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Journal articles on the topic 'Virchow triad'

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Published: 7 June 2025

Last updated: 17 July 2025

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Bennett, Philip, Stanley Silverman, Paramjit Gill, and Gregory Lip. "Peripheral arterial disease and Virchow’s triad." Thrombosis and Haemostasis 101, no. 06 (2009): 1032–40. http://dx.doi.org/10.1160/th08-08-0518.

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SummaryPeripheral arterial disease (PAD) is an important global health-care problem associated with considerable morbidity and mortality. This disease is an important manifestation of atherosclerosis and the pathophysiological processes involved in its development, progression and complications are atherothrombosis and thromboembolism. Over 150 years ago, Virchow described a triad of abnormalities (abnormal blood flow, abnormal vessel wall and abnormal blood constituents) associated with thrombus formation (thrombogenesis). An improvement in biochemical techniques has allowed quantification of various components of Virchow’s triad, and as a consequence, there has been increasing interest in the measurement of such biomarkers in understanding the development and progression of PAD, as well as its symptomatic complications. This review discusses quantifiable components of Virchow’s triad that have been associated with PAD and their clinical utility as risk factors for PAD.

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HARRISON, S. E., J. BERNSDORF, D. R. HOSE, and P. V. LAWFORD. "DEVELOPMENT OF A LATTICE BOLTZMANN FRAMEWORK FOR NUMERICAL SIMULATION OF THROMBOSIS." International Journal of Modern Physics C 18, no. 04 (2007): 483–91. http://dx.doi.org/10.1142/s0129183107010711.

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The interacting factors relating to thrombogenesis were defined by Virchow in 1856 to be abnormalities of blood chemistry, the vessel wall and haemodynamics. Together, these factors are known as Virchow's triad. Many attempts have been made to simulate numerically certain aspects of the complex phenomena of thrombosis, but a comprehensive model, which includes the biochemical and physical aspects of Virchow's triad, and is capable of predicting thrombus development within physiological geometries has not yet been developed. Such a model would consider the role of platelets and the coagulation cascade along with the properties of the flow in the chosen vessel. A lattice Boltzmann thrombosis framework has been developed, on top of an existing flow solver, to model the formation of thrombi resulting from platelet activation and initiation of the coagulation cascade by one or more of the strands of Virchow's triad. Both processes then act in parallel, to restore homeostasis as the deposited thrombus disturbs the flow. Results are presented in a model of deep vein thrombosis (DVT), resulting from hypoxia and associated endothelial damage.

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Yamashita, Takeshi. "Virchow triad and beyond in atrial fibrillation." Heart Rhythm 13, no. 12 (2016): 2377–78. http://dx.doi.org/10.1016/j.hrthm.2016.09.007.

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Dorobantu-Lungu, Luiza-Roxana, Viviana Dinca, Andrei Gegiu, et al. "The Relevance of the Virchow Node and Virchow Triad in Renal Cancer Diagnosis." Clinics and Practice 15, no. 1 (2025): 18. https://doi.org/10.3390/clinpract15010018.

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Background: The purpose of this article is to overview the clinical significance of left supraclavicular adenopathy and review the etiology of inferior vena cava (IVC) thrombosis, starting from a presentation of a rare case of renal cell carcinoma (RCCs) with Xp11.2 translocation involving TFE3 gene fusion. This article also aims to review the literature to understand the characteristics of this rare type of renal tumor. Renal cell carcinoma (RCC) associated with Xp11.2 translocation/gene fusion TFE3 is a rare subtype of kidney cancer that was classified in 2016 as belonging to the family of renal carcinomas with MiT gene translocation (microphthalmia-associated transcription factor). The prognosis for these kidney cancers is poorer compared to other types. Methods: We present a case of a 66-year-old man with Virchow–Troisier adenopathy during physical examination, which raises the suspicion of infra-diaphragmatic tumor. The echocardiography highlighted a heterogeneous mass in the right cardiac cavities, and the abdominal ultrasound exam revealed a solid mass at the upper pole of the left kidney. Results: Following computed tomography, magnetic resonance imaging, PET-CT, and histopathological and immunohistochemical examinations, the patient was diagnosed with renal carcinoma with Xp11.2 translocation and TFE3 gene fusion. Conclusions: IVC thrombosis is often associated with neoplastic disease due to the procoagulant state of these patients, the most common malignancies related to IVC thrombosis being represented by RCCs (38%), genitourinary cancers (25%), bronchus and lung cancers, retroperitoneal leiomyosarcoma, and adrenal cortical carcinoma. Imaging methods play a crucial role in differential diagnosis, allowing for the localization of the primary tumor and assessment of its characteristics.

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Safavi-Abbasi, Sam, Cassius Reis, Melanie C. Talley, et al. "Rudolf Ludwig Karl Virchow: pathologist, physician, anthropologist, and politician." Neurosurgical Focus 20, no. 6 (2006): 1–6. http://dx.doi.org/10.3171/foc.2006.20.6.1.

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✓ The history of apoplexy and descriptions of stroke symptoms date back to ancient times. It was not until the mid-nineteenth century, however, that the contributions of Rudolf Ludwig Karl Virchow, including his descriptions of the phenomena he called “embolism” and “thrombosis” as well as the origins of ischemia, changed the understanding of stroke. He suggested three main factors that conduce to venous thrombosis, which are now known as the Virchow triad. He also showed that portions of what he called a “thrombus” could detach and form an “embolus.” Thus, Virchow coined these terms to describe the pathogenesis of the disorder. It was also not until 1863 that Virchow recognized and differentiated almost all of the common types of intracranial malformations: telangiectatic venous malformations, arterial malformations, arteriovenous malformations, cystic angiomas (possibly what are now called hemangioblastomas), and transitional types of these lesions. This article is a review of the contributions of Rudolf Virchow to the current understanding of cerebrovascular pathology, and a summary of the life of this extraordinary personality in his many roles as physician, pathologist, anthropologist, ethnologist, and politician.

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Bagot, Catherine N., and Roopen Arya. "Virchow and his triad: a question of attribution." British Journal of Haematology 143, no. 2 (2008): 180–90. http://dx.doi.org/10.1111/j.1365-2141.2008.07323.x.

