Thrombosis of the deep veins of the legs is a relatively common occurrence initiated by venous stasis, endothelial damage or hypercoagulable states. Prolonged sitting has also been associated with thrombotic events. A case is reported where immobility caused by drug overdose resulted in lethal pulmonary thromboembolism. Case report: A 50-year-old male was found sitting in the driver's seat of his car slumped forward. A suicide note was present. At autopsy finely granular tablet residue was found in the stomach. Deep venous thrombosis was present in both calves with bilateral pulmonary thromboembolism. Toxicological examination of blood revealed elevated levels of amitriptyline (0.92 mg/L), nortriptyline (0.41 mg/L) and oxycodone (0.17 mg/L). Death was due to pulmonary thromboembolism arising from bilateral deep venous thromboses complicating mixed drug toxicity. Prolonged immobility should be considered a possible mechanism for venous thrombosis in drug takers.

Our study is centered around a pivotal question: How does the increase in adipose tissue, which defines obesity, impact hemorheological parameters? By delving into this question, we aim to underscore the crucial role of fat tissue increase in obesity, a topic of significant interest and importance in the field of physiology and obesity research.

Individuals with a body mass index (BMI) of 25 and above were included in this study. Height was measured with bare feet on flat surface, then, using the bioimpedance device (Tanita-BC418), weight, BMI, fat percentage, fat mass (FM), and fat-free mass were determined. Using the Brookfield viscometer, several shear rates were utilized (for whole blood, 75, 150, 300, and 450 sec-1; for plasma 450 sec-1) in accordance with established standards and test procedures. Whole blood and plasma viscosity were studied in Hamidiye Medical Faculty Hemorheology laboratory.

Plasma viscosity in the obese group was significantly (P = 0.01) higher than in the non-obese group, and increased statistically in proportion to weight, BMI, FM, fat-free mass (P < 0.05) in the obese group. At shear rates of 300 and 450 sec-1 (P < 0.05) were determined statistically significant differences between the obese and nonobese groups in whole blood viscosity (WBV). In the obese group, WBV at a shear rate of 75, 150, 300, and 450 sec-1 showed a positive correlation with weight, BMI, FM (P < 0.05).

Increased adipose tissue significantly affect plasma and blood viscosities in obesity. The increase in plasma and WBV is directly associated with the increase in adipose tissue.

Thrombophilia is characterized by a hypercoagulable state that predisposes individuals to venous and arterial thrombotic events, posing significant challenges for clinical evaluation and management. This narrative review critically examines the current landscape of thrombophilia testing, focusing on the utility and limitations of both circulating and genetic biomarkers. Circulating biomarkers-such as D-dimer, antithrombin, protein C, and protein S-offer dynamic insights into the coagulation process yet often suffer from low specificity in varied clinical settings. In contrast, genetic biomarkers, notably Factor V Leiden and the prothrombin G20210A mutation, provide stable risk stratification but are limited by their low prevalence in the general population. Emerging markers, including selectins, Factor VIII, Factor XI, neutrophil extracellular traps, and extracellular vesicles, are also discussed for their potential to refine thrombotic risk assessment. By integrating evidence-based guidelines from international health organizations, this review underscores the need for a personalized approach to thrombophilia evaluation that balances comprehensive risk assessment with the avoidance of over-testing. Such an approach is crucial for optimizing patient outcomes and informing the duration and intensity of anticoagulant therapy.

Thrombotic and cardiovascular events are among the leading causes of death for patients with polycythemia, more specifically for those with primary origin. It has been suggested that the high hematocrit (Hct) would favor hypercoagulability. However, the impact of Hct on coagulation in patients with polycythemia has not been investigated so far. The aim of our study was to compare the coagulation profiles of healthy subjects and patients with polycythemia and to evaluate the in vitro impact of Hct on coagulation. Blood from healthy individuals (n = 100 for blood viscosity; n = 19 for coagulation) and patients with primary/secondary polycythemia (n = 29 for blood viscosity; n = 20 for coagulation) was used to perform measurements at native Hct. The impact of Hct modulation (20% vs. 50%) on coagulation was tested in vitro in 9 healthy subjects and 19 patients with polycythemia. Blood viscosity was measured by viscosimetry and coagulation and fibrinolysis by rotational thromboelastometry. In patients with polycythemia, Hct, and blood viscosity were higher, clotting time was prolonged and clot lysis was faster compared to healthy individuals. Our in vitro results showed that the clotting time was faster and the clot firmness higher at 20% versus 50% Hct for both populations, without any difference between the two populations at a given Hct. Our findings suggest that the interpretation of thromboelastometry results should be approached with caution in patients with high Hct. The in vivo hypercoagulable state of patients with polycythemia is probably the consequence of changes in hemodynamic conditions attributed to blood hyper-viscosity, that may promote venous stasis and platelet margination.

ObjectiveDeep vein thrombosis (DVT) is a global health issue caused by abnormal clotting in deep veins, which can lead to serious complications such as pulmonary embolism. This study is the first to validate the regulatory effect of miR-223-3p on the NLRP3 inflammasome in a mouse model of DVT, expanding its potential therapeutic value in venous thrombosis-associated inflammation.MethodsMicroRNA sequencing and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to assess miRNA expression in a DVT mouse model. The downstream target of miR-223-3p, NLRP3, was identified using miRNA target prediction databases and validated by qRT-PCR. Human umbilical vein endothelial cells (HUVECs) and a DVT mouse model were used to explore the functional relationship between miR-223-3p and Nlrp3.ResultsThe expression of miR-223-3p and Nlrp3 was significantly increased in the vein walls of mice with DVT. The tail vein injection of agomiR-223-3p reduced thrombus formation and downregulated the expression of Nlrp3, interleukin 6 (Il-6), interleukin 1 beta (IL-1beta) and Icam-1. In vitro, miR-223-3p overexpression reduced the expression of NLRP3, Il-6, IL-1beta and ICAM-1, whereas NLRP3 overexpression antagonized these effects. Additionally, miR-223-3p enhanced the viability and migration of LPS-stimulated HUVECs by reducing NLRP3 expression.ConclusionsOur findings suggest that miR-223-3p may play a role in alleviating inflammation and reducing the thrombus burden in mice with DVT by downregulating Nlrp3 expression, supporting its potential as a therapeutic target for DVT.

Coronary sinus thrombosis (CST) is a rare and severe disease that remains underrecognized in clinical practice. Most documented cases fall within the acute category, with non-specific symptoms, rapid progression, and a high mortality rate. In contrast, some cases follow an insidious course, leading to the formation of partial or incomplete thrombi that may not cause immediate death but can progress to severe complications over time. This review study the pathophysiology, clinical presentations, diagnostic challenges, and the association with persistent left superior vena cava (PLSVC), emphasizing the utility of imaging modalities such as Echocardiography, Computed Tomography, Magnetic Resonance Imaging and Venography. For management, anticoagulation remains the cornerstone of treatment for CST, with surgical thrombectomy reserved for severe or refractory cases. Post-treatment follow-up is highlighted as essential for monitoring recurrence and managing complications. In brief, the aim of this review is to enhance the understanding of CST and improve clinical outcomes through early recognition, tailored interventions, and multidisciplinary care.

