1,721,004 research outputs found
Venous thromboembolism and heparin use in COVID-19 patients: juggling between pragmatic choices, suggestions of medical societies
Full text linkThe disease caused by coronavirus SARS-CoV-2, named COVID-19, has become a global emergency. The virus spreads via respiratory droplets and is mainly responsible for infections of the respiratory airways, with potentially fatal pneumonia. Although mortality is higher in elderly frail patients presenting with comorbidities, cases of deaths have been reported also in younger age groups. Physicians treating patients with COVID-19 are facing novel and unexpected challenges. One of these is the proper prevention and diagnosis of venous thromboembolism (VTE) and, more generally, how to deal with coagulative activation apparently existing in these patients. In this article, we discuss the many doubts currently existing on the use of heparins and the correct prevention and diagnosis of VTE in COVID-19 patients, with physicians that juggle between pragmatic choices, different suggestions being released on a daily by hospital and medical societies, and the lack of solid evidence or guidelines. Finally, we highlight the need for a call to action by the medical and scientific community
Prophylaxis against venous thromboembolism in patients with cancer
No full textProphylaxis against venous thromboembolism in patients with cancer
Prevalence of pulmonary embolism on hospital admission in COVID-19 patients: is there a role for pre-test probability scores and home treatment?
No full text: Further confirmation that COVID-19 patients are at high risk of venous thromboembolism https://bit.ly/2OfPR5
Polycythemia vera.
No full textThe diagnostic approach to a patient with polycythemia has been greatly simplified by the introduction of new genetic testing in addition to traditional tests, such as measurement of red cell mass and serum erythropoietin (Epo) level. Clonal erythrocytosis, which is the diagnostic feature of polycythemia vera (PV), is almost always associated with a JAK2 mutation (JAK2V617F or exon 12). Therefore, in a patient with acquired erythrocytosis, it is reasonable to begin the diagnostic work-up with JAK2 mutation analysis to distinguish PV from secondary erythrocytosis. The clinical course of PV is marked by a high incidence of thrombotic complications that represent the main cause of morbidity and mortality in these patients. Blood hyperviscosity as well as platelet and leukocyte quantitative, and qualitative abnormalities play a major role in the pathogenesis of thrombophilia. Prevention of vascular events and minimizing the risk of disease transition into acute leukaemia are the main targets of the whole PV treatment strategy. This can rely on the use of low-dose aspirin in most patients, while the choice of the optimal cytoreductive strategy is based on the individual vascular risk. Phlebotomy is still the preferred treatment in subjects at low risk, while hydroxyurea or pipobroman is usually administered to most elderly subjects or subjects with a previous vascular history. The use of pegylated interferon, imatinib, and JAK2 inhibitors is currently being evaluated
Controversies in venous thromboembolism: the unique case of isolated distal deep vein thrombosis
No full textVenous thromboembolism (VTE) represents the third leading cause of cardiovascular mortality, and it is the main cause of preventable mortality in hospitalized patients. Among VTE, there is the unique case of isolated distal deep vein thrombosis (IDDVT), which still lacks an agreement in terms of optimal therapeutic strategy. Although most IDDVTs are self-limiting and associated with a very low risk of embolic complications, still not all IDDVTs can be safely identified as stable. Lack of strong scientific evidence, fear of thromboembolic complications, and risk of bleeding upon initiation of anticoagulant treatment result in very heterogeneous therapeutic strategies among physicians. Here, we provide a comprehensive review of the literature, highlight the many controversial issues regarding IDDVTs, and call for a consensus of experts aimed to shed new light on the gray areas of IDDVT management and therapy
Clinical Correlates of In-Hospital Mortality in Patients Undergoing Inferior Vena Cava Filter Placement for Acute Deep Vein Thrombosis