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Rakhmatova, Sanobar Nizamovna Usmonov Surat Rustamovich. "COMPARATIVE STUDY OF RISK FACTORS FOR TIA AND ISCHEMIC STROKES.INITIAL DETERMINATION." INTERNATIONAL BULLETIN OF APPLIED SCIENCE AND TECHNOLOGY 3, no. 7 (2023): 154–59. https://doi.org/10.5281/zenodo.8150100.

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the duration of neurological symptoms for more than 30 minutes increases the likelihood of developing a cerebral infarction. The pathogenesis of focal cerebral ischemia is characterized by the classical Virchow triad: it is manifested by a decrease in blood flow, damage to the vascular wall and increased blood clotting.The occurrence of molecular and biochemical changes in the skull substance is caused by acute focal ischemia of the skull

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Pfliegler, György, and Árpád Illés. "COVID–19 és haemostasis." Hematológia–Transzfuziológia 54, no. 4 (2022): 184–91. http://dx.doi.org/10.1556/2068.2021.54.4.4.

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Összefoglaló. A szerzők a SARS-CoV-2 vírus okozta járványnak (COVID–19) a haemostasist érintő, klinikailag fontosabb szempontjait tekintik át röviden. Felhívják a figyelmet a thromboemboliás szövődmények súlyossága és gyakorisága mögött levő patomechanizmus jellegzetességére, vagyis a Virchow-triász három alkotója időben egyszerre történő aktiválódására. A továbbiakban a kórállapotot és -lefolyást jelző fontosabb haemostasis laboratóriumi leleteket érintik, majd rátérnek a megelőzés és a kezelés kérdéseire, mely utóbbiakat a betegség súlyossági csoportokra történő bontásában tárgyalják, a jelenlegi nemzetközi irányelvekre támaszkodva. Végezetül egy összefoglaló táblázatban, a nemzetközi ajánlásokon alapuló, de a hazai szempontokat is figyelembe vevő, általánosan elfogadható antikoagulálási útmutatót igyekeznek adni, hangsúlyozva a kezelés személyre szabásának fontosságát. Summary. In the present paper the most important, clinically relevant haemostatic effects of SARS-Cov-2 virus infection (COVID-19) is reviewed and an awareness is raised of the unique pathomechanism which allows a concurrent activation of each side of the Virchows’ triad responsible for the aggressivity of thrombotic events in the disease. Subsequently characteristic haemostatic prognostic and staging laboratory results are discussed followed by a brief survey of anticoagulant prophylaxis and therapy in the different severity stages of the disease. Finally a brief guidance is given based on various international guidelines with an adoption of current Hungarian situation and emphasizing the importance of personalized decisions.

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KAMADA, Keisuke, Shinsuke KIKUCHI, Daiki UCHIDA, Atsuhiro KOYA, Kazuhiko HANZAWA, and Nobuyoshi AZUMA. "Virchow triad and venous thromboembolism in disaster—Our experience in the Hokkaido East Iburi Earthquake—." Japanese Journal of Thrombosis and Hemostasis 33, no. 6 (2022): 661–66. http://dx.doi.org/10.2491/jjsth.33.661.

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Zhou, Xianghui, Zhipeng Cheng, and Yu Hu. "COVID-19 and Venous Thromboembolism: From Pathological Mechanisms to Clinical Management." Journal of Personalized Medicine 11, no. 12 (2021): 1328. http://dx.doi.org/10.3390/jpm11121328.

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Coronavirus disease 2019 (COVID-19), which is becoming a global pandemic, is caused by SARS-CoV-2 infection. In COVID-19, thrombotic events occur frequently, mainly venous thromboembolism (VTE), which is closely related to disease severity and clinical prognosis. Compared with historical controls, the occurrence of VTE in hospitalized and critical COVID-19 patients is incredibly high. However, the pathophysiology of thrombosis and the best strategies for thrombosis prevention in COVID-19 remain unclear, thus needing further exploration. Virchow’s triad elements have been proposed as important risk factors for thrombotic diseases. Therefore, the three factors outlined by Virchow can also be applied to the formation of venous thrombosis in the COVID-19 setting. A thorough understanding of the complex interactions in these processes is important in the search for effective treatments for COVID-19. In this work, we focus on the pathological mechanisms of VTE in COVID-19 from the aspects of endothelial dysfunction, hypercoagulability, abnormal blood flow. We also discuss the treatment of VTE as well as the ongoing clinical trials of heparin anticoagulant therapy. In addition, according to the pathophysiological mechanism of COVID-19-associated thrombosis, we extended the range of antithrombotic drugs including antiplatelet drugs, antifibrinolytic drugs, and anti-inflammatory drugs, hoping to find effective drug therapy and improve the prognosis of VTE in COVID-19 patients.

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Jorge, Elpidio Moreno Carranza, Suarez Ortega Manuel, Fernando Romero Espinosa Jesús, et al. "Acute Symmetric Arterial Thrombosis of the Four Extremities Associated with Pregnancy: Case Report." International Journal of Medical Science and Clinical Research Studies 5, no. 04 (2025): 638–41. https://doi.org/10.5281/zenodo.15294175.

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During the normal process of pregnancy, there is a procoagulant state derived from the alteration of all the components of the Virchow Triad. Multiple biochemical and structural changes lead to an increased risk of thromboembolic events. Although venous embolic events are more common, arterial thrombosis generally leads to devastating outcomes. Anticoagulation in pregnant patients has very specific indications, primarily in patients with a history of thromboembolism or poor obstetric history. There are multiple drugs used for venous or arterial thrombosis, some of which are associated with teratogenic effects, the most commonly used being low molecular weight heparin. In cases of valve prosthesis and antiphospholipid syndrome, antiplatelet drugs should be added.Shock is the main cause of admission and mortality in intensive care units. In the absence of myocardial dysfunction, hypotension is primarily caused by hypovolemia and the physiological inability to self-regulate and adequately perfuse. In these cases, there are guidelines for the use of vasopressors, aimed at maintaining adequate perfusion to essential organs. However, the use of these drugs may be associated with adverse effects, including the possibility of ischemia in some anatomical regions.In this article, we present the case of a multi-pregnant patient with the presence of several etiopathogenic factors that triggered distal necrosis of all four extremities, requiring amputation.