Implementing Enhanced Recovery After Surgery (ERAS) guidelines has been demonstrated to reduce complications; however, it is unknown if ERAS may influence incidence of postoperative venous thromboembolism, a particularly challenging complication. The objective of this study was to examine the association between ERAS compliance and venous thromboembolism across multiple surgery types.

This retrospective cohort study included adult patients undergoing one of seven ERAS-guided surgeries between 2017 and 2021 at nine hospitals in Alberta, Canada, that implemented ERAS guidelines. The exposure was overall ERAS compliance (categorized as low, moderate, high) and compliance with each ERAS element. The primary outcome was venous thromboembolism within 30 days of surgery. Secondary outcomes included 30-day hospital readmission, emergency department visits and healthcare costs.

Of the 8118 included patients, most had colorectal (52.8%) and gynaecologic (26.1%) surgery. There were 118 (1.5%) patients who experienced a postoperative venous thromboembolism. ERAS compliance was associated with developing a venous thromboembolism; each unit increase in the ERAS compliance score was associated with a 23% decrease in the occurrence of venous thromboembolism. More patients with venous thromboembolism had low (11.0%) or moderate (44.1%) overall ERAS compliance compared with those with no venous thromboembolism (5.6% and 34.5% respectively, P = 0.001). Using logistic regression analysis, the overall ERAS compliance score and American Society of Anesthesiologists class remained significant risk factors for developing a venous thromboembolism.

ERAS compliance was associated with decreased odds of postoperative venous thromboembolism across multiple surgical disciplines, highlighting the importance of improving ERAS compliance to decrease postoperative venous thromboembolism.

Janus kinase inhibitors (JAKi) have been associated with an increased risk of venous thromboembolism (VTE) limiting the use of JAKi-based therapy. To improve risk stratification and drug development, it is crucial to understand the implication of dysregulated JAK-Signal Transducers and Activators of Transcription (STAT) signaling in the pathogenesis of VTE. The objective of this study is to clarify the putative genomic vulnerability to dysregulated JAK-STAT signaling in VTE through systematic mining of large-scale datasets generated from studies comparing VTE patients with healthy controls. Particularly, we assess the representation of entities of the JAK-STAT signaling pathway including STAT target genes among sets of miRNA, mRNA, and proteins differentially abundant in VTE patients, and we explore the putative cumulative genetic association of JAK-STAT signaling gene sets to VTE. Genes related to the JAK-STAT pathway were found significantly altered in VTE patients compared to healthy controls, indicating that genes under transcriptional control of STAT may be dysregulated in VTE. In support of this notion, we find a significant overrepresentation of predicted STAT target genes among genes downregulated in VTE patients, and promoter sequences of differentially regulated genes were significantly enriched with STAT transcription factor binding site motifs. Further linking STAT signaling to the molecular signature of VTE, genes targeted by miRNAs differentially regulated in patients are significantly enriched with STAT target genes and genes acting in the JAK-STAT signaling pathway. Together, our findings indicate that disruptions in the JAK-STAT pathway contribute to the molecular profile of VTE. This offers hope for identifying ways to interact with the JAK-STAT pathway that do not carry the risk of VTE.

A previously healthy 15-year-old female developed sudden onset right lower extremity swelling, pain, and erythematous linear streaking from the ankle to mid-thigh. Duplex venous ultrasound revealed multiple superficial and deep venous thrombi in the right lower extremity. Incidentally, the patient was also noted to have elevated transaminases and a microcytic anemia with significant iron deficiency. Additional evaluation ultimately led to the diagnosis of 2 distinct but interconnected chronic conditions, one of which progressed to requiring liver transplantation.

The purpose of this study was to sonographically evaluate whether intravenous (IV) flucloxacillin administration was associated with an increased risk of peripheral intravenous catheter (PIVC) thrombus formation.

This observational study included participants enrolled as a convenience sample from a larger prospective study of patients with cellulitis receiving IV antibiotics in the emergency department. Point-of-care ultrasound was used to evaluate the PIVCs for thrombus formation after insertion and at specified timepoints after IV administration of antibiotic or saline solution through to discharge. The primary endpoint included the presence and length of the thrombus in proximity of the catheter tip.

Between May 2021 and June 2022, 25 participants were enrolled and received either IV flucloxacillin (n = 10), other IV antibiotics (n = 8) or no IV antibiotics (control; n = 7). PIVC thrombus formation was sonographically detected in 100%, 67% and 17% of patients in flucloxacillin, other and control groups at 6-12 h (flucloxacillin vs. control; P = 0.015), with a mean length of 17.4 ± 8.1 (flucloxacillin vs. control; P = 0.46), 15.5 ± 13.4 (other vs. control; P = 0.73) and 7.3 ± 17.9 mm (control), respectively. Thrombus formation increased significantly in the flucloxacillin group over time (0->12 h; P = 0.03) but did not increase in the other or control groups.

The administration of IV flucloxacillin appears to promote the formation of a PIVC thrombus visible on ultrasound, but the clinical implications are uncertain. Although the vast majority appear to be asymptomatic, they have the potential to become a precursor to thrombophlebitis and lead to early PIVC failure.

It was feasible to identify and measure PIVC thrombus sonographically. Ultrasound showed that IV flucloxacillin administration appeared to be associated with more frequent formation of PIVC thrombus, with these increasing in length over time. Further research is required to confirm these findings in larger studies and to identify any clinical implications of the findings.

The protease thrombin, which increases its levels with various pathologies, can signal through the G protein-coupled receptors protease-activated receptors 1 and 4 (PAR1/PAR4). PAR1 is a high-affinity receptor for thrombin, whereas PAR4 is a low-affinity receptor. Finding functions for PAR4 in endothelial cells (ECs) has been an elusive goal over the last two decades. Several studies have demonstrated a lack of functionality for PAR4 in ECs, with many claiming that PAR4 function is confined mostly to platelets. A recent study from our lab identified low expressing but functional PAR4 in hepatic ECs in vivo. We also found that PAR4 likely has a higher signaling potency than PAR1. Given this potency, ECs seem to limit PAR4 signaling except for extreme cases. As a result, we claim PAR4 is not an impotent receptor because it is low expressing, but rather PAR4 is low expressing because it is a very potent receptor. Since we have finally shown PAR4 to be present and functional on ECs in vivo, it is important to outline why such controversy arose over the last two decades and, more importantly, why the receptor was undervalued on ECs. This timely review aims to inspire investigators in the field of vascular biology to study the regulatory aspect of endothelial PAR4 and its relationship with the more highly expressed PAR1.

