4 edition of Venous and Arterial Thrombosis: Pathophysiological and Clinical Aspects found in the catalog.
Venous and Arterial Thrombosis: Pathophysiological and Clinical Aspects
by Not Avail
Written in English
|Contributions||S. Levy-Toledano (Editor), H. C. Hemker (Editor)|
|The Physical Object|
|Number of Pages||116|
Arterial thrombosis is the cause of myocardial infarction (MI) and stroke, while venous thrombosis (VT) leads to venous thromboembolism (VTE) and pulmonary embolism (PE). Structurally, arterial and venous thrombi are distinct. Arterial thrombi are rich in platelets and form at the sides of or around ruptured atherosclerotic plaques. In the past, arterial and venous thrombosis have been accepted as two completely different diseases. Recently, the thesis of two separate pathogenetic mechanisms of venous and arterial thrombosis has been challenged by accumulation of evidence which suggest that patients with atherothrombosis are at increased risk for venous thrombosis.
Background and objectives. Cerebral venous and sinus thrombosis (CVST) is a rare condition which accounts for. This issue of Seminars in Thrombosis & Hemostasis is focused on the role of TF in arterial and venous thrombosis, providing insights that span from pathophysiology to clinical implications. First, Gajsievwicz and Morrissey review the structure–function relationship of the interaction between TF and FVIIa, providing insights into their.
Get this from a library! Cerebral sinus thrombosis: experimental and clinical aspects. [Karl Einhäupl; Oliver Kempski; A Baethmann;] -- Contrary to the neurological manifestations of arterial cerebral blood flow disturbances, respective conditions resulting fram obstruction of the cerebro-venous system are far less well understood. Free 2-day shipping. Buy Cerebral Sinus Thrombosis: Experimental and Clinical Aspects (Paperback) at
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We speculate that venous and arterial thrombosis are two aspects of the same disease (ie, thrombosis), and that this disease may electively affect genetically predisposed individuals resulting in clinically manifestations that are, in turn, depending on a variety of elements including the age of patients, their lifestyle, and the occurrence of co-morbidities and circumstantial factors: the venous thrombotic Cited by: Contrary to the neurological manifestations of arterial cerebral blood flow disturbances, respective conditions resulting fram obstruction of the cerebro-venous system are far less well understood.
Hence, cerebral sinus vein thrombosis (CSVT) ranks prominently among Brand: Springer US. Buy Venous and Arterial Thrombosis: Pathophysiological and Clinical Aspects: 15th International Congress on Thrombosis, Antalya, October Selected Plenary Lectures 15th Congress, Antal by Toledano, S.
L., Hemker, H. C., Levy-Toledano, Sylviane (ISBN: ) from Amazon's Book Store. Everyday low prices and free delivery on eligible orders.4/5(1). Current concepts suggest that the basic mechanisms of venous and arterial thrombosis are different variations of similar pathogenetic pathways.
Both v Cited by: 5. Nevertheless, of PubMed citations of works on arterial and venous thrombosis, approximately 25% are to arterial thrombosis. An additional aspect of thrombosis and cancer is the inevitably adverse effect of chemotherapy (often anti-neoplastic and cytotoxic) in promoting thrombosis [ by: Prevention and Treatment of Venous and Arterial Thrombosis in Patients with Specific Conditions: Diabetes, Hypercoagulable States, Pregnancy, and Renal Insufficiency (Pages: ) Meyer Michel Samama MD.
Jacqueline Conard PhD. Grigoris Gerotziafas MD. Caplan's Stroke - edited by Louis R. Caplan September The relationship between cancer and venous thromboembolism (VTE) has been recognised for almost two centuries.
Historically, the French physician, Armand Trousseau, is credited with initially describing the relationship between VTE and cancer in a seminal book published in (Trousseau, ); however, it has since been recognised that the first description of deep vein thrombosis.
The book features comprehensive information ranging from molecular mechanisms of diseases to the clinical features, diagnosis, and therapeutic regimens for treating a variety of clinical conditions. It has a broad appeal to scientists and research students as well as busy clinicians engaged in patient care, who will all find something important.
Venous thromboembolism (VTE) refers to a blood clot that starts in a vein. It is the third leading vascular diagnosis after heart attack and stroke, affecting betweentoAmericans each year.
There are two types: Deep vein thrombosis (DVT) Deep vein thrombosis is a clot in a deep vein, usually in the leg. DVT sometimes affects. Arterial and venous thrombosis share common risk factors, for example, age, smoking or hypercholesterolemia. 24 In addition, patients with venous thrombosis have more frequent adverse.
Srinivasan, K. Puerperial cerebral venous and arterial thrombosis. Pathophysiological aspects of cerebral sinus venous thrombosis Haley, EC, Brashear, R, Barth, JT et al.
Deep cerebral venous thrombosis. clinical, neuroradiological, and neuropsychological correlates. Although the embolus can be a blood clot (thrombus), fat, air, amniotic fluid, or tumour, a PE is usually caused by a thrombus originating from the deep veins in the legs (deep venous thrombosis, DVT).
Arterial vs. venous thrombosis. Thromb Haemost. Apr;(4) The coagulation cascade is an essential part of hemostasis. Thus, arterial thrombosis is a major contributing factor to myocardial infarction and its pathophysiology therefore deserves every attention. Arterial thrombi as a rule start from a vascular lesion, most often from ruptured atheromas and have been shown to progress from a primary deposite of blood platelets.
The book is organized into 20 chapters. The first is an introductory chapter on the basic physiology of hemostasis, focusing on blood vessels, platelets, and plasma proteins that comprise the. Arterial thrombosis usually occurs after the erosion or rupture of an atherosclerotic plaque and, through platelet-mediated thrombi, can cause ischaemic injuries especially in tissues with a terminal vascular bed.
Indeed, cardiac ischaemia and stroke are the most severe clinical manifestations of atherothrombosis. Risk factors for venous and arterial thrombosis Article Literature Review (PDF Available) in Blood transfusion = Trasfusione del sangue 9(2) October with Reads.
Clinical presentation will vary based upon the anatomic location and extent of thrombosis. This chapter will discuss the epidemiology, etiology, and clinical presentation of venous thrombosis in multiple organ systems and provide up-to-date strategies for diagnosis and management of the disease.
Thrombosis. Arterial and venous thrombosis can be present in APS, distinguishing this from other prothrombotic states such as protein C, S, or antithrombin deficiency, in which only venous thrombosis occurs.
Any organ and any size of vessel (small, medium, or large) can be affected; thus, the range of clinical features is extremely wide. Atherosclerosis is the most common cause of major disability and death in the United States.
The most devastating complication of this disease occurs when a platelet-rich thrombus abruptly occludes arterial blood flow, resulting in acute MI, stroke, or sudden cardiac death.
This chapter reviews the basic pathophysiology of arterial thrombosis. The prevalence of deep venous reflux, superficial venous reflux, and coincident deep and superficial venous reflux in clinical class C4-C6 limbs was higher than in clinical class C0-C3 limbs.Cerebral venous sinus thrombosis is a challenging condition because of its variability of clinical symptoms and signs.
It is very often unrecognised at initial presentation. All age groups can be affected. Large sinuses such as the superior sagittal sinus are most frequently involved. Extensive collateral circulation within the cerebral venous system allows for a significant degree of.Induced venous thrombus in the presence of radiolabelled platelets shows early platelet accumulation at the ‘head’ of the thrombus.
Then, the acquisition of platelets by the thrombi slows and the clots become ‘red’, being predominantly composed of fibrin and erythrocytes.