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Agnesha, Fahmi, and Sri Rahardjo. "TROMBOEMBOLI PADA KEHAMILAN." Jurnal Komplikasi Anestesi 5, no. 3 (2018): 75–85. http://dx.doi.org/10.22146/jka.v5i3.7343.

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Tromboemboli pada kehamilan merupakan salah satu kejadian yang angka kejadiannya jarang namun dapat berakibat fatal apabila tidak dikenali sejak dini. Gambaran klinis tromboemboli vena pada kehamilan adalah trombosis vena dalam (deep vein thrombosis) dan tromboemboli pulmonal. Patofisiologi terjadinya tromboemboli dijelaskan melalui triad Virchow yang menggambarkan faktor yang menyebabkan peningkatan risiko tromboemboli antara lain adalah (1) stasis vena, (2) kerusakan vaskular, dan (3) hiperkoagulabilitas. Diagnosis dilakukan dengan menggunakan alat penunjang ultrasonografi pada vena proksimal pada pasien dengan onset baru atau tanda mengarah ke trombosis vena dalam. Tata laksana tromboemboli pada kehamilan dengan diberikan antikoagulan yang diberikan selama hamil dan periode post partum berupa low mollecular weight heparin dan unfractioned heparin. Pemberian terapi tersebut memiliki implikasi pada pasien yang dilakukan neuraxial anestesi berupa hematom spinal dan epidural. Sehingga beberapa rekomendasi terkait hal ini dapat dilakukan untuk pencegahan berupa penghentian konsumsi heparin sebelum prosedur dilakukan.

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Adeel, Jamil, Jamil Umer, Kumar Sunny, Akrmah Muhammad, Ghaffarpasand Eiman, and Chi Gerald. "Inflammation and Atherothrombosis: The Beginning of the End of a Hypothesis." EC Cardiology 5, no. 1 (2018): 05–09. https://doi.org/10.5281/zenodo.1202054.

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Abstract: The inflammatory hypothesis for atherothrombosis posits that inflammation drives the development of atherosclerotic plaque and its progression to thrombosis. Empirical data have suggested the relation of inflammation to the Virchow’s triad: endothelial injury, blood stasis, and hypercoagulable state. Evidence from clinical studies also pointed to a potential benefit in thrombotic risk reduction from inhibiting inflammation. Until recently, interleukin-1β blockade with canakinumab has been investigated for preventing recurrent cardiovascular events among patients with prior myocardial infarction and demonstrated compelling outcomes. Furthermore, the results ascertain that a downstream inflammatory biomarker, high-sensitivity C-reactive protein, could be utilized to identify at-risk patient subsets associated with significant benefits from anti-inflammatory therapy. As research efforts are closing the knowledge gap between inflammation and thrombosis, the potential role of inflammation in other cardiovascular diseases also presents new challenges for future studies.

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Denise, Francisca dos Santos Pattricia Ferreira do Amaral Romulo Gonçalves de Moura Lucena Daniel Carvalho dos Santos Aline Carvalho Gouveia de Almeida Sérgio Botelho Fiuza Arnon Henrique Teschima Rezende Christiane de Sousa Martins José Joceilson Cruz de Assis Daniela Lins de Queiroz Campos Khaila Corrêa Batista Izabella Manso Heinzen Gustavo Snidarcis Berti Sérgio Botelho Fiuza Cassiana de Moura e. Costa Matheus Hermano Caldas Giovanna Pires Barcelos Beatriz Matta Ferro Couri Eric Zaneti Teixeira Baptista Nuno Brandão Di Barros Cachapuz Caiado Ana Karine Laranjeira de Sá José Mateus Rabelo Diniz Sampaio Fabiana Falco dos Santos Joao Victor Araujo Guimaraes Mateus Pimentel Rodrigues Santana Aline Magalhães Vargas Victor Diniz Borges Valéria de Carvalho Fagundes Thais Aguilhera Bruno de Oliveira José Lucas campos Rodrigues Milena Cilião Salvadori Kélen Klein Heffel Jose Songlei da Silva Rocha Isadora Dias Lopes Ferrari Ygor Borges Anna Cristina Rocha de Carvalho Batista Bruno Matheus Ribeiro Matos Luciano Gouvêa de Moraes Silva Alexandre Estevam Montenegro Diniz Ana Carolina Bueno de Bueno Rainally Sabrina freire de Morais Sofia Perroni Leonardo Francisco Ribeiro Uanderson Pereira da Silva Anne Brandão Silva Larissa Miranda Silva Lara Morais Batista Katia Aparecida Scarpari Bourdokan Luiz Augusto Germano Borges Ubiratan Rodrigues de Godoy Neto Isabella Hayashi Diniz Luiza Rodrigues leão Pina Ana Paula de Souza Lima Jarlene Cristiana Pereira da Silva Brasileiro Raissa Desyree Duarte Pereira Bruna Larissa Passos Nunes Carvalho Eduardo Viníccius Ramos dos Santos Danilo de Brito Campos Jaqueline Maria Pinheiro de Araujo Vanessa Araújo Alves. "AS ATRIBUIÇÕES CLÍNICAS DO TROMBOEMBOLISMO VENOSO." Revistaft 27, no. 122 (2023): 81. https://doi.org/10.5281/zenodo.7982981.

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O tromboembolismo venoso é uma condição que pode ser fracionada em trombose venosa profunda e tromboembolismo pulmonar. Estas compõe este espectro a qual proporcionalmente ao estado hemodinâmico, cursando não obrigatoriamente com o trio típico, exemplificada pela dispneia, dor torácica pleurítica e hemoptise, sendo a dispneia o mais clássico. Estima-se que a minoria dos portadores desta condição são devidamente identificados e tratados, devido o enquadramento isolado não propiciar confirmação ou exclusão patológica. Objetivos: Descrever o quadro clínico do paciente portador de tromboembolismo venoso, no intuito de favorecer o diagnóstico e manejo precoce e principalmente o bom prognóstico do mesmo. Trata-se de uma revisão bibliográfica de literatura fundamentada nas plataformas do SciELO, PubMed, Lilacs e Google Scholar no período de janeiro a março de 2023, utilizando se os seguintes descritores tromboembolismo venoso; embolia pulmonar. Resultados e Discussão: O trombobolismo venoso é uma condição de elevada morbidade e complicações, associado ao fato de que este pode cursar de modo silencioso e culminar em deteriorações e até ao óbito.