There are many recognised risk factors for retinal vein occlusions. It is plausible that musicians who play wind instruments or use their voice as their primary instrument may be at increased risk of branch retinal vein occlusions through repeated Valsalva manoeuvre.

Repeated valsalva manoeuvres are commonly performed by musicians using high resistance wind instruments. This also true for singers. This case series illustrates a correlation between repeated Valsalva manoeuvres and retinal vein occlusion in three patients and explores the clinical and functional underlying mechanisms.

A retrospective review of three cases presenting to a private Ophthalmology clinic.

Case 1 is an 85-year-old male, French Horn player and Case 2 is a 77-year-old male, bass-baritone singer each presented with a left-sided non-ischaemic branch retinal vein occlusion. Case 3 is a 79-year-old male Tenor presented with a left -sided ischaemic branch retinal vein occlusion. All cases were treated with intravitreal anti-vascular endothelial growth factor stabilising vision.

Repeated Valsalva manoeuvre as demonstrated in wind musicians and singers may play a role in pathogenies of branch retinal vein occlusions in susceptible individuals.

Venous thromboembolism, characterized by deep vein thrombosis and pulmonary embolism, is the third cardiovascular disease in the world. Deep vein thrombosis occurs when a blood clot forms in areas of impaired blood flow, and it is significantly affected by environmental factors. Local hypoxia, caused by venous stasis, plays a critical role in deep vein thrombosis under normal conditions, and this effect is intensified when the Po2 decreases, such as during air travel or high-altitude exposure. The lower oxygen levels and reduced pressure at high altitudes further contribute to deep vein thrombosis development. These conditions increase the pro-coagulant activity of neutrophils, platelets, and red blood cells, which interact on the surface of activated endothelial cells, promoting clot formation. Understanding the mechanisms involved in thrombus formation when Po2 is reduced, with or without pressure reduction, is crucial for preventing the development of venous thromboembolisms in such conditions and identifying innovative therapeutic targets. This literature review explores the mechanisms involved in thrombus formation related to high-altitude conditions and discusses the pro-coagulant consequences induced by environmental disturbances.

The Woven EndoBridge (WEB) device has become a prominent treatment for wide-neck bifurcation intracranial aneurysms since its FDA approval in 2018. However, the impact of anticoagulant therapy on its efficacy and patient outcomes remains underexplored. This study aims to evaluate the effects of postoperative anticoagulant use on aneurysm occlusion, retreatment rates, and functional outcomes following WEB device implantation. This retrospective multicenter study included 457 patients treated with the WEB device across 10 academic institutions in the United States between January 2012 and June 2024. Patients were categorized based on postoperative anticoagulant use: 91 patients (19.9%) received anticoagulants, while 366 patients (80.1%) did not. Propensity score matching (PSM) was employed to control for potential confounders, resulting in 316 matched patients (229 non-anticoagulant and 87 anticoagulant). After PSM, the anticoagulant group had lower rates of excellent functional outcomes (mRS 0-1: 73% vs. 85%, p = 0.026) and higher mortality rates (6.7% vs. 3.7%, p = 0.33), though the latter difference was not statistically significant. No significant differences in the last follow-up adequate occlusion were observed between the two groups (p = 0.7). However, patients in the anticoagulant group had lower major device compaction (> 50%) (4.9% vs. 12%, p = 0.12) and retreatment rates (4.6% vs. 12%, p = 0.045). Postoperative anticoagulant use is associated with poor functional outcomes and higher tendency for higher mortality rate. No significant differences in the last follow-up adequate occlusion rate were observed between the anticoagulant group and non-anticoagulant group. However, patients in the anticoagulant group had lower major compaction and retreatment rates. These findings suggest that the WEB mechanism of occlusion is more complex than what have been hypothesized and highlight the need for individualized management strategies to optimize outcomes in patients requiring anticoagulation post-WEB. Further studies are needed.

Obesity is a recognized risk factor for venous thromboembolism (VTE), associated with distinct challenges in managing anticoagulation therapy. There is still limited evidence regarding the impact of extreme body weight on the pharmacokinetics, pharmacodynamics, efficacy, and safety of various anticoagulant medications. To our knowledge, this is the first comprehensive review to address both prophylactic and therapeutic anticoagulant dosages specifically for managing VTE in patients with a body mass index (BMI) ≥40 kg/m2 or weight ≥120 kg. Our aim was to synthesize the findings of relevant studies alongside the latest recommendations on anticoagulation in this unique population. We gathered and analyzed data on all classes of anticoagulants available for VTE management, including vitamin K antagonists (VKAs), unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), fondaparinux, and direct oral anticoagulants (DOACs), offering insights into their efficacy and safety profiles. Additionally, we explored special subpopulations of morbidly obese patients, such as those with cancer, renal dysfunction, or those undergoing bariatric surgery, recognizing the nuanced therapeutic challenges they present. The current evidence for anticoagulant therapy in morbidly obese patients with VTE is evidently insufficient, underscoring the need for a tailored approach and meticulous monitoring to achieve an optimal therapeutic balance.

The relationship between thromboelastogram (TEG) hypercoagulation status and perioperative deep vein thrombosis (DVT) in patients with femoral and pelvic fractures is not well understood. We aimed to investigate the relationship between hypercoagulation status identified by thromboelastography and postoperative DVT formation in patients with femoral and pelvic fractures, as well as to evaluate the role of thromboelastography in assessing hypercoagulation status and predicting postoperative DVT formation.

Data from 2,065 patients with femoral and pelvic fractures who underwent surgical treatment at a hospital in China between May 2018 and December 2023 were retrospectively analysed. Hypercoagulable TEG was defined as reaction time (R) < 5 min, coagulation time (K) < 1 min, alpha angle (α) > 72 degrees, maximum amplitude (MA) > 70 mm, and/or coagulation index (CI) > 3. The correlation between preoperative hypercoagulability identified by TEG and postoperative DVT formation was assessed using multivariate logistic regression. Propensity score matching (PSM) was performed to control for confounding factors.

Compared to the non-DVT group, the DVT group had decreased R and K values, while the α, MA, and CI values significantly increased (P < 0.05). Multivariate logistic regression analysis demonstrated that hypercoagulable TEG findings were predictive of postoperative DVT formation. PSM, using a 0.1 calliper value, matched 296 patients from the hypercoagulation and non-hypercoagulation groups in a 1:1 ratio. Before PSM, hypercoagulable TEG was associated with DVT in femoral and pelvic fractures (P < 0.001, odds ratio [OR]:1.860, 95% confidence interval: 1.389-2.492). After PSM, these two variables remained correlated (P = 0.001, OR = 1.878, 95% confidence interval:1.301 - 2.709).

The hypercoagulable state identified by TEG can predict thromboembolic events in patients with femoral and pelvic fractures.

The study was registered in the Chinese Clinical Trial Register ( https://www.chictr.org.cn/bin/home ) on April 16, 2024, with registration number ChiCTR2400083135.

