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Arterial Thrombosis—Diagnosis and Management
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
H. Patrick McNeil, Steven A. Krilis, Colin N. Chesterman
This chapter will be divided into three sections. First we will discuss the various situations in which aPL-associated arterial thromboembolism occurs. It appears that the presence of aPL characterizes a group of people, some of whom have a prothrombotic diathesis, and are at risk of spontaneous vascular thrombosis, usually in the absence of other vascular disease. More recently, an association between aPL in the presence of pre-existing vascu-lopathy such as ischemic heart disease has been found suggesting a role for these antibodies as an additional risk factor in progression of the underlying disease. Second, diagnostic considerations will be discussed and finally, the management of arterial thromboembolism will be reviewed, both with respect to management of the acute event and prevention of recurrences.
The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
A sudden critical decrease in blood supply to the intestines threatens the viability of the bowel and the life of the patient. The most common cause is arterial thromboembolism, followed by in situ thrombus formation and non-occlusive vascular disease. Cellular injury is caused by anoxia and also often by reperfusion injury, in a manner analogous to that seen in the myocardium (see Chapter 7). The clinical features and severity of injury depend on the depth of intestinal damage. If infarction is confined to the mucosa, then complete regeneration is possible. Submucosal extension (mural infarction) can lead to fibrous stricture. Transmural infarction (gangrene) will lead to perforation if not surgically resected. Even before perforation, septicaemia may ensue as a result of unimpeded invasion by bacteria from the bowel lumen.
Management problems
Published in Brian J Pollard, Gareth Kitchen, Handbook of Clinical Anaesthesia, 2017
The source of arterial thromboembolism is often the heart. The majority of emboli of cardiac origin are the result of atrial fibrillation, particularly when this is associated with mitral stenosis or thyrotoxicosis. Other predisposing conditions include prosthetic heart valves, recent myocardial infarction with mural thrombus formation and low cardiac output states. Cardiac emboli may travel peripherally, or more commonly to the cerebral circulation, producing a stroke. NICE guidelines recommend that the majority of patients will benefit from anticoagulation (similarly to VTE, the risk of bleeding and the risk of stroke must be assessed and considered). Heparin is used initially, followed by long-term treatment with apixaban, dabigatran, rivaroxaban or warfarin.
Association of PC and AT levels in the early phase of STEMI treated with pPCI with LV systolic function and 6-month MACE
Published in Acta Clinica Belgica, 2021
Slobodan Obradovic, Edin Begic, Slobodan Jankovic, Radoslav Romanovic, Nemanja Djenic, Boris Dzudovic, Zoran Jovic, Dragana Malovic, Vesna Subota, Milena Stavric, Farid Ljuca, Zumreta Kusljugic
The question remains which stimulus leads to increased PC activity after STEMI. Our assumption is that increased PC activity can be triggered as a response to a thrombogenic process, that is, by an extensiveness of the thrombogenic process. Releasing increased levels and/or activity of PC can be a response to STEMI, and it may represent a protective mechanism against atherothrombosis. The idea of the potential benefit of recombinant PC in the treatment of no-reflow phenomena and reperfusion injury after STEMI may emerge from this research, but more research is needed to confirm this. Therefore, our study warrants further studies to be conducted in order to understand the molecular mechanisms of PC secretion in STEMI. It would be important to determine whether there exists an association between the risk factors for venous thromboembolism and the risk factors for arterial thromboembolism, which would lead to more optimized treatment of these conditions, and whether the use of oral anticoagulants would improve the prevention and the treatment of acute myocardial infarction.
A drug safety review of treating eosinophilic asthma with monoclonal antibodies
Published in Expert Opinion on Drug Safety, 2019
Patrick Mitchell, Richard Leigh
Concerns were raised in an earlier study that reported an imbalance of cardiovascular (CV) and cerebrovascular serious adverse events observed in the omalizumab group compared to the placebo [26]. This prompted, amongst other reasons, the FDA to request EXCELS (An Epidemiologic Study of Xolair [omalizumab] Evaluating Clinical Effectiveness and Long-term Safety in Patients With Moderate-to-Severe Asthma) which was a prospective observational cohort study to better understand the long-term safety of omalizumab in clinical practice [27]. Analysis of the EXCELS data showed that at baseline, the 2 cohorts had similar demographic characteristics, but severe asthma was more common in the omalizumab versus the non-omalizumab treated group (50% vs 23%). Omalizumab-treated patients did have a higher rate of CV serious adverse events (13.4 per 1,000 person years [PYs]) than did non-omalizumab-treated patients (8.1 per 1,000 PYs) as peer the analysis [27]. A further analysis of this concern, using data from more than 6200 participants in 25 randomized control trials (RCTs), revealed few cardiovascular events in either the omalizumab group (n = 5) or the placebo group (n = 4). Rates for arterial thromboembolism were similar between the 2 groups. The secondary analysis, which included nonserious events, showed no difference between the omalizumab and placebo groups. The authors concluded that the rates of observed arterial thromboembolic events were similar between the omalizumab and placebo groups. However, the low number of events and wide confidence intervals likely limit the ability to exclude small differences in CV risk [27,28].
Improving fibrinolysis in venous thromboembolism: impact of fibrin structure
Published in Expert Review of Hematology, 2019
Among acquired thrombophilias such as heparin-induced thrombocytopenia or paroxysmal nocturnal hemoglobinuria, the most common disorder (5% of VTE patients) is antiphospholipid syndrome (APS) that characterizes by the presence of IgG and/or IgM antiphospholipid antibodies with the most prothrombotic lupus anticoagulant. The recurrent VTE is observed in 60% of APS patients with triple antibody positivity, and up to 20% of APS patients suffered also from ischemic cerebrovascular event [62]. In 2014 we demonstrated reduced plasma clot permeability and lysability with dense fiber network formation, the so-called prothrombotic clot phenotype assessed in vivo, in patients with APS [63]. Vikerfors et al. [64] also reported formation of more compact fibrin clots in APS patients compared to healthy individuals and patients after VTE without APS, however lysability was not assessed. Of note, during a median follow-up of 62 months, clot lysis time, in contrast to Ks, failed to predict recurrent venous or arterial thromboembolism in patients with APS [65]. We found that at baseline CLT was similar in APS patients with recurrent events and those free of such events.