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The risk of recurrent events among survivors of acute myocardial infarction (AMI) is understudied. The aim of this alysis was to investigate the role of residual high thrombotic risk (HTR) as a predictor of recurrent in-hospital events after AMI. This retrospective cohort study included 186,646 patients admitted with AMI from 2009 to 2010 in all Italian hospitals who were alive 30 days after the index event. HTR was defined as at least one of the following in the 5 years preceding AMI: previous myocardial infarction, ischemic stroke/other vascular disease, type 2 diabetes mellitus, rel failure. Risk adjustment was performed in all multivariate survival alyses. Rates of major cardiac and cerebrovascular events (MACCE) within the following 5 years were calculated in both patients without fatal readmissions at 30 days and in those free from in-hospital MACCE at 1 year from the index hospitalization. The overall 5-year risk of MACCE was higher in patients with HTR than in those without HTR, in both survivors at 30 days [hazard ratio (HR), 1.49; 95% confidence interval (CI), 1.45-1.52; p<0.0001] and in those free from MACCE at 1 year (HR, 1.46; 95% CI, 1.41-1.51; p<0.0001). The risk of recurrent MACCE increased in the first 18 months after AMI (HR, 1.49) and then remained stable over 5 years. The risk of MACCE after an AMI endures over 5 years in patients with HTR. This is also true for patients who did not have any new cardiovascular event in the first year after an AMI. All patients with HTR should be identified and addressed to intensive preventive care strategies.

A great number of studies confirm the fact that haemostatic anomalies occur rather often in endocrine diseases. Multiple endocrine and metabolic disorders can alter the haemostatic balance and favour thrombotic risk, with stroke being the most frequent and feared clinical manifestation. Hormonal factors are important, especially in arterial thrombosis, and, to a lesser extent, in venous thrombosis. This process causes ischaemic lesions, with the most severe clinical manifestations being stroke and myocardial ischaemia.

In type 2 diabetes, anti-thrombotic management is challenging, and current anti-platelet agents have demonstrated reduced efficacy. Old and new anti-diabetic drugs exhibited—besides lowering blood glucose levels—direct and indirect effects on platelet function and on thrombotic milieu, eventually conditioning cardiovascular outcomes. The present review summarizes existing evidence on the effects of glucose-lowering agents on platelet properties, addressing pre-clinical and clinical research, as well as drug–drug interactions with anti-platelet agents. We aimed at expanding clinicians’ understanding by highlighting new opportunities for an optimal management of patients with diabetes and cardiovascular disease. We suggest how an improvement of the thrombotic risk in this large population of patients may be achieved by a careful and tailored combination of anti-diabetic and anti-platelet therapies.

In 10% of ischemic strokes, non-valvular atrial fibrillation (NVAF) is detected retroactively. Milder, or even asymptomatic forms of NVAF have shown high mortality, thrombotic risk, and deterioration of cognitive function. The current guidelines for the diagnosis and treatment of AF contain \"grey areas\", such as the one related to anticoagulant treatment in men with CHA2DS2-VASc score 1 and women with score 2. Moreover, parameters such as renal function, patient weight or left atrium remodelling are missing from the recommended guidelines scores. Vulnerable categories of patients including the elderly population, high hemorrhagic risk patients or patients with newly diagnosed paroxysmal episodes of atrial high rate at device interrogation are at risk of underestimation of the thrombotic risk. This review presents a systematic exposure of the most important gaps in evaluation of thrombotic and hemorrhagic risk in patients with NVAF. The authors propose new algorithms and risk factors that should be taken into consideration for an accurate thrombotic and hemorrhagic risk estimation, especially in vulnerable categories of patients.In 10% of ischemic strokes, non-valvular atrial fibrillation (NVAF) is detected retroactively. Milder, or even asymptomatic forms of NVAF have shown high mortality, thrombotic risk, and deterioration of cognitive function. The current guidelines for the diagnosis and treatment of AF contain \"grey areas\", such as the one related to anticoagulant treatment in men with CHA2DS2-VASc score 1 and women with score 2. Moreover, parameters such as renal function, patient weight or left atrium remodelling are missing from the recommended guidelines scores. Vulnerable categories of patients including the elderly population, high hemorrhagic risk patients or patients with newly diagnosed paroxysmal episodes of atrial high rate at device interrogation are at risk of underestimation of the thrombotic risk. This review presents a systematic exposure of the most important gaps in evaluation of thrombotic and hemorrhagic risk in patients with NVAF. The authors propose new algorithms and risk factors that should be taken into consideration for an accurate thrombotic and hemorrhagic risk estimation, especially in vulnerable categories of patients.