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Poston, Robert, Charles White, Katrina Read, et al. "Virchow Triad, but Not Use of an Aortic Connector Device, Predicts Early Graft Failure after Off-Pump Coronary Bypass." Heart Surgery Forum 7, no. 5 (2004): E428—E433. http://dx.doi.org/10.1532/hsf98.20041090.

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Akrivou, Dimitra, Garifallia Perlepe, Paraskevi Kirgou, Konstantinos I. Gourgoulianis, and Foteini Malli. "Pathophysiological Aspects of Aging in Venous Thromboembolism: An Update." Medicina 58, no. 8 (2022): 1078. http://dx.doi.org/10.3390/medicina58081078.

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The aim of this review is to highlight all the factors that associate venous thromboembolism (VTE) with aging. Elderly people are characterized by a higher incidence of thrombosis taking into account the co-existing comorbidities, complications and fatality that arise. Based on the Virchow triad, pathophysiological aspects of venous stasis, endothelium injury and hypercoagulability in elderly people (≥65 years) are described in detail. More precisely, venous wall structure, nitric oxide (NO) and endothelin-1 expression are impaired in this age group. Furthermore, an increase in high-molecular-weight kininogen (HMWK), prekallikrein, factors V, VII, VIII, IX and XI, clot lysis time (CLT) and von Willebrand factor (vWF) is observed. Age-dependent platelet dysfunction and changes in anticoagulant factors are also illustrated. A “low-grade inflammation stage” is delineated as a possible risk factor for thrombosis in the elderly. Consequently, clinical implications for frail elderly people related to diagnosis, treatment, bleeding danger and VTE recurrence emerge. We conclude that aging is an acquired thrombotic factor closely related to pathophysiological changes.

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Vorobev, Alexander Viktorovich, Alexander Davidovich Makatsaria, Andrey Mikhailovich Chabrov, and Alexander Anatol’evich Savchenko. "Pathogenesis of Trousseau’s syndrome." Journal of obstetrics and women's diseases 64, no. 4 (2015): 85–94. http://dx.doi.org/10.17816/jowd64485-94.

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Malignancies and thrombosis have common pathogenetic features that was shown by A. Trousseau in 1865. There is now no doubt that the cancer patients occur much more frequently thromboembolism, and migratory venous thrombosis is a manifestation of paraneoplastic syndrome in cancer patients. In general, any manifestation of thrombohemorrhagic complications in cancer patients called Trousseau’s syndrome. While thrombotic complications such as venous thromboembolism are most frequent in cancer patients, may also experience severe bleeding symptoms due to systemic coagulopathies, including disseminated intravascular coagulation, haemolytic thrombotic microangiopathy, and hyperfibrinolysis. The basis of the pathophysiology of Trousseau’s syndrome, except the classic triad of Virchow, is overproduction of tissue factor (TF), the main initiator of extrinsic coagulation pathway. Thus a significant release of microparticles from tumor cells bearing tissue factor is critical not only for the formation of a blood clot, but the growth and progression of tumors. Tumor cells activate the coagulation cascade or fibrinolysis system, providing conditions for its further spread, stimulation of angiogenesis, increased vascular permeability, which in turn promotes metastasis.

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Labianca, Alice, Tommaso Bosetti, Alice Indini, Giorgia Negrini, and Roberto Francesco Labianca. "Risk Prediction and New Prophylaxis Strategies for Thromboembolism in Cancer." Cancers 12, no. 8 (2020): 2070. http://dx.doi.org/10.3390/cancers12082070.

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In the general population, the incidence of thromboembolic events is 117 cases/100,000 inhabitants/year, while in cancer patient incidence, it is four-fold higher, especially in patients who receive chemotherapy and who are affected by pancreatic, lung or gastric cancer. At the basis of venous thromboembolism (VTE) there is the so-called Virchow triad, but tumor cells can activate coagulation pathway by various direct and indirect mechanisms, and chemotherapy can contribute to VTE onset. For these reasons, several studies were conducted in order to assess efficacy and safety of the use of anticoagulant therapy in cancer patients, both in prophylaxis setting and in therapy setting. With this review, we aim to record principal findings and current guidelines about thromboprophylaxis in cancer patients, with particular attention to subjects with additional risk factors such as patients receiving chemotherapy or undergoing surgery, hospitalized patients for acute medical intercurrent event and patients with central venous catheters. Nonetheless we added a brief insight about acute and maintenance therapy of manifested venous thromboembolism in cancer patients.

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Sugraliyev, Akhmetzhan, and Рlinio Cirillo. "Microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome. Prevention of venous thromboembolism in patients with COVID-19." Journal "Medicine" 3-4, no. 213-214 (2020): 2–7. http://dx.doi.org/10.31082/1728-452x-2020-213-214-3-4-2-7.

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In this review, the authors describe the new concept of MicroCLOTS (microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome) - proposed by Italian multidisciplinary team headed by Ciceri F, et al. as the cause of atypical acute respiratory distress syndrome. Ciceri F, etal. hypothesise that, in predisposed individuals, alveolar viral damage is followed by an inflammatory reaction and by microvascular pulmonary thrombosis. This progressive endothelial thromboinflammatory syndrome may also involve the microvascular bed of the brain and other vital organs, leading to multiple organ failure and death. In addition, patients with COVID-19 often develop macrovascular venous thrombosis as a result of the activation of the Virchow triad. Microvascular and macrovascular thrombosis development in patients with COVID-19 is confirmed by ultrasound examination of the veins of the lower extremities and complete autopsy study. The data obtained indicate the importance of the prevention of venous thrombosis with LMWH (nadroparin, enoxaparin) and Fondaparinux sodium in all hospitalized patients with COVID-19. Keywords: COVID-19, аtypical acute respiratory distress syndrome, MicroCLOTS (microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome), thrombosis, hemostasis.