Full text linkBackground: It is reasonable to place an Inferior Vena Cava Filter (IVCF) when an acute deep vein thrombosis (DVT) of the lower limbs occurs in a patient with absolute contraindication to therapeutic anticoagulation. An additional potential reason for placing an IVCF is the need to stop therapeutic anticoagulation in a patient with acute DVT who must undergo urgent non-deferrable surgery. However, IVCFs are often used outside of such established indications and many authors argue about their actual utility, especially in terms of survival. In this retrospective study, we looked for clinical correlates of in-hospital mortality among patients who underwent IVCF placement, limiting our analysis to the cases for which a correct indication to IVCF placement existed. Methods: We retrospectively analyzed the electronic database of our University Hospital, searching for consecutive hospitalized patients who had acute DVT and underwent IVCF placement because of an established contraindication to therapeutic anticoagulation and/or because it was necessary to stop anticoagulation due to urgent surgery. The search covered the period between 1 January 2010 and 31 December 2020. Results: The search resulted in the identification of 168 individuals. An established contraindication to therapeutic anticoagulation was present in 116 patients (69.0%), while urgent non-deferrable surgery was the reason for IVCF placement in 52 patients (31.0%). A total of 24 patients (14.3%) died during the same hospital stay in which the IVCF was placed. Mortality rate was significantly higher in patients with a contraindication to anticoagulation than in patients who underwent IVCF placement because of urgent surgery (19.0% vs. 3.8%, OD 5.85 vs. 0.17). In-hospital mortality was also significantly higher among patients with chronic kidney disease and those who needed blood cell transfusion during hospitalization. Conclusions: This study provides novel information on clinical correlates of in-hospital mortality among patients with acute DVT who undergo IVCF. Prospective observational studies are needed to substantiate these findings
Factor V Leiden, prothrombin, MTHFR, and PAI-1 gene polymorphisms in patients with arterial disease. A comprehensive systematic-review and meta-analysis
Full text linkIntroduction: The role of inherited thrombophilia in arterial disease is uncertain. We performed a systematic review and meta-analysis of inherited thrombophilia in cerebrovascular (CVD), coronary heart (CHD), and peripheral artery disease (PAD) patients.Materials and methods: MEDLINE and EMBASE were searched up to February 2022. Pooled prevalences (PPs) and odds ratios (ORs) with 95 % confidence intervals (95%CI) were calculated in a random-effects model. Factor V Leiden (G1691A), prothrombin (G20210A), MTHFR C677T/A1298C and PAI-1 4G/5G were evaluated.Results: 377 studies for 98,186 patients (32,791 CVD, 62,266 CHD, 3129 PAD) and 108,569 controls were included. Overall, 37,249 patients had G1691A, 32,254 G20210A, 42,546 MTHFR C677T, 8889 MTHFR A1298C, and 19,861 PAI-1 4G/5G gene polymorphisms. In CVD patients, PPs were 6.5 % for G1691A, 3.9 % for G20210A, 56.4 % for MTHFR C677T, 51.9 % for MTHFR A1298C, and 77.6 % for PAI-1. In CHD, corresponding PPs were 7.2 %, 3.8 %, 52.3 %, 53.9 %, and 76.4 %. In PAD, PPs were 6.9 %, 4.7 %, 55.1 %, 52.1 %, and 75.0 %, respectively. Strongest ORs in CVD were for homozygous G1691A (2.76; 95 %CI, 1.83-4.18) and for homozygous G20210A (3.96; 95 %CI, 2.05-7.64). Strongest ORs in CHD were for homozygous G1691A (OR 1.68; 95%CI, 1.02-2.77) and G20210A (heterozygous 1.49 95%CI, 1.22-1.82; homozygous 1.54 95%CI, 0.79-2.99). The OR for PAI-1 4G/4G in PAD was 5.44 (95%CI, 1.80-16.43). Specific subgroups with higher PPs and ORs were identified according to age and region. Conclusions: Patients with arterial disease have an increased prevalence and odds of having some inherited thrombophilia. Some thrombophilia testing may be considered in specific subgroups of patients
Gut dysbiosis-related thrombosis in inflammatory bowel disease: Potential disease mechanisms and emerging therapeutic strategies
