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Due to their very wide range of indications, anticoagulants are one of the most commonly used drug groups. Although these drugs are characterized by different mechanisms of action, the most common complication of their use is still bleeding episodes, the frequency of which depends largely on the clinical condition of the patient using such therapy. For this reason, to this day, the best method of preventing bleeding complications remains the assessment of bleeding risk using scales such as HAS-BLED. There are many reports in the literature assessing the occurrence of this type of complication after the use of drugs affecting the coagulation process, as well as many reports comparing individual groups of drugs with different mechanisms of action. However, there are still no clear guidelines that would indicate which group of anticoagulants should be preferred in particular groups of patients. The aim of our article is to summarize the data collected so far regarding the safety of using specific groups of anticoagulants and the frequency of bleeding complications after their use. [ABSTRACT FROM AUTHOR]

Abstract Background Anticoagulation is recommended as a standardized therapy for COVID-19 patients according to the WHO guidelines. However, bleeding events have also been reported. Hemorrhage or hematoma was observed in sites including the retroperitoneum, brain, alimentary tract, muscles, and soft tissues. Reduction or suspension of anticoagulants is a common intervention. Transfusion, endoscopic hemostasis, and vascular interventional therapy have been used to improve the condition. Case presentation In this article, we present two cases of concurrent multisite hematomas and bleeding at other sites in patients with SARS-CoV-2 infection. Both patients were treated with heparins and experienced bleeding after the anticoagulation therapy. Both patients were older with more than two comorbidities, and critical COVID-19. Laboratory tests revealed a considerable decrease in hemoglobin levels and alterations in the coagulation system. In the first patient, the main intervention was embolization using angiography. However, we only adjusted the anticoagulation strategy in the second case. The first patient recovered and was discharged; however, the second died of other causes. This study provides a retrospective review of typical hemorrhagic cases during anticoagulation in COVID-19 patients over the course of four years. A relatively comprehensive search was performed in Pubmed by constructing MeSH subject terms on limiting the search period and specific contents. It summarizes and synthesizes the research related to heparins and other novel anticoagulants in the context of COVID-19 from the onset of the pandemic to the present disseminated phase. This study aimed to offer valuable insights and reference points for developing anticoagulation treatment strategies for patients with COVID-19. Conclusions Anticoagulation is a crucial treatment option for patients with COVID-19. The difference in anticoagulant effects is related to the severity of COVID-19. Nafamostat can reduce thrombosis in the extracorporeal circuits in critically ill patients with COVID-19. The efficacy and safety of novel anticoagulants require further clinical data. Routine bedside assessments and real-time laboratory monitoring are essential for early identification of bleeding events during anticoagulant therapy and administering intervention.

Due to their very wide range of indications, anticoagulants are one of the most commonly used drug groups. Although these drugs are characterized by different mechanisms of action, the most common complication of their use is still bleeding episodes, the frequency of which depends largely on the clinical condition of the patient using such therapy. For this reason, to this day, the best method of preventing bleeding complications remains the assessment of bleeding risk using scales such as HAS-BLED. There are many reports in the literature assessing the occurrence of this type of complication after the use of drugs affecting the coagulation process, as well as many reports comparing individual groups of drugs with different mechanisms of action. However, there are still no clear guidelines that would indicate which group of anticoagulants should be preferred in particular groups of patients. The aim of our article is to summarize the data collected so far regarding the safety of using specific groups of anticoagulants and the frequency of bleeding complications after their use.

Novel coronavirus 2019 (COVID-19) represents a significant risk factor for the development of venous thromboembolism (VTE) in hospitalized with both moderate and severe/critical COVID-19. Herein, we present a brief updated review on emerging robust data on diverse thromboprophylaxis strategies used to mitigate VTE complications, as well as a personal point of view of current controversies in regards the use of therapeutic and prophylactic anticoagulation strategies, particularly in the moderately-ill subgroup of patients with COVID-19. [ABSTRACT FROM AUTHOR]

