FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2136072189> ?p ?o ?g. }

• W2136072189 endingPage "1228" @default.
• W2136072189 startingPage "1223" @default.
• W2136072189 abstract "Copyright © Polskie Towarzystwo Kardiologiczne INTRODUCTION Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), and atherothrombosis have long been considered to be separate entities with distinct pathogenic mechanisms. The traditional rationale for this concept has been based on: (1) pathologic data showing platelet-rich thrombi in the arteries in contrast to ‘red clots’ observed in veins; (2) clinical data on a substantial efficacy of antiplatelet agents in the prevention of arterial thromboembolic events in contrast to negligible benefits from these drugs in patients with VTE; (3) experimental data demonstrating diffuse inflammatory infiltrates, extracellular cholesterol deposits, neovessel formation and calcification within advanced atherosclerotic lesions within the arterial wall in contrast to minor lesions largely within the endothelial layer of the thrombosed veins. A key component of this concept is the assumption that deranged local processes occurring inside the vessel wall account for arterial thrombosis with a minor contribution by blood-borne abnormalities, whereas a combination of extrinsic factors ranging from venous blood stasis to hypercoagulable blood that act on a normal wall of a vein determine the occurrence of venous thrombosis. Experimental data derived from biochemical laboratories, cell cultures and animal models has shown however many similarities in the pathophysiology of arterial and venous thrombosis [1]. Coagulation pathways and their regulation are in fact identical in arteries and veins. Blood circulating in the two types of vessels is the same in terms of coagulation proteins. All kinds of thrombosis are triggered with the same major physiological initiator of blood coagulation, i.e. tissue factor (TF) [2]. Finally, thrombus composition assessed following thrombectomy in patients with ST-segment elevation acute myocardial infarction (MI) is frequently hard to differentiate from that of thrombi obtained from thrombosed veins, as evidenced by the fact that fibrin represents the largest portion of the thrombotic mass in both types of vessels [3, 4]. Despite the key role of activated platelets as a driving factor of thrombus formation under high shear stress conditions, there is convincing evidence for a significant contribution of thrombin and blood coagulation proteins in arterial thrombosis, as well as for their expression in macrophages and other cells within atherosclerotic lesions [5]. Until the beginning of the current century, there was no clinical data to support basic science findings indicating that thrombus formation in most vessels follows the same pattern and once deranged haemostasis tilted toward thrombosis results in increased risk of thromboembolic events putting in danger both the arterial and venous beds. Within the last decade, accumulating evidence has indicated that patients following VTE are at risk of MI or ischaemic stroke and vice versa. However a lot of experimental and clinical questions are to be answered including those as to whether all affected patients are indeed prone to develop the other type of thrombosis and which diagnostic and therapeutic strategy should be adopted in such a clinical setting. This review summarises the most important clinical and experimental data on the association between arterial and venous thrombosis." @default.
• W2136072189 created "2016-06-24" @default.
• W2136072189 creator A5047958060 @default.
• W2136072189 date "2013-12-13" @default.
• W2136072189 modified "2023-10-03" @default.
• W2136072189 title "Atherosclerosis and venous thromboembolism — similarities" @default.
• W2136072189 cites W1517429669 @default.
• W2136072189 cites W1593008417 @default.
• W2136072189 cites W164116990 @default.
• W2136072189 cites W1761341737 @default.
• W2136072189 cites W1968749966 @default.
• W2136072189 cites W1974640470 @default.
• W2136072189 cites W1974642901 @default.
• W2136072189 cites W1975990989 @default.
• W2136072189 cites W1976260077 @default.
• W2136072189 cites W1989165392 @default.
• W2136072189 cites W1993164009 @default.
• W2136072189 cites W1999994926 @default.
• W2136072189 cites W2005369178 @default.
• W2136072189 cites W2006666326 @default.
• W2136072189 cites W2013688099 @default.
• W2136072189 cites W2017527722 @default.
• W2136072189 cites W2046051565 @default.
• W2136072189 cites W2046693913 @default.