The immune and inflammatory responses of platelets to human immunodeficiency virus 1 (HIV-1) and its envelope proteins are of great significance to both the treatment of the infection, and to the comorbidities related to systemic inflammation. Platelets can interact with the HIV-1 virus itself, or with viral membrane proteins, or with dysregulated inflammatory molecules in circulation, ensuing from HIV-1 infection. Platelets can facilitate the inhibition of HIV-1 infection via endogenously-produced inhibitors of HIV-1 replication, or the virus can temporarily hide from the immune system inside platelets, whereby platelets act as HIV-1 reservoirs. Platelets are therefore both guardians of the host defence system, and transient reservoirs of the virus. Such reservoirs may be of particular significance during combination antiretroviral therapy (cART) interruption, as it may drive viral persistence, and result in significant implications for treatment. Both HIV-1 envelope proteins and circulating inflammatory molecules can also initiate platelet complex formation with immune cells and erythrocytes. Complex formation cause platelet hypercoagulation and may lead to an increased thrombotic risk. Ultimately, HIV-1 infection can initiate platelet depletion and thrombocytopenia. Because of their relatively short lifespan, platelets are important signalling entities, and could be targeted more directly during HIV-1 infection and cART.

Hormone receptor-positive, HER2-negative (HR+/HER2-) is the most common subtype of breast cancer in women. Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors, such as palbociclib, ribociclib, and abemaciclib play an important role in the treatment of advanced HR+/HER2- breast cancer. However, CDK4/6 inhibitors might be associated with an increased risk of thrombotic events, including venous thromboembolism (VTE). We conducted a retrospective study at two centers in Saudi Arabia, analyzing data from 447 patients treated with CDK4/6 inhibitors for HR+/HER2- breast cancer between 2016 and 2023. Patients with early-stage, high-risk breast cancer receiving abemaciclib for at least one month were included. The primary outcomes were the incidence of VTE and arterial thrombosis. A total of 505 patients were screened in which 447 breast cancer patients receiving CDK4/6 inhibitors were included. Majority of patients were on palbociclib (70.4%), followed by abemaciclib (28.8%), and then ribociclib (0.67%). The thrombotic events were 11.8% (n=53), with 37.7% of these being pulmonary embolism (PE) and 18.8% symptomatic deep vein thrombosis (DVT). Patients with a prior history of VTE had a significantly higher risk of thrombosis (p=0.03). Abemaciclib was associated with a higher incidence of thrombosis (16.3%), followed by palbociclib (10.2%), and none of the three patients on ribociclib developed thrombosis. The median time to develop thrombosis while receiving CDK4/6 inhibitor therapy was 11.8 months. There was no significant difference in overall survival in breast cancer patients who developed thrombosis compared to patients without thrombosis (p=0.55). This study shows a higher incidence of thrombotic events in real-world settings than clinical trials, emphasizing the need for risk assessment and possible thromboprophylaxis in patients receiving CDK4/6 inhibitors. Future risk assessment tools needed to be applied in breast cancer patients receiving CDK4/6 inhibitors and risk of developing thrombosis.

