient air particle pollution and premature cardiovascular mortality, and offers insights into public health solutions that extend beyond regulatory environmental protections to actions that can be taken by individuals, public health officials, healthcare professionals, city and regional planners, local and state governmental officials and all those who possess the capacity to improve cardiovascular health within the population. The foundation of the framework rests on the contribution of traditional cardiovascular risk factors acting alone and in concert with long-term exposures to air pollutants to create a conditional susceptibility for clinical vascular events, such as myocardial ischemia and infarction; stroke and lethal ventricular arrhythmias. The conceptual framework focuses on the fact that short-term exposures to ambient air particulate matter (PM) are associated with vascular thrombosis (acute coronary syndrome, stroke, deep venous thrombosis, and pulmonary embolism) and electrical dysfunction (ventricular arrhythmia); and that individuals having prevalent heart disease are at greatest risk. Moreover, exposure is concomitant with changes in autonomic nervous system balance, systemic inflammation, and prothrombotic/anti-thrombotic and profibrinolytic-antifibrinolytic balance. Thus, a comprehensive solution to the problem of premature mortality triggered by air pollutant exposure will require compliance with regulations to control ambient air particle pollution levels, minimize exposures to air pollutants, as well as a concerted effort to decrease the number of people at-risk for serious clinical cardiovascular events triggered by air pollutant exposure by improving the overall state of cardiovascular health in the population. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
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PMID:Proposed pathophysiologic framework to explain some excess cardiovascular death associated with ambient air particle pollution: Insights for public health translation. 2745 57

Diabetes and chronic kidney disease (CKD) are associated with a higher rate of complications in patients undergoing total knee arthroplasty (TKA). The purpose of this study was to determine the effects of CKD and diabetes in patients after TKA. Diabetic patients who received unilateral primary TKA between January 2008 and December 2011 were enrolled. The follow-up period was more than 6 months. The primary outcome was a TKA-related infection and the secondary outcome was all-cause mortality. The study cohort included 13844 patients who were followed for a mean period of 2 years, of whom 1459 (10.5%) had CKD. The patients with CKD were older than those without CKD (71.6 versus 70.3 years, P<0.0001) and had higher rates of hypertension, gouty arthritis, ischemic heart disease, chronic pulmonary obstructive disease, pulmonary embolism and deep vein thrombosis (all P<0.0001). After adjustment of comorbidities, the CKD group had a higher incidence of urinary tract infections (OR: 1.61, 95% CI: 1.19-2.17). There were no significant differences in wound infections, pneumonia, pulmonary embolism or in-hospital death between the two groups. After adjustment of confounders, the CKD group had higher rates of myocardial infarction (HR: 2.06, 95% CI: 1.26-3.39) and mortality (HR: 1.99, 95% CI: 1.59-2.48). The risk of TKA-related infection during follow-up was comparable between the two groups (HR: 1.31, 95% CI: 0.94-1.82). In conclusion, CKD is associated with increased risks of urinary tract infections, myocardial infarction and all-cause mortality after TKA. Surgeons should be aware of this when evaluating TKA patients with renal disease.
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PMID:Chronic kidney disease is associated with a risk of higher mortality following total knee arthroplasty in diabetic patients: a nationwide population-based study. 2924 78

Ca2+ entry via Orai1 store-operated Ca2+ channels in the plasma membrane is critical to cell function, and Orai1 loss causes severe immunodeficiency and developmental defects. The tetraspanins are a superfamily of transmembrane proteins that interact with specific 'partner proteins' and regulate their trafficking and clustering. The aim of this study was to functionally characterize tetraspanin Tspan18. We show that Tspan18 is expressed by endothelial cells at several-fold higher levels than most other cell types analyzed. Tspan18-knockdown primary human umbilical vein endothelial cells have 55-70% decreased Ca2+ mobilization upon stimulation with the inflammatory mediators thrombin or histamine, similar to Orai1-knockdown. Tspan18 interacts with Orai1, and Orai1 cell surface localization is reduced by 70% in Tspan18-knockdown endothelial cells. Tspan18 overexpression in lymphocyte model cell lines induces 20-fold activation of Ca2+ -responsive nuclear factor of activated T cell (NFAT) signaling, in an Orai1-dependent manner. Tspan18-knockout mice are viable. They lose on average 6-fold more blood in a tail-bleed assay. This is due to Tspan18 deficiency in non-hematopoietic cells, as assessed using chimeric mice. Tspan18-knockout mice have 60% reduced thrombus size in a deep vein thrombosis model, and 50% reduced platelet deposition in the microcirculation following myocardial ischemia-reperfusion injury. Histamine- or thrombin-induced von Willebrand factor release from endothelial cells is reduced by 90% following Tspan18-knockdown, and histamine-induced increase of plasma von Willebrand factor is reduced by 45% in Tspan18-knockout mice. These findings identify Tspan18 as a novel regulator of endothelial cell Orai1/Ca2+ signaling and von Willebrand factor release in response to inflammatory stimuli.
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PMID:Tspan18 is a novel regulator of the Ca2+ channel Orai1 and von Willebrand factor release in endothelial cells. 3057 9