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Finianos, Elie S., Stephanie F. Yacoub, and Mary F. Chammas. "Ovarian Vein Thrombosis Complicated by Pulmonary Embolism after Cesarean Delivery in the Presence of a Large Fibroid: Case Report and Literature Review of Contributing Factors." Case Reports in Obstetrics and Gynecology 2021 (September 8, 2021): 1–7. http://dx.doi.org/10.1155/2021/6389713.

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Ovarian vein thrombophlebitis is rare and mostly occurs during the puerperal period and in higher rates after a cesarean delivery. The objective of this case report and literature review is to highlight the rare occurrence of an ovarian vein thrombosis in a 37-year-old woman postcesarean delivery in the setting of a large uterine fibroid who subsequently developed a pulmonary embolism. The patient presented with severe abdominal pain, fever, and chills. Imaging showed a right ovarian vein thrombosis. Following initiation of anticoagulation therapy, she developed dyspnea and testing showed a subsegmental pulmonary embolism. Further investigation showed that the patient had an undiagnosed thrombophilia thus meeting the classic Virchow triad. Complete clinical recovery was observed, and anticoagulation therapy was continued for 1 year. Our case highlights the importance of recognizing ovarian vein thrombosis because of the risk of fatal complications such as pulmonary embolus. The presence of large fibroids should raise our awareness for OVT in the setting of abdominal pain and fever. The absence of complications in previous pregnancies should not alter our clinical suspicion.

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Vuckovic, Biljana. "A neoteric approach to understanding thrombosis." Medicinski pregled 77, no. 3-4 (2024): 79–82. http://dx.doi.org/10.2298/mpns2404079v.

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Pathophysiology of thrombosis. Thrombosis, a leading cause of morbidity and mortality worldwide, results from an imbalance between procoagulant, anticoagulant, and fibrinolytic factors. Virchow?s triad - endothelial injury, stasis of blood flow, and hypercoagulability - has long been the cornerstone for understanding thrombosis. However, evolving knowledge has refined our interpretation of how these factors contribute to venous and arterial thrombosis. Arterial thrombosis. Historically, arterial and venous thromboses were viewed as distinct pathophysiological entities. Over the past two decades, research has highlighted the complexity of etiopathogenesis of the thrombotic process, recognizing mutual risk factors offering a more comprehensive understanding the pathophysiological mechanism behind these diseases. Venous thrombosis. Recent insights focus on thrombotic potential, defined as an individual?s susceptibility to thrombosis resulting from a combination of congenital and acquired risk factors.. It has become clear that the interaction of these factors is not merely additive but synergistic, significantly increasing the risk of thrombosis. The significant social impact of thrombosis underscores the necessity of thoroughly understanding its underlying mechanisms to develop effective preventive and therapeutic strategies.

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Baghestanian, M., H. C. Bankl, C. Sillaber, et al. "New Aspects in Thrombosis Research: Possible Role of Mast Cells as Profibrinolytic and Antithrombotic Cells." Thrombosis and Haemostasis 87, no. 05 (2002): 786–90. http://dx.doi.org/10.1055/s-0037-1613084.

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SummaryVenous thromboembolism represents a significant cause of morbidity worldwide. The factors that underly thrombophilia are manifold. The concept of Virchow defines the well known triad of stasis, humoral factors, and pathologies of the vascular wall. In the current article, an additional factor, the “accumulation of repair cells” is discussed. This novel concept highlights the mast cell that accumulates around thrombosed vessels and provides a number of important repair molecules including heparin, profibrinolytic tPA, and fibrinogenolytic β-tryptase. Thus, mast cell recruitment and activation may result in local thrombolysis and prevention of coagulation. In line with this concept, mast cell-deficient mice are more susceptible to lethal thrombogenic stimuli compared to normal mice. The factors (cytokines) that trigger mast cell accumulation and release of repair molecules have also been identified – the most important one appears to be stem cell factor (SCF). All in all, our novel concept suggests that the patho-physiology of thrombosis may involve a “physiologic” cell that provides the same repair molecules that are used for treatment of thrombotic disorders by the physician. Whether an altered availability of components of this cellular repair system can predispose for thrombophilia remains to be determined.

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Ozolinya, Lyudmila A., та Angelina A. Anikeeva. "Hemostatic system in patients with endometrial hyperplasia and the risk of venous thrombosis: А literature review". V.F.Snegirev Archives of Obstetrics and Gynecology 9, № 4 (2022): 193–201. http://dx.doi.org/10.17816/2313-8726-2022-9-4-193-201.

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While treating patients with endometrial hyperplasia, the physician may face both bleeding and thrombotic complications, particularly, during hormonal or surgical treatment, which significantly increases the risk of these complications. In addition, thrombotic complications in gynecological patients may result from congenital or acquired thrombophilia, blood flow disorders (blood stasis), and vascular wall damage, that is, the classic Virchow triad. This study aimed to review the recent scientific literature on the peculiarities of the blood coagulation system in patients with endometrial hyperplasia. The review reflects the results of studies conducted by Russian and foreign authors on the status of the blood coagulation system in patients with endometrial hyperplasia. The features of vascular, thrombocytic, plasma (procoagulant and anticoagulant), and fibrinolytic elements of hemostasis in these patients are considered. The data from the literature on the state of hemostasis before treatment and following hormone therapy and surgical treatment are presented. Moreover, the data of some studies on the genetic features of the hemostatic system in patients with endometrial hyperplasia are summarized. An analysis of the literature indicates the need for a careful choice of drugs and methods of treatment of these patients to avoid venous thromboembolic complications.

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Regazzoli, Damiano, Francesco Ancona, Nicola Trevisi, et al. "Left Atrial Appendage: Physiology, Pathology, and Role as a Therapeutic Target." BioMed Research International 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/205013.