Background Antiphospholipid syndrome (APS) is notably linked to thrombotic events, particularly cardiovascular disease (CVD). The role of remnant cholesterol (RC) in predicting CVD risk is established, yet its relationship with thrombotic risk in APS patients remains to be elucidated. This study aims to assess the association between RC and recurrent thrombotic risk in patients with APS. Methods A prospective analysis was conducted based on a cohort of APS patients who met the 2006 Sydney revised classification criteria. Thrombotic risks associated with varying levels of RC were evaluated using Kaplan–Meier survival analysis and Cox proportional hazards regression models. Mendelian randomization (MR) was applied to examine the causal link between RC and different types of thrombotic events. Results A total of 325 patients with APS were enrolled in this study. Over a median follow-up of 35 months, 51 patients experienced thrombotic events, including 24 venous, 19 arterial, and 16 microvascular incidents. Patients with RC levels above 0.60 mmol/L exhibited significantly higher risks, with multivariable-adjusted hazard ratio (and 95% confidence interval) for all-cause, venous, arterial thrombosis, and microvascular disease being 5.05 (2.23–11.41), 6.34 (1.71–23.54), 3.79 (1.00–14.32), and 4.36 (1.08–17.58), respectively. Notably, elevated RC remained a significant thrombotic risk factor even in patients with normal conventional lipid profiles. MR analysis revealed a significant causal association between RC and arterial thrombosis, but not venous thrombosis. Conclusions Elevated RC is linked to a substantial increase in the risk of thrombotic events in APS patients. These findings suggest that RC could be a valuable marker for thrombotic risk in this population and a potential target for therapeutic intervention. Highlights A more than 5-fold increase in thrombotic risk, including arterial, venous, and microvascular events, is linked to individuals with RC levels >0.60 mmol/L in APS. Elevated RC remains a significant risk factor even in patients with normal conventional lipid indices (LDL-C, TC, TG, and non-HDL-C). Through MR analysis, there was a significant causal relationship between RC and AT in the general population, but not with VT, suggesting the complexity of the pathogenesis of VT in patients with APS. Patients with APS treated with hydroxychloroquine have lower RC levels, and hydroxychloroquine may have the potential to reduce RC. Graphical Abstract

Background All available recommendations about the management of antithrombotic therapies (ATs) in patients who experienced traumatic brain injury (TBI) are mainly based on expert opinion because of the lack of strength in the available evidence-based medicine. Currently, the withdrawal and the resumption of AT in these patients is empirical, widely variable, and based on the individual assessment of the attending physician. The main difficulty is to balance the thrombotic and hemorrhagic risks to improve patient outcome. Methods Under the endorsement of the Neurotraumatology Section of Italian Society of Neurosurgery, the Italian Society for the Study about Haemostasis and Thrombosis, the Italian Society of Anaesthesia, Analgesia, Resuscitation, and Intensive Care, and the European Association of Neurosurgical Societies, a working group (WG) of clinicians completed two rounds of questionnaires, using the Delphi method, in a multidisciplinary setting. A table for thrombotic and bleeding risk, with a dichotomization in high risk and low risk, was established before questionnaire administration. In this table, the risk is calculated by matching different isolated TBI (iTBI) scenarios such as acute and chronic subdural hematomas, extradural hematoma, brain contusion (intracerebral hemorrhage), and traumatic subarachnoid hemorrhage with patients under active AT treatment. The registered indication could include AT primary prevention, cardiac valve prosthesis, vascular stents, venous thromboembolism, and atrial fibrillation. Results The WG proposed a total of 28 statements encompassing the most common clinical scenarios about the withdrawal of antiplatelets, vitamin K antagonists, and direct oral anticoagulants in patients who experienced blunt iTBI. The WG voted on the grade of appropriateness of seven recommended interventions. Overall, the panel reached an agreement for 20 of 28 (71%) questions, deeming 11 of 28 (39%) as appropriate and 9 of 28 (32%) as inappropriate interventions. The appropriateness of intervention was rated as uncertain for 8 of 28 (28%) questions. Conclusions The initial establishment of a thrombotic and/or bleeding risk scoring system can provide a vital theoretical basis for the evaluation of effective management in individuals under AT who sustained an iTBI. The listed recommendations can be implemented into local protocols for a more homogeneous strategy. Validation using large cohorts of patients needs to be developed. This is the first part of a project to update the management of AT in patients with iTBI.