Full text linkPatients with inflammatory bowel disease (IBD) have an increased risk of developing venous thromboembolic events, which have a considerable impact on morbidity and mortality. Chronic inflammation plays a crucial role in the pathogenesis of thrombotic events in patients with IBD. However, many unresolved questions remain, particularly regarding the mechanisms that determine the persistent inflammatory state independent of disease activity. This review explored the role of gut microbiota dysbiosis and intestinal barrier dysfunction, which are considered distinctive features of IBD, in determining pro-thrombotic tendencies. Gut-derived endotoxemia due to the translocation of bacterial lipopolysaccharides (LPS) from the intestine to the bloodstream and the bacterial metabolite trimethylamine-N-oxide (TMAO) are the most important molecules involved in gut dysbiosis-related thrombosis. The pathogenic prothrombotic pathways linked to LPS and TMAO have been discussed. Finally, we present emerging therapeutic approaches that can help reduce LPS-mediated endotoxemia and TMAO, such as restoring intestinal eubiosis, normalizing intestinal barrier function, and counterbalancing the effects of LPS and TMAO
Major Bleeding Risk Assessment in Patients with Cancer-Associated Venous Thromboembolism Treated with DOACs: Data from a Multicenter Cohort
No full textIn cancer-associated venous thromboembolism (CAT), extended anticoagulation should be considered when the risk-benefit profile is favorable. However, optimal predictors of major bleeding (MB) remain unclear.This multicenter observational study included CAT patients treated with direct oral anticoagulants (DOACs). Study objectives were: (i) assess the performance of nine bleeding risk scores (ATRIA, CAT-BLEED, CHAP, DOAC, HAS-BLED, Kuijer, ORBIT, RIETE, VTE-BLEED), (ii) identify predictors of MB (ISTH definition), and (iii) propose an improved bleeding risk model (Perform score).Overall, 823 patients were followed (mean 1.6 years). MB occurred in 44 cases (3.4% per patient-year). The predictive performance of bleeding risk scores was modest (c-statistics range 0.513-0.606). Risk factors included increasing age (HR 1.04, 95% CI 1.00-1.07), use of steroids (HR 2.69, 95% CI 1.34-5.40), antimetabolites (HR 2.51, 95% CI 1.28-4.93), and unresected gastrointestinal cancer (HR 7.30, 95% CI 1.70-31.30). Conversely, prior cancer surgery (HR 0.41, 95% CI 0.20-0.82) and anticancer hormones (HR 0.22, 95% CI 0.05-0.92) showed a possible protective effect toward MB risk. The Perform score provided a slight enhancement in risk prediction (c-statistics 0.678), but remained suboptimal.In this real-world cohort of CAT patients treated with DOACs, unresected gastrointestinal cancer and use of steroids or antimetabolites were associated with increased MB risk, while prior cancer surgery and anticancer hormones were linked to a lower risk. These factors, not considered in current bleeding risk scores, may refine bleeding prediction. Further studies should clarify their role in guiding anticoagulation decisions and improving personalized risk assessment
Reversible coronary microvascular dysfunction: a common pathogenetic mechanism in Apical Ballooning or Tako-Tsubo Syndrome
No full textAims To study coronary microvascular dysfunction as possible pathogenetic mechanism in Apical Ballooning Syndrome (ABS). Methods and results Fifteen ABS patients (all women, 68 +/- 14 years) underwent myocardial contrast echocardiography at baseline during adenosine infusion (140 microg/kg/min) and at 1-month follow-up and compared with a group of anterior ST-elevation myocardial infarction (STEMI) patients with similar clinical characteristics. Myocardial perfusion was assessed by contrast score index (CSI) and endocardial length of contrast defect (contrast defect length, CDL), whereas myocardial dysfunction by wall motion score index (WMSI), endocardial length of contractile dysfunction (wall motion defect length, WMDL), and LV ejection fraction (LVEF). At baseline, no difference in myocardial perfusion and dysfunction were present between the two groups. During adenosine challenge, while no changes were observed in STEMI group, in ABS patients CSI, CDL, WMSI, and WMDL significantly decreased compared with baseline (P < 0.001 vs. baseline for all parameters) and LVEF significantly increased (P = 0.01 vs. baseline). At 1-month follow-up, myocardial perfusion and dysfunction completely recovered in ABS patients (P < 0.001 vs. baseline for all parameters), whereas no significant changes were observed in STEMI group. Conclusion Our data strongly suggest that in ABS, irrespectively of its underlying aetiology, acute and reversible coronary microvascular vasoconstriction could represent a common pathophysiological mechanism
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