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Atrial fibrillation (AF) is the most common clinically relevant cardiac arrhythmia. AF poses patients at increased risk of thromboembolism, in particular ischemic stroke. The CHADS2 and CHA2DS2-VASc scores are useful in the assessment of thromboembolic risk in nonvalvular AF and are utilized in decision-making about treatment with oral anticoagulation (OAC). However, OAC is underutilized due to poor patient compliance and contraindications, especially major bleedings. The Virchow triad synthesizes the pathogenesis of thrombogenesis in AF: endocardial dysfunction, abnormal blood stasis, and altered hemostasis. This is especially prominent in the left atrial appendage (LAA), where the low flow reaches its minimum. The LAA is the remnant of the embryonic left atrium, with a complex and variable morphology predisposing to stasis, especially during AF. In patients with nonvalvular AF, 90% of thrombi are located in the LAA. So, left atrial appendage occlusion could be an interesting and effective procedure in thromboembolism prevention in AF. After exclusion of LAA as an embolic source, the remaining risk of thromboembolism does not longer justify the use of oral anticoagulants. Various surgical and catheter-based methods have been developed to exclude the LAA. This paper reviews the physiological and pathophysiological role of the LAA and catheter-based methods of LAA exclusion.

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Hackett, Thomas R., and Jonathan A. Godin. "Editorial Commentary: Should the Virchow Triad Have Been a Quartet? Is High Altitude a Risk Factor for Deep Venous Thrombosis After Knee Arthroscopy?" Arthroscopy: The Journal of Arthroscopic & Related Surgery 32, no. 11 (2016): 2355–56. http://dx.doi.org/10.1016/j.arthro.2016.09.002.

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Hasstedt, Sandra J., Mark F. Leppert, George L. Long, and Edwin G. Bovill. "Hereditary Thrombophilia as a Model for Multigenic Disease." Thrombosis and Haemostasis 82, no. 08 (1999): 662–66. http://dx.doi.org/10.1055/s-0037-1615894.

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IntroductionNearly 150 years ago, Virchow postulated that thrombosis was caused by changes in the flow of blood, the vessel wall, or the composition of blood. This concept created the foundation for subsequent investigation of hereditary and acquired hypercoagulable states. This review will focus on an example of the use of modern genetic epidemiologic analysis to evaluate the multigenic pathogenesis of the syndrome of juvenile thrombophilia.Juvenile thrombophilia has been observed clinically since the time of Virchow and is characterized by venous thrombosis onset at a young age, recurrent thrombosis, and a positive family history for thrombosis. The pathogenesis of juvenile thrombophilia remained obscure until the Egeberg observation, in 1965, of a four generation family with juvenile thrombophilia associated with a heterozygous antithrombin deficiency subsequently identified as antithrombin Oslo (G to A in the triplet coding for Ala 404).1,2 The association of a hereditary deficiency of antithrombin III with thrombosis appeared to support the hypothesis, first put forward by Astrup in 1958, of a thrombohemorrhagic balance.3 He postulated that there is a carefully controlled balance between clot formation and dissolution and that changes in conditions, such as Virchow’s widely encompassing triad, could tip the balance toward thrombus formation.The importance of the thrombohemorrhagic balance in hypercoagulable states has been born out of two lines of investigation: evidence supporting the tonic activation of the hemostatic mechanism and the subsequent description of additional families with antithrombin deficiency and other genetically abnormal hemostatic proteins associated with inherited thrombophilia. Assessing the activation of the hemostatic mechanism in vivo is achieved by a variety of measures, including assays for activation peptides generated by coagulation enzyme activity. Activation peptides, such as prothrombin fragment1+2, are measurable in normal individuals, due to tonic hemostatic activity and appear elevated in certain families with juvenile thrombophilia.4 In the past 25 years since Egeberg’s description of antithrombin deficiency, a number of seemingly monogenic, autosomal dominant, variably penetrant hereditary disorders have been well established as risk factors for venous thromboembolic disease. These disorders include protein C deficiency, protein S deficiency, antithrombin III deficiency, the presence of the factor V Leiden mutation, and the recently reported G20210A prothrombin polymorphism.5,6 These hereditary thrombophilic syndromes exhibit considerable variability in the severity of their clinical manifestations. A severe, life-threatening risk for thrombosis is conferred by homozygous protein C or protein S deficiency, which if left untreated, leads to death.7,8 Homozygous antithrombin III deficiency has not been reported but is also likely to be a lethal condition. Only a moderate risk for thrombosis is conferred by the homozygous state for factor V Leiden or the G20210A polymorphism.9,10 In contrast to homozygotes, the assessment of risk in heterozygotes, with these single gene disorders, has been complicated by variable clinical expression in family members with identical genotypes.11 Consideration of environmental interactions has not elucidated the variability of clinical expression. Consequently, it has been postulated that more than one genetic risk factor may co-segregate with a consequent cumulative or synergistic effect on thrombotic risk.12 A number of co-segregating risk factors have been described in the past few years. Probably the best characterized interactions are between the common factor V Leiden mutation, present in 3% to 6% of the Caucasian population,13,14 and the less common deficiencies of protein C, protein S, and antithrombin III. The factor V Leiden mutation does not, by itself, confer increased risk of thrombosis. The high prevalence of the mutation, however, creates ample opportunity for interaction with other risk factors when present.The G20210A prothrombin polymorphism has a prevalence of 1% to 2% in the Caucasian population and, thus, may play a similar role to factor V Leiden. A number of small studies have documented an interaction of G20210A with other risk factors.15-17 A limited evaluation of individuals with antithrombin III, protein C, or protein S deficiency revealed a frequency of 7.9% for the G20210A polymorphism, as compared to a frequency of 0.7% for controls.18 The G20210A polymorphism was observed in only 1 of the 6 protein C-deficient patients.18 In the present state, the elucidation of risk factors for venous thromboembolic disease attests to the effectiveness of the analytical framework constructed from the molecular components of Virchow’s triad, analyzed in the context of the thrombohemorrhagic balance hypothesis. Two investigative strategies have been used to study thromobophilia: clinical case-control studies and genetic epidemiologic studies. The latter strategy has gained considerable utility, based on the remarkable advances in molecular biology over the past two decades. Modern techniques of genetic analysis of families offer important opportunities to identify cosegregation of risk factors with disease.19 The essence of the genetic epidemiologic strategy is the association of clinical disease with alleles of specific genes. It is achieved either by the direct sequencing of candidate genes or by demonstration of linkage to genetic markers.