Venous thromboembolism (VTE) is a significant concern in vascular surgery due to its potentially severe consequences. Effective prophylactic measures are essential to minimize the risks associated with VTE. However, considerable controversy remains regarding the optimal strategies for VTE prevention in patients undergoing vascular procedures.

This review critically analyzes key clinical research, guidelines, and expert opinions to explore the advantages and limitations of various VTE prophylaxis approaches. The pharmacological and mechanical methods are explored, with a focus on balancing the risk of VTE against the potential for bleeding complications, particularly in high-risk patients.

The review addresses controversial issues such as the choice of anticoagulants, dosage, timing, and duration of prophylaxis. The lack of consensus in existing guidelines and the variability in clinical practice regarding VTE prevention in vascular surgery patients is highlighted. The role of patient-specific risk factors, including the use of intraoperative anticoagulation and bleeding risks, is also examined.

This review provides a comprehensive evaluation of VTE prophylaxis strategies in vascular surgery, emphasizing the need for individualized, evidence-based approaches. Clarifying these controversies is crucial for optimizing patient outcomes and minimizing both thrombotic and hemorrhagic complications.

The literature analysis conducted in this review discusses the latest achievements in the identification of cardiovascular damage induced by oxidative stress with secondary platelet mitochondrial dysfunction. Damage to the platelets of mitochondria as a result of their interactions with reactive oxygen species (ROS) and reactive nitrogen species (RNS) can lead to their numerous ischemic events associated with hypoxia or hyperoxia processes in the cell. Disturbances in redox reactions in the platelet mitochondrial membrane lead to the direct oxidation of cellular macromolecules, including nucleic acids (DNA base oxidation), membrane lipids (lipid peroxidation process) and cellular proteins (formation of reducing groups in repair proteins and amino acid peroxides). Oxidative changes in biomolecules inducing tissue damage leads to inflammation, initiating pathogenic processes associated with faster cell aging or their apoptosis. The consequence of damage to platelet mitochondria and their excessive activation is the induction of cardiovascular and neurodegenerative diseases (Parkinson's and Alzheimer's), as well as carbohydrate metabolism disorders (diabetes). The oxidation of mitochondrial DNA can lead to modifications in its bases, inducing the formation of exocyclic adducts of the ethano and propano type. As a consequence, it disrupts DNA repair processes and conduces to premature neoplastic transformation in critical genes such as the p53 suppressor gene, which leads to the development of various types of tumors. The topic of new innovative methods and techniques for the analysis of oxidative stress in platelet mitochondria based on methods such as a nicking assay, oxygen consumption assay, Total Thrombus formation Analysis System (T-Tas), and continuous-flow left ventricular assist devices (CF-LVADs) was also discussed. They were put together into one scientific and research platform. This will enable the facilitation of faster diagnostics and the identification of platelet mitochondrial damage by clinicians and scientists in order to implement adequate therapeutic procedures and minimize the risk of the induction of cardiovascular diseases, including ischemic events correlated with them. A quantitative analysis of the processes of thrombus formation in cardiovascular diseases will provide an opportunity to select specific anticoagulant and thrombolytic drugs under conditions of preserved hemostasis.

Acute pancreatitis, a sudden inflammatory condition, can lead to a hypercoagulable state resulting in complications such as deep vein thrombosis (DVT) or pulmonary embolism (PE). This case report discusses a unique presentation of a massive PE in a patient with acute pancreatitis despite being on appropriate prophylactic anticoagulation. A 27-year-old man presented with acute abdominal pain, nausea, and vomiting. He was diagnosed with diabetic ketoacidosis (DKA) and acute pancreatitis and admitted to the ICU. He was treated with prophylactic enoxaparin. On day 16, he experienced acute respiratory decompensation, and CT angiography revealed bilateral PEs, including a right main pulmonary artery saddle embolus. The patient underwent emergent thrombectomy with the immediate resolution of symptoms. He was transitioned to therapeutic heparin and later discharged on apixaban. A two-month follow-up showed no recurrence of PE. This case underscores the critical need to consider PE in patients with inflammatory conditions, even when on prophylactic anticoagulation. The hypercoagulable state induced by pancreatitis can overcome standard anticoagulation measures, leading to severe complications. Current guidelines may not adequately address the anticoagulation needs in such inflammatory states. Therefore, weight-based dosing of anticoagulants should be considered for patients with significant inflammation. This report highlights the necessity for vigilance in monitoring for PE in similar clinical scenarios to improve patient outcomes and inform future guidelines.

Trauma and cancer are the leading causes of death in the US. There is a paucity of data describing the impact of cancer on trauma patients. We aimed to determine the influence of cancer on outcomes of trauma patients.

In this retrospective analysis of American College of Surgeons-Trauma Quality Improvement Program 2019-2021, we included all adult trauma patients (≥18 y) and excluded patients with severe head injuries and nonmelanomatous skin cancers. Patients were stratified into cancer (C), and no cancer (No-C). Propensity score matching (1:3) was performed. Outcomes were complications and mortality.

A matched cohort of 3236 patients (C, 809; No-C, 2427) was analyzed. The mean age was 70 y, 50.5% were males, and the median injury severity score was 8 (4-10). There were no differences in terms of receiving thromboprophylaxis (C 51%: No-C 50%, P = 0.516). Compared to No-C group, the C group had higher rates of deep vein thrombosis (C 1.1% versus No-C 0.3%, P = 0.004), but there was no difference in terms of overall complications. Patients in the C group had higher mortality (C 7.5% versus No-C 2.7%, P < 0.001).

Trauma patients with cancer have nearly 4 times higher odds of deep vein thrombosis and 3 times higher odds of mortality. Developing pathways specific to cancer patients might be necessary to improve the outcomes of trauma patients with cancer.

Patients with severe mitral stenosis (MS) in normal sinus rhythm (NSR), presenting with left atrial appendage (LAA) inactivity and associated left atrial spontaneous echo contrast (LASEC) are prone to left atrium (LA) or LAA thrombus formation. But unlike for atrial fibrillation, oral anticoagulants are not commonly prescribed for this patient subset. This study aimed to compare the levels of procoagulants and fibrinogen in both local (LA) and systemic contexts between patients with severe MS in NSR vs those in healthy control subjects.

The study involved 35 patients with severe MS in NSR with LAA inactivity and LASEC who were eligible for balloon mitral valvuloplasty vs 35 healthy controls. All patients underwent transthoracic and transesophageal echocardiography to assess MS severity, LAA activity, and LASEC grade, and had blood samples analyzed for procoagulant levels.

Results showed comparable baseline characteristics between groups, with most patients in the New York Heart Association II or III functional classes, and with varying LASEC grades. Patients exhibited significantly higher levels of prothrombin fragment 1 + 2 [patient vs control, 9017 pg/mL (6228.0-10,963.5) vs 1790 pg/mL (842.3-2712), P < 0.0001], thrombin-antithrombin III [patient vs control, 39 ng/mL (5.45-74.85) vs 2.80 ng/mL (1.6-6.5), P < 0.0001], plasminogen activator inhibitor-1 (patients vs controls, 26.09 ± 8.18 ng/mL vs 8.05 ± 3.53 ng/mL, P < 0.0001), and fibrinogen (3.48 ± 0.89 g/L vs 3.01 ± 0.53 g/L, P = 0.029) in the LA of patients, compared to those in control subjects. Systemic procoagulant levels also were elevated in patients, but D-dimer levels were similar between the 2 groups.

