Arterial Thrombosis—Diagnosis and Management
E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson in Phospholipid-Binding Antibodies, 2020
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
C. Simon Herrington in Muir's Textbook of Pathology, 2020
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 of Acute Intestinal Ischaemia
Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams in Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Patients with mesenteric venous thrombosis often have a less acute presentation as compared with arterial embolism or thrombosis. Symptoms often develop gradually over a period of days. Similar to arterial embolism or thrombosis, patients often have pain out of proportion to the exam. In addition to abdominal pain, patients may experience anorexia and diarrhoea.7 Similar to the other forms of mesenteric ischaemia, CT imaging is often the main stay diagnostic modality. However, the accurate diagnosis of mesenteric venous thrombosis requires delayed venous phase images to properly assess the venous system. Except in the setting of peritonitis, the management of venous thrombosis is often non-surgical and involves systemic anticoagulation, bowel rest and close observation.
Characteristics of platelet count and size and diagnostic accuracy of mean platelet volume in patients with venous thromboembolism. A systematic review and meta-analysis
Published in Platelets, 2019
Sándor Kovács, Zoltán Csiki, Katalin S Zsóri, Zsuzsanna Bereczky, Amir H. Shemirani
Recent studies have suggested associations between VTE and arterial thromboembolism [10]. Platelets are essential in hemostasis and their functions play an important role in the formation of thrombi in both venous and arterial systems [11]. Elevated platelet agreeability and thrombocyte activation are among the known factors attributed to the role of platelets in the pathogenesis of VTE [12]. It has been recognized that platelet is a central element of the atherothrombotic process [13]. Although there is a lack of strong evidence regarding PLT as a risk factor for VTE in the general population [14,15], association of elevated PLT (>350 k) with VTE was demonstrated on hospitalized patients [16]. Some studies show that platelet activation has a role in the pathology of VTE [17]. Experimental evidence has been demonstrated that urinary excretion of thromboxane B2, as a marker of platelet activation in the early phase of thrombosis, was elevated in patients with VTE [18]. The role of platelet volume and platelet count (PLT) in the setting of VTE is still unclear.
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].
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.
Related Knowledge Centers
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- Artery
- Thrombosis
- Embolus
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- Shortness of Breath