Fondaparinux is a synthetic heparin pentasaccharide with a sequence identical to that found in anticoagulant heparin. It is a pure compound with a molecular weight of 1728Da. Fondaparinux catalyzes the conformational change of a serpin or serine protease inhibitor antithrombin III to accelerate the suicidal inactivation of factor Xa over 340-fold, which in turn inhibits thrombin generation in the coagulating signal transduction pathway. Fondaparinux does not inhibit thrombin activity, release tissue factor pathway inhibitor, or possess other properties of heparin such as anti-inflammatory, anti-viral, anti-angiogenesis, anti-neoplastic, and anti-metastatic effects though high affinity interactions with a variety of proteases, protease inhibitors, chemokines, cytokines, growth factors, and their respective receptors. Low antithrombin III levels in blood circulation also affects the efficacy of Fondaparinux. Thus, Fondaparinux represents a refined use of the anti-factor Xa property of heparin. As an anti-factor Xa drug, Fondaparinux has complete bioavailability subcutaneously, instant onset of action, a half-life of 15-20h, and a direct renal excretion without any metabolism. Fondaparinux has been shown to be superior to low molecular weight heparin in preventing deep vein thrombosis. Clinically, Fondaparinux is used for the prevention of deep vein thrombosis in patients who have had orthopedic surgery as well as for the treatment of deep vein thrombosis and pulmonary embolism with limitations of use in elderly, low weight, renal impaired patients and in those receiving spinal anesthesia. Clinical studies showed that Fondaparinux acts in prevention and treatment of venous thromboembolism and in ischemic heart disease without significant risk of bleeding.
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PMID:The clinical use of Fondaparinux: A synthetic heparin pentasaccharide. 3103 Jul 56

Chemotherapy, alone or in association with radiation therapy, has represented the cornerstone of cancer treatment for decades. However, in the last several years, an unprecedented progress in the understanding of cancer biology and the discovery of novel therapeutic targets have led to a paradigm shift in the management of patients with neoplastic diseases. The introduction of tyrosine kinase inhibitors, vascular endothelial growth factor pathway inhibitors, immunomodulatory agents, proteasome inhibitors, immune checkpoint inhibitors, and chimeric antigen receptor T cells, among others, has been associated with prolonged survival in many forms of cancer. A common feature of both chemotherapy and novel cancer treatments is the frequent occurrence of vascular toxicity, mainly mediated by injury to the endothelium. While the mechanisms may vary between agents, the clinical manifestations may overlap and range from hypertension, vasospastic and thrombotic arterial events (myocardial ischemia and infarction, peripheral ischemia, and limb gangrene), venous thromboembolism (deep vein thrombosis and pulmonary embolism) to capillary leak syndrome. Therefore, the effective management of patients with cancer requires a multidisciplinary team approach in which oncologist and cardiovascular medicine specialists work together to prevent, detect, and minimize acute vascular toxicity and long-term consequences of cancer therapy.
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PMID:Vascular effects of cancer treatments. 3253 32

Phlegmasia cerulea dolens is a severe form of deep venous thrombosis (DVT) characterized by severe venous outflow obstruction, marked limb swelling, pain, bluish discoloration, and even venous gangrene if the condition is untreated. In our case, 75-year-old woman, with general abdominal pain, which increases with eating and anorexia and 5 days of coldness and swelling of the left leg, was accepted. The patient had a history of Type II diabetes, ischemic heart disease, congestive heart failure, hyperlipidemic (HLP), hypertension, metastatic ovarian cancer, and previous DVT. She has undergone chemotherapy for the past 3 weeks due to ovarian cancers. Anticoagulation with intravenous administration of heparin and fluid resuscitation started immediately. The evidence of color Doppler sonography approved acute DVT in common femoral vein extending to the left external iliac. The patient did not consent for continuing the procedure in the hospital and succumbed to her illness on the 7th day after discharge.
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PMID:Phlegmasia Cerulea Dolens: A Rare Case Report. 3307 43

(1) Aim: The aim of this study was to assess the preferences of oral anticoagulants (OA) in patients diagnosed with deep vein thrombosis (DVT) of lower limbs or non-valvular atrial fibrillation (AF) requiring anticoagulation for medium/long term. (2) Materials and methods: the study included consecutive patients admitted with a diagnosis of either acute DVT of lower limbs (without signs of pulmonary embolism) or non-valvular AF who required oral anticoagulation, in a time frame of 18 months from January 2017 until June 2018. The following data were recorded: demographic variables, comorbidities (ischemic heart disease, arterial hypertension, heart failure, stroke, peripheral artery disease, diabetes mellitus, obesity), type and dose of OA (acenocoumarol, dabigatran, apixaban, rivaroxaban), complications due to the use of OA. (3) Results: AF patients were older and had considerably more cardiovascular comorbidities than DVT patients. Vitamin K antagonists (VKA) were more likely to be administered in patients with AF, as they had indication for indefinite anticoagulation. VKA were more frequently prescribed in patients with ischemic heart disease, heart failure, and diabetes compared with DVT patients. Moreover, complications related to OA use were more frequent in the VKA group. Almost half of patients with acute DVT (48.5%) were treated with direct OA (DOAC) rather than VKA, and only a quarter of AF patients (24.8%) were treated with DOACs.
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PMID:Oral Anticoagulants Preference in Hospitalized Patients with Acute Deep Vein Thrombosis or Non-Valvular Atrial Fibrillation. 3307 9


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