The findings suggest a hypercoagulable state in patients, similar to that in patients with atrial fibrillation. The study advocates for consideration of use of oral anticoagulants in these patients until LA and LAA function improves, to mitigate thrombus formation.

Deep vein thrombosis (DVT) is a critical complication and concern in hospitalized patients due to its significant morbidity and mortality. Given the complex and multifaceted pathophysiology surrounding DVT formation, patients who have had surgical interventions faced acute or chronic trauma and prolonged immobility are at substantially high risk. Identifying these risk factors early is essential for early intervention and prophylaxis. Current standard-of-care prophylaxis for DVT includes pharmacological agents such as anticoagulants, and recently, there has been an increase in the use of mechanical medical devices such as sequential compression devices (SCDs). Pharmacological prophylaxis, while shown to be effective in some patients, carries certain risks of complications such as bleeding. SCDs offer a safer and more effective approach for these patients. SCDs function by artificially replicating the "pumping mechanism" present in the soleus muscle to enhance venous return and reduce stasis. Various types of SCDs, namely intermittent pneumatic compression and graduated compression stockings, have demonstrated clinical efficacy when used as an adjunctive intervention with anticoagulant medications. This narrative review explores the pathophysiology, risk factors, and prophylactic measures for DVT, focusing on the use of SCDs as a non-pharmacological intervention. Through synthesizing evidence from various studies obtained from PubMed, MEDLINE, and Cochrane Library and evaluating the benefits and limitations of SCD use, this review highlights the need for tailored prophylactic strategies, considering patient-specific risk factors and preferences.

Pulmonary embolism (PE), the most serious presentation of venous thromboembolism (VTE), is associated with a high rate of mortality and expense. Clinical studies on pregnant women with PE are scarce. The aim of this study was to analyze the clinical impact of fibrinolytic enzyme activation inhibitor-1 (PAI-1) 4G/5G genetic polymorphisms, methylenetetrahydrofolate reductase (MTHFR) rs1801131 (A1298C) and rs1801133 (C677T) genetic polymorphisms, and establish a predictive model for pregnant women.

Between September 2022 and August 2023, 53 pregnant women with PE were enrolled. Using the propensity score matching method, 106 consecutive pregnant women without VTE were 1:2 matched. The relevant patient data were collected, and the susceptibility genes for PE were detected to determine genetic polymorphisms, and PE susceptibility in pregnant women, as well as to develop predictive models.

Our study showed that 4G/4G homozygous mutations increased the risk of pregnant PE fourfold (OR = 4.46, 95% CI = 1.59-12.50, P = 0.004), whereas the 4G allele mutation increased the risk twofold (OR = 2.33, 95% CI = 1.35-4.04, P = 0.002). A nomogram was established to predict the risk of pregnant women with PE by four predictive features including PAI-1 genetic polymorphisms, international normalized ratio (INR), antithrombin-III (AT-III) activity, and platelet count (PLT). The area under the curve (AUC) of the nomogram was 0.821 (0.744-0.898). The AUC of the internal validation group was 0.822 (0.674-0.971). Decision curve analysis revealed that the nomogram has a higher net benefit in the following threshold: probability interval of ≥15%.

The PAI-1 4G/4G genotype is an independent risk factor for pregnant women with PE; furthermore, the presence of the 4G allele can increase the risk of PE. The study established a nomogram to predict the risk of PE in pregnant women.

Virchow's law of thrombosis states that thrombosis in a vessel occurs as a combination of the following: (i) injury to the vessel wall, (ii) stasis of blood flow, and (iii) blood hypercoagulability. Injury to the wall includes infection/inflammation and/or injury to the resident cells of the wall. We postulate that in COVID-19, the SARS-CoV-2 virus directly infects the alveolar type II cell or directly or indirectly infects/injures the pericyte, promoting inflammation and interaction with endothelial cells, thereby causing a cascade of events leading to our observation that thrombosis occurred within the walls of the pulmonary vessels and not in the lumen of the vascular circulation.

A retrospective clinical study with confirmatory evaluation in healthy volunteers.

To investigate the association between deep vein thrombosis (DVT) and surgical position after cervical spine surgery.

It is unclear whether posterior cervical surgery using the prone position increases the risk of postoperative DVT relative to anterior cervical surgery.

A total of 340 patients undergoing surgery for degenerative cervical myelopathy were included. Multivariate analysis was used to identify the predictors of postoperative DVT, adjusting for potential confounders. In addition, 45 healthy volunteers were used to study the blood flow velocity and intravascular diameter of the posterior tibial vein (PTV) and popliteal vein (PV) of the subjects, which were monitored by ultrasound and compared among three positions (supine, prone, and prone with iliac cushions).

Multivariate analysis showed that advanced age (above 63.5 yr old), preoperative varicose veins, D-dimer >0.255 mg/L, bleeding volume >303 mL, and prone positioning were significantly associated with DVT after cervical spine surgery. The results of vascular ultrasound showed that the blood flow velocities of the PV and PTV in the prone position with cushions were significantly lower than those in the supine position. The diameter of PV in the prone position with cushions was also significantly larger. The blood flow velocity and diameter of PV in the prone position with cushions were significantly lower and larger, respectively, than those in the prone position without cushions.

Posterior cervical surgery in the prone position was significantly associated with postoperative DVT. The prone position with iliac cushions may decrease venous flow within the lower extremities due to compression of the iliac veins, obstructing venous return and thus increasing the incidence of postoperative DVT. The prone position without iliac cushions may reduce the potential for DVT.

3.

Rudolf Virchow, also known as Rudolf Carl Virchow, was a physician, pathologist, medical scientist, anthropologist, politician, social reformer, and role model. However, he is best known as the founder of the field of cellular pathology. He is known as "the father of modern pathology" and the founder of social medicine. He was born on October 13, 1821, in Prussia (now Swidwin, Poland) and died on September 5, 1902, in Berlin, Germany. He stressed that most diseases of mankind can be understood in terms of the dysfunction of cells. His study subjects were cell theory, disease, embolus, and thrombosis. He actively promoted social reforms and helped establish anthropology as a contemporary scientific field. He was also awarded and honored by the Copley Medal in 1892 for his notable work in "Cellular Pathology as Based Upon Physiological and Pathological Histology" and "Handbuch der Speziellen Pathologie und Therapie." Virchow said, "Medicine is a social science, and politics is nothing more than medicine on a grand scale." He believed that politics and social structures could have a significant positive or negative impact on public health, that medicine and public health practices used politically might change society, and that politicians and doctors had a moral duty to improve society. Knowing about Virchow helps us appreciate his ideas that laid the groundwork for many medical and scientific practices, the historical development of medical science, and the ongoing need to address social health factors. Virchow's contributions are still relevant in today's medical and public health fields. His work on cellular pathology forms the basis for many aspects of contemporary medicine, such as cancer, infectious diseases, and genetic disorders. His focus on social determinants of health remains a core principle in public health. Today, issues such as poverty, education, housing, and nutrition are acknowledged as factors affecting health outcomes. Virchow's beliefs in ethical responsibility, social transformation, and justice have affected medical ethics and the role of health professionals in society. This article highlights Rudolf Virchow's enormous contribution to pathology, medicine, and public health.