Thromboembolic events are common in hospitalized patients with COVID-19, suggesting that SARS-CoV-2 infection may be related to a prothrombotic state. Several clinical trials evaluating different anticoagulation strategies were developed. Thus, we proposed conducting a meta-analysis of randomized clinical trials that evaluated the efficacy and safety of therapeutic anticoagulation with heparins in hospitalized patients with COVID-19. We searched PubMed, Cochrane, and Epistemonikos for studies published until December 22, 2022. Nine studies compared prophylactic/intermediate anticoagulation versus therapeutic anticoagulation with heparins were included. Four efficacy and one safety endpoints were analyzed: all-cause mortality, thromboembolic events, pulmonary embolism, need of intensive care unit or non-invasive ventilation, and major bleeding. Compared with prophylactic/intermediate anticoagulation, therapeutic anticoagulation with heparins was not associated with a reduction in all-cause mortality and need of intensive care unit or non-invasive ventilation in hospitalized patients with COVID-19, but showed a reduction in the number of thromboembolic events (RR 0.54, 95% CI 0.41–0.71, I² = 0 %) and pulmonary embolisms (RR 0.37, 95% CI 0.24–0.57, I² = 0 %), besides an increase in major bleeding (RR 1.67, 95% CI 1.05–2.64, I² = 0 %). This meta-analysis did not show a reduction in all-cause mortality in hospitalized patients with COVID-19 who received anticoagulation with heparin at a therapeutic dose compared to those who received a prophylactic/intermediate dose, as well as no significant differences were found in the need of intensive care unit admission or use of non-invasive ventilation. There was, however, a reduction in thromboembolic events, pulmonary embolism, and increased bleeding (Tab. 1, Fig. 5, Ref. 31). [ABSTRACT FROM AUTHOR]

Since severe acute respiratory syndrome coronavirus 2 led to a world pandemic, extensive research has been conducted to identify its characteristics and form an appropriate management plan. One recognized complication of COVID-19 is coagulation defects that can lead to thromboembolic events. We have reviewed the literature to summarize and present the latest research about the pathophysiology, clinical manifestations, anticoagulation use and appropriate dose in COVID-19 patients, as well as the effect of anticoagulation in outpatient and post-hospital settings. The pathophysiology of coagulation abnormalities in COVID-19 is not fully understood yet, but multiple mechanisms appear to be involved, such as a direct viral attack, hyperinflammation, increased immune response, blood stasis, and endothelial injury. Clinical manifestations are mainly venous thromboembolism (deep vein thrombosis and pulmonary embolism), arterial thromboembolism, ischemic stroke, central venous sinus thrombosis, and central retinal vein occlusion. Anticoagulation is widely used in hospitalized patients with COVID-19, unless it is contraindicated. Heparinoid is the main anticoagulant used. However, the appropriate dosage is still debated as research is trying to find a balance between benefits and risks. In outpatients, it appears that anticoagulation has no benefit in contrast to post-hospitalization use, where benefit could be observed in severely affected patients. We concluded that thromboprophylaxis should be used in treating hospitalized COVID-19 patients, but the dosage is still a matter of debate. More research needs to be done on outpatient and post-hospitalized patients to derive accurate conclusions.

Aim: The present study investigated the risk of bleeding when antidepressants are added to antithrombotics. Methods: Using data registered in VigiBase®, the WHO pharmacovigilance database, between 01/01/2000 and 31/12/2022, we compared the risk of reporting "serious" bleeding (Reporting Odds Ratio, ROR) with antidepressants + antithrombotics versus antithrombotics alone. Results: Increased values of ROR were found for the association Serotonin Reuptake Inhibitors (SRIs) + Direct Oral Anticoagulants (DOACs) versus DOACs alone (ROR=1.49(1.17-1.89)). Similar results were found for Factor Xa inhibitors or Thrombin inhibitors. This association was also found for other antithrombotics: Vitamin K Antagonists (ROR=1.37(1.12-1.68)), Platelet Aggregation Inhibitors PAIs (ROR=1.38(1.21-1.57)) and Heparins (2.04(1.59-2.62)) but not with other antidepressants (Non-Selective Monoamine Reuptake Inhibitors, NSMRIs). Conclusion: The present study suggests an increased risk of "serious" bleeding when SRIs (but not NSMRIs) are associated with antithrombotics (all antithrombotics and not only DOACs). [ABSTRACT FROM AUTHOR]

The laboratory diagnosis of antiphospholipid syndrome (APS) requires the measurement of solid-phase antibodies to cardiolipin or β2-Glycoprotein-I and the search for lupus anticoagulant (LA). The diagnosis of patients whilst on anticoagulation is impaired by the difficult interpretation of results, at least for LA, owing to the fact that prolongations of clotting times induced by LA superimpose those induced by anticoagulants. This is a matter of concern as treating physicians very often need to know the APS status of their patients to make a decision on secondary antithrombotic prophylaxis. This article aims to review the effect brought about by anticoagulants on APS diagnosis and discuss the options that can be used to overcome such an effect. [ABSTRACT FROM AUTHOR]