• W2136072189 cites W2047718818 @default.
• W2136072189 cites W2065276135 @default.
• W2136072189 cites W2068687443 @default.
• W2136072189 cites W2068898353 @default.
• W2136072189 cites W2077420019 @default.
• W2136072189 cites W2079766839 @default.
• W2136072189 cites W2087560474 @default.
• W2136072189 cites W2092241757 @default.
• W2136072189 cites W2094865274 @default.
• W2136072189 cites W2100989562 @default.
• W2136072189 cites W2106087253 @default.
• W2136072189 cites W2107281999 @default.
• W2136072189 cites W2107371049 @default.
• W2136072189 cites W2125102123 @default.
• W2136072189 cites W2126950963 @default.
• W2136072189 cites W2129657984 @default.
• W2136072189 cites W2131940096 @default.
• W2136072189 cites W2133115600 @default.
• W2136072189 cites W2134923719 @default.
• W2136072189 cites W2142738443 @default.
• W2136072189 cites W2147232435 @default.
• W2136072189 cites W2149707766 @default.
• W2136072189 cites W2152502508 @default.
• W2136072189 cites W2154036638 @default.
• W2136072189 cites W2154401812 @default.
• W2136072189 cites W2160044219 @default.
• W2136072189 cites W2161735825 @default.
• W2136072189 cites W2161991083 @default.
• W2136072189 cites W2163666988 @default.
• W2136072189 cites W2170731631 @default.
• W2136072189 cites W2172191543 @default.
• W2136072189 cites W2314873497 @default.
• W2136072189 cites W2330538993 @default.
• W2136072189 cites W2349457619 @default.
• W2136072189 cites W2402738658 @default.
• W2136072189 cites W2407022166 @default.
• W2136072189 cites W2462275437 @default.
• W2136072189 cites W91644420 @default.
• W2136072189 cites W3146483393 @default.
• W2136072189 doi "https://doi.org/10.5603/kp.2013.0322" @default.
• W2136072189 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24399581" @default.
• W2136072189 hasPublicationYear "2013" @default.
• W2136072189 type Work @default.
• W2136072189 sameAs 2136072189 @default.
• W2136072189 citedByCount "8" @default.
• W2136072189 countsByYear W21360721892014 @default.
• W2136072189 countsByYear W21360721892015 @default.
• W2136072189 countsByYear W21360721892016 @default.
• W2136072189 countsByYear W21360721892017 @default.
• W2136072189 countsByYear W21360721892018 @default.
• W2136072189 countsByYear W21360721892019 @default.
• W2136072189 crossrefType "journal-article" @default.
• W2136072189 hasAuthorship W2136072189A5047958060 @default.
• W2136072189 hasBestOaLocation W21360721891 @default.
• W2136072189 hasConcept C126322002 @default.
• W2136072189 hasConcept C164705383 @default.
• W2136072189 hasConcept C177713679 @default.
• W2136072189 hasConcept C2780868729 @default.
• W2136072189 hasConcept C2991741193 @default.
• W2136072189 hasConcept C71924100 @default.
• W2136072189 hasConceptScore W2136072189C126322002 @default.
• W2136072189 hasConceptScore W2136072189C164705383 @default.
• W2136072189 hasConceptScore W2136072189C177713679 @default.
• W2136072189 hasConceptScore W2136072189C2780868729 @default.
• W2136072189 hasConceptScore W2136072189C2991741193 @default.
• W2136072189 hasConceptScore W2136072189C71924100 @default.
• W2136072189 hasIssue "12" @default.
• W2136072189 hasLocation W21360721891 @default.
• W2136072189 hasLocation W21360721892 @default.
• W2136072189 hasLocation W21360721893 @default.
• W2136072189 hasOpenAccess W2136072189 @default.
• W2136072189 hasPrimaryLocation W21360721891 @default.
• W2136072189 hasRelatedWork W2145532404 @default.
• W2136072189 hasRelatedWork W2155855469 @default.

• next