Blood volume shifts during postural adjustment lead to irregular distension of the internal jugular vein (IJV). In microgravity, distension may contribute to flow stasis and thromboembolism, though the regional implications and associated risk remain unexplored. We characterized regional differences in IJV volume distension and flow complexity during progressive head-down tilt (HDT) (0°, -6°, -15°, -30°) using conventional ultrasound and vector flow imaging. We also evaluated low-pressure thigh cuffs (40 mmHg) as a fluid shifting countermeasure during -6° HDT. Total IJV volume expanded 139 ± 95% from supine position (4.6 ± 2.7 mL) to -30° HDT (10.3 ± 5.0 mL). Blood flow profiles had greater vector uniformity at the cranial IJV region (P < 0.01) and became more dispersed with increasing tilt (P < 0.01). Qualitatively, flow was more uniform throughout the IJV during its early flow cycle phase and more disorganized during late flow phase. This disorganized flow was accentuated closer to the vessel wall, near the caudal region, and during greater HDT. Low-pressure thigh cuffs during -6° HDT decreased IJV volume at the cranial region (-12 ± 15%; P < 0.01) but not the caudal region (P = 0.20), although flow uniformity was unchanged (both regions, P > 0.25). We describe a distensible IJV accommodating large volume shifts along its length. Prominent flow dispersion was primarily found at the caudal region, suggesting multidirectional blood flow. Thigh cuffs appear effective for decreasing IJV volume but effects on flow complexity are minor. Flow complexity along the vessel length is likely related to IJV distension during chronic volume shifting and may be a precipitating factor for flow stasis and future thromboembolism risk.NEW & NOTEWORTHY The internal jugular vein (IJV) facilitates cerebral outflow and is sensitive to volume shifts. Concerns about IJV expansion and fluid flow behavior in astronauts have surfaced following thromboembolism reports. Our study explored regional volume distension and blood flow complexity in the IJV during progressive volume shifting. We observed stepwise volume distension and increasing flow dispersion with head-down tilting across all regions. Flow dispersion may pose a risk of future thromboembolism during prolonged volume shifts.

Pancreatic ductal adenocarcinoma (PDAC) accounts for more than 90% of all pancreatic cancers and is the most fatal of all cancers. The treatment response from combination chemotherapies is far from satisfactory and surgery remains the mainstay of curative strategies. These challenges warrant identifying effective treatments for combating this deadly cancer. PDAC tumor progression is associated with the robust activation of the coagulation system. Notably, cancer-associated thrombosis (CAT) is a significant risk factor in PDAC. CAT is a concept whereby cancer cells promote thromboembolism, primarily venous thromboembolism (VTE). Of all cancer types, PDAC is associated with the highest risk of developing VTE. Hypoxia in a PDAC tumor microenvironment also elevates thrombotic risk. Direct oral anticoagulants (DOACs) or low-molecular-weight heparin (LMWH) are used only as thromboprophylaxis in PDAC. However, a precision medicine approach is recommended to determine the precise dose and duration of thromboprophylaxis in clinical setting.

Anesthesia management of patients with dilated cardiomyopathy (DCM) has always been a challenge for anesthesiologists. Eighty percent of patients with DCM have heart failure as the first symptom, which may be accompanied by arrhythmias, thromboembolism, etc. Thrombosis is a significant contributing factor to adverse cardiovascular and cerebrovascular events, and its risk is severely underestimated in the anesthetic management of DCM.

We present a case of a 54-year-old hypersensitive female patient with dilated cardiomyopathy and purpura who underwent an interventional thrombectomy under general anesthesia following a lower limb thromboembolism.

Patient underwent an interventional thrombectomy under general anesthesia, with in situ thrombosis occurring during the surgery.

After maintaining stable hemodynamics, proceed with the intervention to retrieve the embolus.

Patients in the advanced DCM developed acute thrombosis twice during embolization.

This case discusses the causes of intraoperative thrombosis and summarizes and reflects on the anesthesia management of this case, which has always been one of the difficult points for anesthesiologists to master. In the anesthesia management of DCM patients, it is also necessary to maintain hemodynamic stability, enhance perioperative coagulation management, use anticoagulants rationally, and avoid the occurrence of thrombotic events.

Carotid artery webs (CaW) are non-atherosclerotic projections into the vascular lumen and have been linked to up to one-third of cryptogenic strokes in younger patients. Determining how CaW affects local hemodynamics is essential for understanding clot formation and stroke risk. Computational fluid dynamics simulations were used to investigate patient-specific hemodynamics in carotid artery bifurcations with CaW, bifurcations with atherosclerotic lesions having a similar degree of lumen narrowing, and with healthy carotid bifurcations. Simulations were conducted using segmented computed tomography angiography geometries with inlet boundary conditions extracted from 2D phase contrast MRI scans. The study included carotid bifurcations with CaW (n = 13), mild atherosclerosis (n = 7), and healthy bifurcation geometries (n = 6). Hemodynamic parameters associated with vascular dysfunction and clot formation, including shear rate, oscillatory shear index (OSI), low velocity, and flow stasis were calculated and compared between the subject groups. Patients with CaW had significantly larger regions containing low shear rate, high OSI, low velocity, and flow stasis in comparison to subjects with mild atherosclerosis or normal bifurcations. These abnormal hemodynamic metrics in patients with CaW are associated with clot formation and vascular dysfunction and suggest that hemodynamic assessment may be a tool to assess stroke risk in these patients.

Peripheral intravenous catheters (PIVCs) are the most commonly used invasive medical device, yet despite best efforts by end-users, PIVCs experience unacceptably high early failure rates. We aimed to design a new PIVC that reduces the early failure rate of in-dwelling PIVCs and we conducted preliminary tests to assess its efficacy and safety in a porcine model of intravenous access.

We used computer-aided design and simulation to create a PIVC with a ramped tip geometry, which directs the infused fluid away from the vein wall; we called the design the FloRamp™. We created FloRamp prototypes (test device) and tested them against a market-leading device (BD Insyte™; control device) in a highly-controlled setting with five insertion sites per device in four pigs. We measured resistance to infusion and visual infusion phlebitis (VIP) every 6 h and terminated the experiment at 48 h. Veins were harvested for histology and seven pathological markers were assessed.