Since severe acute respiratory syndrome coronavirus 2 led to a world pandemic, extensive research has been conducted to identify its characteristics and form an appropriate management plan. One recognized complication of COVID-19 is coagulation defects that can lead to thromboembolic events. We have reviewed the literature to summarize and present the latest research about the pathophysiology, clinical manifestations, anticoagulation use and appropriate dose in COVID-19 patients, as well as the effect of anticoagulation in outpatient and posthospital settings. The pathophysiology of coagulation abnormalities in COVID-19 is not fully understood yet, but multiple mechanisms appear to be involved, such as a direct viral attack, hyperinflammation, increased immune response, blood stasis, and endothelial injury. Clinical manifestations are mainly venous thromboembolism (deep vein thrombosis and pulmonary embolism), arterial thromboembolism, ischemic stroke, central venous sinus thrombosis, and central retinal vein occlusion. Anticoagulation is widely used in hospitalized patients with COVID-19, unless it is contraindicated. Heparinoid is the main anticoagulant used. However, the appropriate dosage is still debated as research is trying to find a balance between benefits and risks. In outpatients, it appears that anticoagulation has no benefit in contrast to post-hospitalization use, where benefit could be observed in severely affected patients. We concluded that thromboprophylaxis should be used in treating hospitalized COVID-19 patients, but the dosage is still a matter of debate. More research needs to be done on outpatient and post-hospitalized patients to derive accurate conclusions. [ABSTRACT FROM AUTHOR]

Copyright of African Journal of Reproductive Health is the property of Women's Health & Action Research Centre and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Critically ill COVID-19 patients are at risk for venous thromboembolism (VTE). Therefore, they receive thromboprophylaxis and, when appropriate, therapeutic unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH). To monitor heparins in COVID-19 disease, whole-blood rotational thromboelastometry (ROTEM) may be a promising alternative to the aPTT and anti-Xa assays. Objective: To evaluate the ROTEM INTEM/HEPTEM ratios in mechanically ventilated COVID-19 patients treated with UFH and therapeutic LMWH. Material and methods: A subcohort of mechanically ventilated COVID-19 patients of the prospective Maastricht Intensive Care Covid (MaastrICCht) cohort was studied. Anti-Xa, aPTT, and ROTEM measurements following treatment with UFH or therapeutic dose of LMWH (nadroparin) were evaluated using uni- and multivariable linear regression analysis and receiver operating characteristics. Results: A total of 98 patients were included, of which 82 were treated with UFH and 16 with therapeutic LMWH. ROTEM-measured INTEM/HEPTEM CT ratio was higher in patients using UFH (1.4 [1.3–1.4]) compared to patients treated with LMWH (1.0 [1.0–1.1], p

Variances in the patients’ outcomes have been a well-documented challenge in anticoagulant therapy. A clinical encounter with a thromboembolic or a hemorrhagic event, due to subtherapeutic or adverse effects of an anticoagulant, is often managed by switching the anticoagulant agent into another, which is more specific and direct-acting. This management approach is usually associated with a financial burden. Additionally, the certainty of achieving better efficacy and safety profile is still questionable. Genetic variants affecting the protein sites that are involved in the anticoagulant pharmacokinetic and pharmacodynamics interactions have been suggested to contribute to the variability in the response to anticoagulant therapy. The current work reviewed the studies investigating the response variability associated with the anticoagulant therapy (heparins, rivaroxaban, apixaban, and dabigatran) and the potential pharmacogenes contributing to such response variability. Several genetic polymorphisms were reported as potential contributors to variances in response to anticoagulant therapy and were associated with adverse events. A link has been proposed for heparin resistance with single nucleotide polymorphisms (SNPs) of the anti-thrombin-encoding gene (SERPINC1) as well as heparin-induced thrombocytopenia with human leukocyte antigen (HLA) variant allele (HLA-DRB3FNx0101:01). Several investigations also remarked variations in the serum drug level of direct oral anticoagulants (DOACs) that are associated with SNPs in the proteins contributing to the pharmacokinetics of the anticoagulant agent. Several studies discerned significant associations between SNPs in the ABCB1 gene and elevations in the serum levels of rivaroxaban, apixaban, and dabigatran. Moreover, carriers of the variant genotype of the SNP (rs776746) in the cytochrome P450 3A5 enzyme-encoding gene (CYP3A5) had significantly higher drug levels when compared with the non-carriers. In contrast, some SNPs were reported to impart a protective phenotype to the carrier. The SNP (rs2244613) in the carboxylesterase-encoding gene (CES1) has been significantly associated with a decline in dabigatran trough levels and a lower risk of hemorrhage. Further investigations are essential to elucidate the extent of pharmacogenetics-based alterations in the drug levels as well as the subsequent clinical outcomes of anticoagulant therapy.

