The cardiovascular system
C. Simon Herrington in Muir's Textbook of Pathology, 2020
Thrombosis occurs most commonly in veins but can also occur in arteries. The risk of thrombosis is increased by (1) alterations in blood flow, (2) alterations in blood constituents that increase coagulability (e.g. thrombocytosis), and (3) injury to the vascular endothelium – known as Virchow's triad. In rapidly flowing blood, vascular injury results in the formation of platelet-rich thrombus, which grows by accretion of activated platelets and fibrin. Where the vessel is occluded, the blood flow slows and traps red blood cells to form red thrombus. This extends as far as the next branch, where flowing blood will deposit pale thrombus, which in turn will lead to further occlusion. This process is called propagation (Figure 7.9). In veins the blood flow is so slow that the thrombus consists mostly of red thrombus.
Orthopaedic operations
Ashley W. Blom, David Warwick, Michael R. Whitehouse in Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Venous thromboembolism (VTE) is one of the commonest complications of lower limb surgery. It comprises three associated disorders: deep vein thrombosis (DVT), pulmonary embolism (PE) and the later complication of chronic venous insufficiency in some cases. Approximately one in 30–40 patients operated on for hip fractures or hip and knee replacements will develop a symptomatic thromboembolic complication despite the use of prophylaxis during their hospital stay. The most important risk factors are increasing age, obesity, prolonged immobility, malignancy and in particular a personal or family history of previous thrombosis.
Thrombophilia
Efstratios M. Kolibianakis, Christos A. Venetis in Recurrent Implantation Failure, 2019
Thrombosis describes the clotting of blood inside the vessels. Thrombophilia is a condition where the blood has an elevated tendency to form clots (hypercoagulability). The origin of thrombosis was described in 1856 by the Virchow triad, which includes endothelial injury, hypercoagulability, and stasis. Clots usually appear in the venous vessels (e.g., deep vein thrombosis), while their circulation in the blood system can lead to pulmonary embolism. Arterial thrombosis can cause myocardial infarction, apoplectic stroke or in the case of the antiphospholipid syndrome, habitual abortion. Thrombophilia can either be acquired or inherited (Table 8.1). The cause of thrombophilia determines the risk of thrombosis. During a women's reproductive years, lifetime venous thromboembolism (VTE) is a major cause for morbidity and mortality. Its mean incidence ranges from 2/10,000 during the mid-teens to 1/1000 at 50 years of age. Estrogens enhance the risk for VTE, which explains the four-fold increase in relative risk with the use of oral contraceptives (7/10,000) and the increased incidence of VTEs in pregnancy (20/10,000). About 30% of patients with an event of VTE will develop reoccurrence in the next 10 years.
Risk Factors and Clinical Course of Portal and/or Splenic Vein Thrombosis after Partial Splenic Embolization
Published in Acta Radiologica, 2009
Tomohiro Matsumoto, Takuji Yamagami, Koshi Terayama, Takeharu Kato, Tatsuya Hirota, Rika Yoshimatsu, Hiroshi Miura, Hirotoshi Ito, Takeshi Okanoue, Tsunehiko Nishimura
Background: Although portal and/or splenic vein thrombosis after partial splenic embolization (PSE) is a well-known complication, few reports evaluating risk factors have been published. Purpose: To investigate risk factors and clinical course of portal and/or splenic vein thrombosis after PSE. Material and Methods: Sixteen patients with severe hypersplenism underwent PSE between March 2005 and April 2008. The correlation between portal and/or splenic vein thrombosis after PSE detected on multidetector row CT (MDCT) and various factors were retrospectively reviewed. Further, the clinical course of portal and/or splenic vein thrombosis after PSE was observed on follow-up MDCT. Results: Splenic vein thrombosis was detected in eight patients (50%) on MDCT images taken within 9 days after PSE. In one, the thrombosis also involved the portal vein. The infarct volume was identified as a significant risk factor for portal and/or splenic vein thrombosis (P=0.046). In all but one patient, splenic vein thrombosis resolved completely or improved without anticoagulation therapy. In this patient, both portal and splenic vein thrombosis developed after PSE, and anticoagulation therapy was necessary. Conclusion: It is suggested that a large splenic infarct volume is a risk factor for portal and/or splenic vein thrombosis after PSE. Indications for treatment of thrombosis of the portal vein system after PSE may be limited to patients with portal vein thrombosis.
Antiplatelet therapy in the era of drug-eluting stents: current and future perspectives
Published in Expert Review of Cardiovascular Therapy, 2007
Gregory Ducrocq, Victor Serebruany, Jean-Francois Tanguay
The use of drug-eluting stents (DESs) dramatically reduced in-stent restenosis. However, the increasing use of these stents has raised concern about their potential thrombogenicity. Indeed, the particularity of DES thrombosis compared with bare metal stent thrombosis is a high rate of late thrombosis. Antiplatelet therapy is efficient in preventing DES thrombosis. However, this therapy could be optimized and may be improved in the future. This article will review the mechanisms and the epidemiology of stent thrombosis. Then, we will summarize the antiplatelet therapeutic strategies used to prevent stent thrombosis and especially DES-associated thrombosis. Finally, we will present some data with regard to potential advantages and pitfalls in DES thrombosis prevention using novel antiplatelet agents currently under development, as well as future stent designs with improved healing properties.
Impaired responsiveness to clopidogrel and aspirin in patients with recurrent stent thrombosis following percutaneous intervention for peripheral artery disease
Published in Platelets, 2013
Piotr Mazur, Marzena Frołow, Rafał Niżankowski, Jerzy Sadowski, Anetta Undas
Patients with peripheral artery disease (PAD) following peripheral percutaneous transluminal angioplasty (PTA) with stent implantation are prone to stent thrombosis despite treatment with aspirin and clopidogrel. Impaired clopidogrel responsiveness is associated with increased risk of ischemic events in patients following coronary stent implantation. We sought to assess platelet responsiveness to clopidogrel and aspirin in patients with PAD and recurrent stent thrombosis. Platelet aggregation induced by 5 and 20 µmol/l adenosine diphosphate (ADP) and 0.5 mmol/l arachidonic acid (AA), together with platelet reactivity index (PRI) and serum thromboxane B2 (TXB2), were determined in 11 patients with PAD and a history of stent thrombosis (mean, 3.1 ± 1.14) after PTA and in 15 patients with PAD with no such history, also in 11 controls with coronary artery disease (CAD) and previous stent thrombosis. Platelet aggregation to 5 µmol/l ADP was higher in subjects with PAD and stent thrombosis than in those without stent thrombosis (p = 0.0003) and CAD subjects (p = 0.002). Aggregation induced by 20 µmol/l ADP was higher in PAD group with stent thrombosis than in PAD subjects without thrombosis (p = 0.004). The PAD group with stent thrombosis had higher AA-induced platelet aggregation than CAD controls (p = 0.007) and serum TXB2 concentrations higher than PAD group without thrombosis (p = 0.002) and CAD group (p = 0.02). Concluding, platelet responsiveness to clopidogrel and aspirin is impaired in patients with PAD and recurrent stent thrombosis following PTA, as compared with similar individuals with CAD, and PAD with no history of stent thrombosis. This indicates that atherosclerosis burden affects platelet function and might contribute to stent thrombosis following percutaneous intervention in peripheral arteries.