The pathogenesis of venous thromboembolism in multiple myeloma is still poorly understood because multiple factors are involved. In particular, the increase in whole blood viscosity has a key role and, therefore, we performed an evaluation of some hemorheological determinants in multiple myeloma patients, putting them in relation to the thrombotic risk, with the aim to evaluate if an alteration of the hemorheological pattern was associated with a higher thrombotic risk. We performed an observational retrospective cohort study with data collected from January 2017 to September 2022. In a group of 190 patients with newly diagnosed multiple myeloma, we have examined the trend of calculated blood viscosity according to the Merrill formula, and we stratified the patients for the thrombotic risk in accordance with the IMWG/NCCN guidelines and with IMPEDE VTE score. Using the thrombotic risk stratification proposed by IMWG/NCCN any variation in calculated blood viscosity is evident, while, with the IMPEDE VTE score, we observed an increase in calculated blood viscosity in patients with “intermediate + high” risk. The calculated blood viscosity is higher in subjects presenting an “intermediate + high” thrombotic risk according to the IMPEDE VTE score. This association could therefore lay the groundwork for further research with the aim to confirm the role of hemorheological pattern in MM-related thrombotic risk.

Background/Objectives: Tuberculosis and COVID-19 are two major infectious diseases with significant inflammatory and immunological impact on infected hosts and both conditions are independently associated with a prothrombotic state. However, evidence regarding their combined effect on in-hospital thrombotic risk remains limited. In this study, we aimed to explore whether patients with tuberculosis and COVID-19 coinfection are at a higher risk of developing thrombotic events during hospitalization than patients diagnosed with tuberculosis alone. Materials and Methods: We performed a retrospective, single-center cohort study, including adults hospitalized at the Pulmonology Clinic, Adult Tuberculosis ward of Mures County Clinical Hospital, between 2021 and 2023. Two groups were analyzed: patients with pulmonary tuberculosis who developed COVID-19 during hospitalization (n = 40) and patients with pulmonary tuberculosis without documented SARS-CoV-2 infection (n = 40). Demographic, clinical, laboratory, and imaging data were extracted from medical records. Padua and IMPROVE-DD scores were calculated retrospectively, a rapid mini-score was evaluated exploratorily. Comparisons between groups were performed using appropriate statistical tests and unadjusted odds ratios (ORs) with 95% confidence intervals (CIs) were reported. Given the limited number of events, an age-adjusted Firth penalized logistic regression model was used for multivariable analysis. Results: Thrombotic events occurred more frequently in the tuberculosis and COVID-19 co-infection group (22.5% vs. 10%), although statistical significance was not reached (p = 0.22; OR = 2.61). Patients with coinfection had significantly higher proportions of elevated Padua scores (55% vs. 20%, p = 0.002; OR = 4.88), while IMPROVE-DD showed values near the conventional threshold for statistical significance (37.5% vs. 17.5%, p = 0.07). D-dimer values did not reach statistical significance (p = 0.07) and platelet counts were significantly higher in patients with tuberculosis only (p = 0.001). Mortality did not differ significantly between groups (15% vs. 10%, p = 0.73). In age-adjusted multivariable analysis, tuberculosis and COVID-19 coinfection remained associated with higher odds of thrombotic events, with wide confidence intervals. Conclusions: Patients with concomitant tuberculosis and COVID-19 showed a higher thrombotic risk profile (Padua score) and numerically higher rates of in-hospital thrombotic events, without reaching statistical significance. Findings should be interpreted as exploratory and hypothesis-generating. Larger prospective studies with systematic imaging and multivariable adjustment are needed.