The optimal anticoagulation strategy for venous thromboembolism (VTE) prevention among COVID-19 patients, hospitalized or in the community setting, is still challenging and largely based on real-world evidence. We analyzed real-world data regarding the safety and effectiveness of anticoagulant treatment, both parenteral and oral, for VTE prevention or atrial fibrillation (AF)/VTE treatment among COVID-19 patients. The efficacy of low-molecular-weight heparin (LMWH) doses for VTE prevention correlates with COVID-19 disease status. LMWH prophylactic dose may be useful in COVID-19 patients at the early stage of the disease. LMWH intermediate or therapeutic dose is recommended in COVID-19 patients with an advanced stage of the disease. COVID-19 patients on VKA therapy for atrial fibrillation (AF) and VTE should switch to NOACs in the community setting or LMWH in the hospital setting. No definitive data on de-novo starting of NOACs or VKA therapy for VTE prevention in COVID-19 outpatients are available. In patients at high risk discharged after hospitalization due to COVID-19, thromboprophylaxis with NOACs may be considered. [ABSTRACT FROM AUTHOR]

Introduction: The transition to or from direct oral anticoagulants (DOACs) is common in clinical practice., Areas Covered: A literature search was conducted on PubMed, Google Scholar, and UpToDate up to March 2024 for conditions and approaches for transitioning from one agent to the other. No randomized clinical trials were retrieved except for two studies regarding switching to DOAC in well-conducted vitamin K antagonist (VKA) therapy. A narrative review was conducted addressing the conditions for switching from one agent to the other, such as thromboembolic events and major bleeding during anticoagulation, development or worsening of kidney or liver failure, initiation of interfering drugs, adverse events such as allergic reactions, frailty, patients' preferences, and affordability. During transitions from one anticoagulant to the other, the risk of both thromboembolic and bleeding complications should be minimized. The current approaches for such transitions are derived from those employed in clinical trials evaluating DOAC and from product information., Expert Opinion: Many uncertainties remain regarding those circumstances requiring a change in anticoagulant strategies, as they lack evidence-based guidance. It can be envisaged that the problem of switching to and from DOAC will need additional studies especially addressing the conditions and the best approach to such transitions.

The laboratory diagnosis of antiphospholipid syndrome (APS) requires the measurement of solid-phase antibodies to cardiolipin or β2-Glycoprotein-I and the search for lupus anticoagulant (LA). The diagnosis of patients whilst on anticoagulation is impaired by the difficult interpretation of results, at least for LA, owing to the fact that prolongations of clotting times induced by LA superimpose those induced by anticoagulants. This is a matter of concern as treating physicians very often need to know the APS status of their patients to make a decision on secondary antithrombotic prophylaxis. This article aims to review the effect brought about by anticoagulants on APS diagnosis and discuss the options that can be used to overcome such an effect.

Copyright of Journal of Transfusion Medicine is the property of VM Medica-VM Group (Via Medica) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Variances in the patients' outcomes have been a well-documented challenge in anticoagulant therapy. A clinical encounter with a thromboembolic or a hemorrhagic event, due to subtherapeutic or adverse effects of an anticoagulant, is often managed by switching the anticoagulant agent into another, which is more specific and direct-acting. This management approach is usually associated with a financial burden. Additionally, the certainty of achieving better efficacy and safety profile is still questionable. Genetic variants affecting the protein sites that are involved in the anticoagulant pharmacokinetic and pharmacodynamics interactions have been suggested to contribute to the variability in the response to anticoagulant therapy. The current work reviewed the studies investigating the response variability associated with the anticoagulant therapy (heparins, rivaroxaban, apixaban, and dabigatran) and the potential pharmacogenes contributing to such response variability. Several genetic polymorphisms were reported as potential contributors to variances in response to anticoagulant therapy and were associated with adverse events. A link has been proposed for heparin resistance with single nucleotide polymorphisms (SNPs) of the anti-thrombin-encoding gene (SERPINC1) as well as heparin-induced thrombocytopenia with human leukocyte antigen (HLA) variant allele (HLA-DRB3FNx0101:01). Several investigations also remarked variations in the serum drug level of direct oral anticoagulants (DOACs) that are associated with SNPs in the proteins contributing to the pharmacokinetics of the anticoagulant agent. Several studies discerned significant associations between SNPs in the ABCB1 gene and elevations in the serum levels of rivaroxaban, apixaban, and dabigatran. Moreover, carriers of the variant genotype of the SNP (rs776746) in the cytochrome P450 3A5 enzyme-encoding gene (CYP3A5) had significantly higher drug levels when compared with the non-carriers. In contrast, some SNPs were reported to impart a protective phenotype to the carrier. The SNP (rs2244613) in the carboxylesterase-encoding gene (CES1) has been significantly associated with a decline in dabigatran trough levels and a lower risk of hemorrhage. Further investigations are essential to elucidate the extent of pharmacogenetics-based alterations in the drug levels as well as the subsequent clinical outcomes of anticoagulant therapy. [ABSTRACT FROM AUTHOR]