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Mamchich, V. I., and M. A. Chaika. "Classification of acute cholecystitis:etiopathogenetic principles of construction." Herald of Pancreatic Club 44, no. 3 (2019): 70–78. http://dx.doi.org/10.33149/vkp.2019.03.08.

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Aim of study is to suggest a scientifically based pathogenetic classification of acute cholecystitis, corresponding to the classical R. Virchow triad “etiology, pathogenesis, outcome”. Materials and methods.Comparative assessment of the classical classifications by H. Kehr (1907), L. Aschoff (1909), S. P. Fedorov (1934) and modern disease schemes, combining the signs of the three ones, is conducted. Results and discussion.The proposed improved classification of acute cholecystitis (AC) corresponds to research principles, taking into account the etiology, pathogenesis and predicted outcome of the disease. There are 4 groups of AC variants: I — Acute calculous cholecystitis with all options and combinations (cholangitis, choledocholithiasis, Opie syndrome — papillary ileus, Mirizzi syndrome, Bouveres — acute gallstone ileus, hemobilia (80–85%)). II — Acute non-calculous cholecystitis without stones (8–15%) — no obstruction of the cystic duct of the gallbladder. III —Special AC forms. The dominant factors are enzymatic, vascular, non-productive anaerobic microflora, stress factors (severe injury, burns or surgery, childbirth). These forms require urgent surgeries and occur in 2–15% of all cases of AC destructive forms. IV — Специфические формы ОХ.Specific AC forms. Caused by specific microflora: typhoid, salmonella, dysentery, and parasitic (opisthorchosis, alveococcosis, amebiasis, ascariasis, less often — giardiasis). Rare forms are characteristic of endemic zones and in violation of generally accepted sanitary standards. Conclusion.Use of ultrasound, CT, SCT, MRI, endoscopic and endovascular interventions allows to diagnose almost all the AC various forms in the pre-operative period and individualize therapeutic and surgical tactics by taking into account the possible outcome. The proposed pathogenetic classification of AC can serve as a scheme for general practitioners, physicians, surgeons, anesthesiologists, and intensive care workers.

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Filip, Catalina, Sofia Alexandra Socolov, Daniela Roxana Matasariu, et al. "The Burden of Deep Vein Thrombosis and Risk Factors in Pregnancy and Postpartum—Mirroring Our Region’s Particularities." Journal of Clinical Medicine 13, no. 16 (2024): 4705. http://dx.doi.org/10.3390/jcm13164705.

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(1) Background: The three factors within the Virchow triad play the leading role in the development of deep vein thrombosis (DVT) during pregnancy. (2) Methods: This research approaches the various risk factors associated with DVT and its most representative complications, pulmonary thromboembolism and cerebral venous thrombosis, in pregnant and postpartum women across a 15-year period (2007–2021). (3) Results: A total of 201 out of 287 patients with DVT had associated risk factors, while 86 did not present with any. Out of the 201 patients with risk factors, 47 developed pulmonary thromboembolism, while 12 experienced cerebral thrombosis. The statistical analysis of risk factors involved in DVT revealed high significance for obesity (OR 3.676; CI 2.484–5.439), gestational diabetes (OR 3.394; CI 2.101–5.483), hypertension (OR 2.325; CI 1.591–3.397), preeclampsia (OR 4.753; CI 2.342–9.645), thrombophilia (OR 12.138; CI 8.973–16.417), and varicose veins (OR 9.678; CI 7.321–12.793); for pulmonary thromboembolism, there was high significance for obesity (OR 7.867; CI 4.297–14.401), hypertension (OR 2.605; CI 1.246–5.446), preeclampsia (OR 7.483; CI 2.346–23.872), thrombophilia (OR 11.035; CI 5.910–20.602), and varicose veins (OR 6.837; CI 3.665–12.757); and for cerebral thromboembolism (CTE), the risk factors identified were obesity (OR 6.755; CI 1.954–23.347), hypertension (OR 1.167; CI 0.155–8.770), preeclampsia (OR 9.655; CI 1.283–72.672), and thrombophilia (OR 33.275; CI 12.884–85.939). (4) Conclusions: Obesity was the only significant factor found to influence DVT, pulmonary embolism and CTE risks, and hereditary thrombophilia was the main factor influencing the risk for pulmonary thromboembolism and CTE. Systemic lupus erythematosus and gestational diabetes revealed conflicting results that require further investigation.

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Sikiric, Predrag, Mario Udovicic, Ivan Barisic, et al. "Stable Gastric Pentadecapeptide BPC 157 as Useful Cytoprotective Peptide Therapy in the Heart Disturbances, Myocardial Infarction, Heart Failure, Pulmonary Hypertension, Arrhythmias, and Thrombosis Presentation." Biomedicines 10, no. 11 (2022): 2696. http://dx.doi.org/10.3390/biomedicines10112696.

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In heart disturbances, stable gastric pentadecapeptide BPC 157 especial therapy effects combine the therapy of myocardial infarction, heart failure, pulmonary hypertension arrhythmias, and thrombosis prevention and reversal. The shared therapy effect occurred as part of its even larger cytoprotection (cardioprotection) therapy effect (direct epithelial cell protection; direct endothelium cell protection) that BPC 157 exerts as a novel cytoprotection mediator, which is native and stable in human gastric juice, as well as easily applicable. Accordingly, there is interaction with many molecular pathways, combining maintained endothelium function and maintained thrombocytes function, which counteracted thrombocytopenia in rats that underwent major vessel occlusion and deep vein thrombosis and counteracted thrombosis in all vascular studies; the coagulation pathways were not affected. These appeared as having modulatory effects on NO-system (NO-release, NOS-inhibition, NO-over-stimulation all affected), controlling vasomotor tone and the activation of the Src-Caveolin-1-eNOS pathway and modulatory effects on the prostaglandins system (BPC 157 counteracted NSAIDs toxicity, counteracted bleeding, thrombocytopenia, and in particular, leaky gut syndrome). As an essential novelty noted in the vascular studies, there was the activation of the collateral pathways. This might be the upgrading of the minor vessel to take over the function of the disabled major vessel, competing with and counteracting the Virchow triad circumstances devastatingly present, making possible the recruitment of collateral blood vessels, compensating vessel occlusion and reestablishing the blood flow or bypassing the occluded or ruptured vessel. As a part of the counteraction of the severe vessel and multiorgan failure syndrome, counteracted were the brain, lung, liver, kidney, gastrointestinal lesions, and in particular, the counteraction of the heart arrhythmias and infarction.