Computer simulations showed that the optimum FloRamp tip reduced maximum endothelial shear stress by 60%, from 12.7 Pa to 5.1 Pa, compared to a typical PIVC tip and improved the infusion dynamics of saline in the blood stream. In the animal study, we found that 2/5 of the control devices were occluded after 24 h, whereas all test devices remained patent and functional. The FloRamp created less resistance to infusion (0.73 ± 0.81 vs 0.47 ± 0.50, p = 0.06) and lower VIP scores (0.60 ± 0.93 vs 0.31 ± 0.70, p = 0.09) than the control device, although neither findings were significantly different. Histopathology revealed that 5/7 of the assessed markers were lower in veins with the FloRamp.

Herein we report preliminary assessment of a novel PIVC design, which could be advantageous in clinical settings through decreased device occlusion and reduced early failure rates.

Pulmonary embolism (PE) is the third most common cause of cardiovascular death. Every specialty of medical practitioner will encounter PE in their patients, and should be prepared to employ contemporary strategies for diagnosis and initial risk-stratification. Treatment of PE is based on risk-stratification, with anticoagulation for all patients, and advanced modalities including systemic thrombolysis, catheter-directed therapies, and mechanical circulatory supports utilized in a manner paralleling PE severity and clinical context.

Venous thromboembolism (VTE) is a massive clinical challenge, annually affecting millions of patients globally. VTE is a particularly consequential pathology, as incidence is correlated with extremely common risk factors, and a large cohort of patients experience recurrent VTE after initial intervention. Altered hemodynamics, hypercoagulability, and damaged vascular tissue cause deep-vein thrombosis and pulmonary embolism, the two permutations of VTE. Venous valves have been identified as likely locations for initial blood clot formation, but the exact pathway by which thrombosis occurs in this environment is not entirely clear. Several risk factors are known to increase the likelihood of VTE, particularly those that increase inflammation and coagulability, increase venous resistance, and damage the endothelial lining. While these risk factors are useful as predictive tools, VTE diagnosis prior to presentation of outward symptoms is difficult, chiefly due to challenges in successfully imaging deep-vein thrombi. Clinically, VTE can be managed by anticoagulants or mechanical intervention. Recently, direct oral anticoagulants and catheter-directed thrombolysis have emerged as leading tools in resolution of venous thrombosis. While a satisfactory VTE model has yet to be developed, recent strides have been made in advancing in silico models of venous hemodynamics, hemorheology, fluid-structure interaction, and clot growth. These models are often guided by imaging-informed boundary conditions or inspired by benchtop animal models. These gaps in knowledge are critical targets to address necessary improvements in prediction and diagnosis, clinical management, and VTE experimental and computational models.

The potentially fatal consequences of pulmonary embolism emphasize the need for more effective diagnostic methods. The Qanadli obstruction index has been described as a convenient tool for risk stratification to determine and quantify the degree of obstruction. This study aimed to assess the correlations between the Qanadli index with clinical and paraclinical findings (D-dimer, troponin, and echocardiographic findings) in patients with pulmonary embolism.

A total of 102 patients with pulmonary embolism underwent echocardiography and CT pulmonary angiography at a single tertiary referral center between 2019 and 2020. The clinical and paraclinical findings, pulmonary arterial obstruction index, atrial measurements, right and left ventricle size and function, tricuspid annular plane systolic excursion, pulmonary artery pressure, and pulmonary hypertension (PH) were analyzed. Vital signs were recorded and assessed. The Qanadli index score was measured, and graded risk stratification was measured based on the quantified index score.

The total mean Qanadli index was 28.75 ± 23.75, and there was no significant relationship between the Qanadli index and gender. Patients' most common clinical findings were exertional dyspnea (84.3%; n = 86) and chest pain (71.7%; n = 73). There were significant correlations between the Qanadli index and pulse rate (PR), troponin, D-dimer levels, and PH. Four patients died during the study, including one from a cardiac condition and three with non-cardiac conditions.

It is possible to determine the severity, prognosis, and appropriate treatment by the Qanadli index based on strong correlations with PR, troponin, D-dimer levels, and PH.

Patients undergoing oncologic resection are at risk of developing venous thromboembolism (VTE), and this can lead to increased morbidity and hospital costs. Low-molecular weight heparin (LMWH) is recommended as extended thromboprophylaxis (ETP) in high-risk patients and has been shown to reduce rates of VTE.

This is a retrospective review of consecutive patients undergoing resection for oncologic indications at a single institution from May 2016 to May 2019. This study evaluated the use of apixaban as ETP at discharge. The primary outcomes were deep vein thrombosis (DVT), pulmonary embolism (PE), or mesenteric/portal venous thromboembolism at 30, 60, and 90 days postoperatively.

A total of 600 patients were included; 449 patients received no ETP, and 151 patients received apixaban. PE occurred in 1.1, 1.6, and 2.3% of patients without ETP and 0, 0, and .7% of patients in the apixaban group (at 30, 60, and 90 days; P = .338, P = .201, and P = .306, respectively). DVT occurred in 1.8, 2.1, and 2.8% of patients without ETP and 0, 0, and 1.4% in the apixaban group (P = .211, P = .121, and P = .535, respectively). The total cost, including ETP and readmission for VTE, per patient was US $5.51 more in the apixaban group.

Apixaban therapy for ETP did not produce a statistically significant reduction in VTE events in our patients. Future studies should include more patients in a prospective multicenter trial.

Cancer is associated with an increased risk of developing venous thromboembolism, due to its direct influence on the three pillars of Virchow's triad (e.g., compression on the blood vessels by the tumour, blood vessels invasion, and cytokine release), together with the effect of exogenous factors (such as chemotherapy, radiotherapy, surgery). In cancer patients, the risk of thrombosis at unusual sites, such as splanchnic, ovarian and renal vein thrombosis, is also increased. Abdominal vein thromboses are frequently incidental findings on abdominal imaging performed as part of the diagnostic/staging workup or the follow-up care of malignancies. There is little evidence on the management of unusual site venous thromboembolism in cancer patients since there are only a few specific recommendations; thus, the management follows the general principles of the treatment of cancer-associated deep vein thrombosis and pulmonary embolism. This narrative review summarises the latest evidence on cancer-associated abdominal vein thrombosis, i.e., thrombosis of the splanchnic, ovarian and renal veins.

Venous thrombosis (VT) is multifactorial trait that contributes to the global burden of cardiovascular diseases. Although abundant single nucleotide polymorphisms (SNPs) provoke the susceptibility of an individual to VT, research has found that the five most strongly associated SNPs, namely, rs6025 (F5 Leiden), rs2066865 (FGG), rs2036914 (F11), rs8176719 (ABO), and rs1799963 (F2), play the greatest role. Association and risk prediction models are rarely established by using merely the five strongly associated SNPs. This study aims to explore the combined VT risk predictability of the five SNPs and well-known non-genetic VT risk factors such as aging and obesity in the Hungarian population.