Since the beginning of the COVID-19 pandemic, there has been an urgent need to find effective treatment. It is widely known that virus attacks and damages mostly the lungs, but also infect vascular endothelial cells. Therefore, the protection of the endothelium is a promising target in the therapy of COVID-19 and its complications. In this review article, we focused on several groups of drugs with potential to protect the endothelium. The most promising ones are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, drugs targeting angiotensin-converting enzyme 2, heparins, sulodexide, acetylsalicylic acid, statins, tocilizumab, baricitinib, and defibrotide. Although the short period of trials and the lack of data necessitate further research, endothelial protection remains a promising target for COVID-19 therapy. [ABSTRACT FROM AUTHOR]

Support with VV-ECMO requires anticoagulation with unfractionated heparin to prevent thrombotic complications. This must be monitored due to bleeding risk. A point-of-care (POC) method of testing aPTT and APR was evaluated for agreement with laboratory methods. In a prospective observational study, patients supported on VV-ECMO as a result of severe respiratory failure secondary to Covid-19 infection were given heparin as part of standard therapy. The aPTT was measured (i) at the bedside using the Hemochron Signature Elite device and (ii) at the hospital laboratory. Duplicate results were compared. Agreement between the POC and laboratory tests was poor, as assessed using the Bland-Altman method. The maximum difference between POC and laboratory methods was 133% and the minimum was 0%. Overall bias was 7.3% and limits of agreement were between −43.8% and 58.5%. Correlation increased when results were normalised to platelet count and creatinine. This POC test is insufficiently accurate for use as the primary method of heparin monitoring in patients requiring VV-ECMO for Covid-19. Platelets and renal function may influence the result of this whole blood POC test. [ABSTRACT FROM AUTHOR]

The aim was to describe inpatients with COVID-19 empirically prescribed heparinoid anticoagulants and compare resource utilization between prophylactic/low-dose and therapeutic/high-dose groups. Methods: This retrospective observational study used real-world data from 880 US hospitals in the PINC AI™ Healthcare Database during 4/1/2020–11/30/2020. Descriptive analysis was used to characterize patients. Multivariable regression was used to evaluate intensive care unit (ICU) admissions, length of stay (LOS), mortality, and costs by anticoagulation dose group, adjusting for cohort characteristics. Among 122,508 inpatients, 29,225 (23.9%) received therapeutic/high-dose, and 93,283 (76.1%) received prophylactic/low-dose anticoagulation. The high-dose group had more comorbidities and worse laboratory values compared with low-dose. Respectively, ICU admission rates were 36.7% and 19.1% and LOS median (Q1, Q3) was 8 (5, 15) and 5 (3, 9) days. In separate adjusted models, high-dose anticoagulation was associated with a 45% increase in odds of ICU admission, 26% increase in odds of in-hospital mortality, 21% longer average LOS, and 28% greater average total cost compared with low-dose (each P < 0.001). Prophylactic/low-dose anticoagulation treatment was associated with decreased healthcare resource utilization (HRU) in hospitalized patients with COVID-19. [ABSTRACT FROM AUTHOR]

Heparins show great anticoagulant effect with few side effects, and are administered by subcutaneous or intravenous route in clinics. To improve patient compliance, oral administration is an alternative route. Nonetheless, oral administration of heparins still faces enormous challenges due to the multiple obstacles. This review briefly analyzes a series of barriers ranging from poorly physicochemical properties of heparins, to harsh biological barriers including gastrointestinal degradation and pre-systemic metabolism. Moreover, several approaches have been developed to overcome these obstacles, such as improving stability of heparins in the gastrointestinal tract, enhancing the intestinal epithelia permeability and facilitating lymphatic delivery of heparins. Overall, this review aims to provide insights concerning advanced delivery strategies facilitating oral absorption of heparins.