SNPs were genotyped in the VT group (n = 298) and control group (n = 400). Associations were established using standard genetic models. Genetic risk scores (GRS) [unweighted GRS (unGRS), weighted GRS (wGRS)] were also computed. Correspondingly, the areas under the receiver operating characteristic curves (AUCs) for genetic and non-genetic risk factors were estimated to explore their VT risk predictability in the study population.

rs6025 was the most prevalent VT risk allele in the Hungarian population. Its risk allele frequency was 3.52-fold higher in the VT group than that in the control group [adjusted odds ratio (AOR) = 3.52, 95% CI: 2.50-4.95]. Using all genetic models, we found that rs6025 and rs2036914 remained significantly associated with VT risk after multiple correction testing was performed. However, rs8176719 remained statistically significant only in the multiplicative (AOR = 1.33, 95% CI: 1.07-1.64) and genotypic models (AOR = 1.77, 95% CI: 1.14-2.73). In addition, rs2066865 lost its significant association with VT risk after multiple correction testing was performed. Conversely, the prothrombin mutation (rs1799963) did not show any significant association. The AUC of Leiden mutation (rs6025) showed better discriminative accuracy than that of other SNPs (AUC = 0.62, 95% CI: 0.57-0.66). The wGRS was a better predictor for VT than the unGRS (AUC = 0.67 vs. 0.65). Furthermore, combining genetic and non-genetic VT risk factors significantly increased the AUC to 0.89 with statistically significant differences (Z = 3.924, p < 0.0001).

Our study revealed that the five strongly associated SNPs combined with non-genetic factors could efficiently predict individual VT risk susceptibility. The combined model was the best predictor of VT risk, so stratifying high-risk individuals based on their genetic profiling and well-known non-modifiable VT risk factors was important for the effective and efficient utilization of VT risk preventive and control measures. Furthermore, we urged further study that compares the VT risk predictability in the Hungarian population using the formerly discovered VT SNPs with the novel strongly associated VT SNPs.

A small percentage of acute pulmonary thromboembolisms (PTE) persist as chronic fibrin clots, potentially leading to chronic thromboembolic pulmonary hypertension (CTEPH). A scoring system for evaluating the burden of acute PTE based on computed tomography pulmonary angiogram (CTPA) findings was tested for its association with CTEPH within one year.

In this retrospective cohort of 475 patients with a definitive diagnosis of acute PTE, the Qanadli score (QS) was calculated on the initial CTPA. Through regular follow-up over 1 year, symptomatic patients underwent extensive evaluation.

Of the 475 patients enrolled in the study [age 58.3 ± 16.6, 195 (41.1%) female, QS: 13.01 ± 7.37/40], 321 patients completed the study. A total of 22 (6.8%) patients were definitively diagnosed with CTEPH. In univariate analysis, the initial QS was significantly higher in patients with subsequent CTEPH than in patients without (17 ± 5.6 vs. 13 ± 7.6, P = .009). QS was directly associated with CTEPH (odds ratio: 1.08, 95% confidence interval: 1.0-1.16, P = .042). The evolution of CTEPH in men could be predicted with a sensitivity of 100% and a specificity of 54% when a cut-off point of 14.5 (43.5%) was set for QS. The area under the receiver operating characteristic curve in this setting was 0.74 with a P-value of .032. Qanadli score failed to predict CTEPH in women.

Scoring the clot burden in the pulmonary arteries through the Qanadli method can predict the evolution of CTEPH only in men 1 year after acute PTE. Women comprise most of the CTEPH patients. Thus, strict follow-up adherence seems to be even more important in women.

Thrombolytic and antithrombotic therapies are limited by short circulation time and the risk of off-target hemorrhage. Integrating a thrombus-homing strategy with photothermal therapy are proposed to address these limitations. Using glycol chitosan, polypyrrole, iron oxide and heparin, biomimicking GCPIH nanoparticles are developed for targeted thrombus delivery and thrombolysis. The nanoassembly achieves precise delivery of polypyrrole, exhibiting biocompatibility, selective accumulation at multiple thrombus sites, and enhanced thrombolysis through photothermal activation. To simulate targeted thrombolysis, a microfluidic model predicting thrombolysis dynamics in realistic pathological scenarios is designed. Human blood assessments validate the precise homing of GCPIH nanoparticles to activated thrombus microenvironments. Efficient near-infrared phototherapeutic effects are demonstrated at thrombus lesions under physiological flow conditions ex vivo. The combined investigations provide compelling evidence supporting the potential of GCPIH nanoparticles for effective thrombus therapy. The microfluidic model also offers a platform for advanced thrombolytic nanomedicine development.

Continuous advances in prehabilitation research over the past several decades have clarified its role in improving preoperative risk factors, yet the evidence demonstrating reduced surgical complications remains uncertain. Describing the potential mechanisms underlying prehabilitation and surgical complications represents an important opportunity to establish biological plausibility, develop targeted therapies, generate hypotheses for future research, and contribute to the rationale for implementation into the standard of care. In this narrative review, we discuss and synthesize the current evidence base for the biological plausibility of multimodal prehabilitation to reduce surgical complications. The goal of this review is to improve prehabilitation interventions and measurement by outlining biologically plausible mechanisms of benefit and generating hypotheses for future research. This is accomplished by synthesizing the available evidence for the mechanistic benefit of exercise, nutrition, and psychological interventions for reducing the incidence and severity of surgical complications reported by the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP). This review was conducted and reported in accordance with a quality assessment scale for narrative reviews. Findings indicate that prehabilitation has biological plausibility to reduce all complications outlined by NSQIP. Mechanisms for prehabilitation to reduce surgical complications include anti-inflammation, enhanced innate immunity, and attenuation of sympathovagal imbalance. Mechanisms vary depending on the intervention protocol and baseline characteristics of the sample. This review highlights the need for more research in this space while proposing potential mechanisms to be included in future investigations.

Biological applications of microfluidics technology is beginning to expand beyond the original focus of diagnostics, analytics and organ-on-chip devices. There is a growing interest in the development of microfluidic devices for therapeutic treatments, such as extra-corporeal haemodialysis and oxygenation. However, the great potential in this area comes with great challenges. Haemocompatibility of materials has long been a concern for blood-contacting medical devices, and microfluidic devices are no exception. The small channel size, high surface area to volume ratio and dynamic conditions integral to microchannels contribute to the blood-material interactions. This review will begin by describing features of microfluidic technology with a focus on blood-contacting applications. Material haemocompatibility will be discussed in the context of interactions with blood components, from the initial absorption of plasma proteins to the activation of cells and factors, and the contribution of these interactions to the coagulation cascade and thrombogenesis. Reference will be made to the testing requirements for medical devices in contact with blood, set out by International Standards in ISO 10993-4. Finally, we will review the techniques for improving microfluidic channel haemocompatibility through material surface modifications-including bioactive and biopassive coatings-and future directions.