Thrombosis, the formation of blood clots within a blood vessel, can lead to severe complications including pulmonary embolism, cardiac arrest, and stroke. The most widely administered class of anticoagulants is heparin-based anticoagulants such as unfractionated heparin, low-molecular weight heparins (LMWHs), and fondaparinux. Protamine is the only FDA-approved heparin antidote. Protamine has limited efficacy neutralizing LMWHs and no reversal activity against fondaparinux. The use of protamine can lead to complications, including excessive bleeding, hypotension, and hypersensitivity, and has narrow therapeutic window. In this work, a new concept in the design of a universal heparin antidote: switchable protonation of cationic ligands, is presented. A library of macromolecular polyanion inhibitors (MPIs) is synthesized and screened to identify molecules that can neutralize all heparins with high selectivity and reduced toxicity. MPIs are developed by assembling cationic binding groups possessing switchable protonation states onto a polymer scaffold. By strategically selecting the identity and modulating the density of cationic binding groups on the polymer scaffold, a superior universal heparin reversal agent is developed with improved heparin-binding activity and increased hemocompatibility profiles leading to minimal effect on hemostasis. The activity of this heparin antidote is demonstrated using in vitro and in vivo studies., (© 2024 The Authors. Advanced Healthcare Materials published by Wiley‐VCH GmbH.)

Heparin-induced thrombocytopenia (HIT) is a serious and potentially life-threatening side effect of heparinotherapy. It is an antibody-mediated process that causes platelet activation, increases the procoagulant characteristics of the blood and, as a result, endangering limbs and life-threatening thrombosis. Venous thrombosis is more common than arterial thrombosis, especially deep vein thrombosis of the lower limbs and pulmonary artery thrombosis. Mortality from complications of heparinotherapy occurs with a frequency of 20–30 % of cases. Diagnosis of HIT is difficult. Such basic symptoms as thrombocytopenia and thrombosis are extremely non-specific and may be present in cancer patients and patients with cardiosurgical pathologies without the impact of heparin. Women are twice as likely to have HIT as men. This review describes pathogenesis, clinical features, modern diagnostic methods, risk factors for the emergence of this formidable complication of heparinotherapy, gives an overview of the most frequent use of drugs for the treatment of HIT, and gives modern clinical recommendations for different groups of patients.

OBJECTIVE: Patients with 2019-nCoV infection have a high risk to develop venous thrombotic events. Several guidelines recommend the use of either unfractionated heparin or low molecular weight heparins in preventing thrombotic events in these patients. However, results from clinical studies, so far published, reached controversial conclusions on heparin efficacy in this kind of patients since the incidence of venous thromboembolism remains high despite prophylaxis. This narrative review aims to provide an overview of the antiviral and anti-inflammatory properties of heparins and their efficacy and safety in SARSCoV-2 medical ward-patients. Moreover, anatomical findings and ongoing trials are also reported. Finally, this narrative review tries to explain why heparins fail to prevent venous thrombosis. MATERIALS AND METHODS: We searched for the most relevant published studies on heparins and 2019-nCoV infected patients using the MEDLINE electronic database in the period between January and December 2020. Articles were preliminarily defined as eligible if they: a) were in English language, b) enrolled 250 or more medical ward-patients and 100 or more ICU-patients, c) reported results on patients treated with heparins in a percentage of at least 70% and d) performed an objectively confirmed diagnosis of VTE. RESULTS: Data from medium to large scientific studies show that the incidence of venous thrombotic events in medical ward-patients with SARS-CoV-2 vary between 0% and 8.3%, while this rate is higher, from 6.2% to 49%, in Intensive Care Unit-patients. However, heparins reduce the mortality rate in these patients of about 50%. Histological findings show that thrombosis could affect capillaries, main and small-midsized vessels, and it is associated with diffuse alveolar damage. CONCLUSIONS: Heparins have anti-inflammatory and anti-viral properties, which may be of help in reducing mortality in SARS-CoV-2 patients. Failure of heparins at prophylactic dosages in preventing VTE, especially in ICU-patients, could be due to the severity of the disease. Data on the use of heparins in an early phase of the 2019-nCoV infection are still lacking. [ABSTRACT FROM AUTHOR]