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Strbe, Sanja, Ivan Maria Smoday, Ivan Krezic, et al. "Innate Vascular Failure by Application of Neuroleptics, Amphetamine, and Domperidone Rapidly Induced Severe Occlusion/Occlusion-like Syndromes in Rats and Stable Gastric Pentadecapeptide BPC 157 as Therapy." Pharmaceuticals 16, no. 6 (2023): 788. http://dx.doi.org/10.3390/ph16060788.

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Even before behavioral disturbances, neuroleptics, amphetamine, and domperidone application rapidly emerged severe occlusion/occlusion-like syndrome, shared innate vascular and multiorgan failure in rats, comparable to occlusion/occlusion-like syndrome described with vessel(s) occlusion or similar noxious procedures application. As therapy, i.e., activation of the collateral pathways, “bypassing key” (activated azygos vein pathway, direct blood flow delivery), the stable gastric pentadecapeptide BPC 157 is a novel solution. Recently, BPC 157 therapy particularly counteracted neuroleptic- or L-NAME-induced catalepsy, lithium intoxication, and schizophrenia positive and negative symptoms (amphetamine/methamphetamine/apomorphine/ketamine). In rats with complete calvariectomy, medication (BPC 157 10 µg/kg, 10 ng/kg ip or ig) was given 5 min after distinctive dopamine agents (mg/kg ip) (haloperidol (5), fluphenazine (5), clozapine (10), risperidone (5), olanzapine (10), quetiapine (10), or aripiprazole (10), domperidone (25), amphetamine (10), and combined amphetamine and haloperidol) and assessed at 15 min thereafter. All neuroleptic-, domperidone-, and amphetamine-induced comparable vascular and multiorgan failure severe syndrome was alleviated with BPC 157 therapy as before major vessel(s) occlusion or other similar noxious procedures. Specifically, all severe lesions in the brain (i.e., immediate swelling, hemorrhage), heart (i.e., congestion, arrhythmias), and lung (i.e., congestion, hemorrhage), as well as congestion in the liver, kidney, and gastrointestinal (stomach) tract, were resolved. Intracranial (superior sagittal sinus), portal, and caval hypertension and aortal hypotension were attenuated or eliminated. BPC 157 therapy almost annihilated arterial and venous thrombosis, peripherally and centrally. Thus, rapidly acting Virchow triad circumstances that occur as dopamine central/peripheral antagonists and agonist essential class-points, fully reversed by BPC 157 therapy, might be overwhelming for both neuroleptics and amphetamine.

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Smoday, Ivan Maria, Ivan Krezic, Luka Kalogjera, et al. "Pentadecapeptide BPC 157 as Therapy for Inferior Caval Vein Embolization: Recovery of Sodium Laurate-Post-Embolization Syndrome in Rats." Pharmaceuticals 16, no. 10 (2023): 1507. http://dx.doi.org/10.3390/ph16101507.

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After inferior caval vein embolization therapy, post-embolization syndrome (sodium laurate 10 mg/kg, 0.1 mL into rat inferior caval vein, assessment at 15, 30, 60 min, prime lung lesions, thromboemboli occluding lung vessels), as a severe occlusion/occlusion-like syndrome, might be resolved as a whole by stable gastric pentadecapeptide BPC 157 therapy. At 5 min after laurate injection, stable gastric pentadecapeptide BPC 157 was implemented as therapy (10 µg/kg, 10 ng/kg intraperitoneally or intragastrically). As before, confronted with the occlusion of major vessel(s) or similar noxious procedures, such as rapidly acting Virchow triad circumstances, the particular effect of the therapy (i.e., collateral pathways activation, “bypassing vascular key”, i.e., direct blood flow delivery via activation of azygos vein) assisted in the recovery of the vessel/s and counteracted multiorgan failure due to occlusion/occlusion-like syndrome as a whole in the laurate-injected rats. Along with prime lung lesions and thromboemboli occluding lung vessels, post-embolization syndrome rapidly occurred peripherally and centrally as a shared multiorgan and vessel failure, brain, heart, lung, liver, kidney, and gastrointestinal tract lesions, venous hypertension (intracranial (superior sagittal sinus), portal, and caval), aortal hypotension, progressing thrombosis in veins and arteries and stasis, congested and/or failed major veins, and severe ECG disturbances. Whatever the cause, these were all counteracted, eliminated, or attenuated by the application of BPC 157 therapy. As recovery with BPC 157 therapy commonly and rapidly occurred, reversing the collapsed azygos vein to the rescuing collateral pathway might initiate rapid direct blood delivery and start blood flow reorganization. In conclusion, we suggest BPC 157 therapy to resolve further vascular and embolization injuries.

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Sikiric, Predrag, Sven Seiwerth, Anita Skrtic, et al. "Acute Compartment Syndrome and Intra-Abdominal Hypertension, Decompression, Current Pharmacotherapy, and Stable Gastric Pentadecapeptide BPC 157 Solution." Pharmaceuticals 18, no. 6 (2025): 866. https://doi.org/10.3390/ph18060866.

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In this study, pharmacotherapies of abdominal compartment syndrome (ACS) and intra-abdominal hypertension (IAH) in animal studies were reviewed from the perspective of ACS/IAH as failed cytoprotection issues, as non-specific injuries, and from the point of view of the cytoprotection concept as resolution. Therefore, this review challenges the unresolved theoretical and practical issues of severe multiorgan failure, acknowledged significance in clinics, and resolving outcomes (i.e., open abdomen). Generally, the reported agents not aligned with cytoprotection align with current pharmacotherapy limitations and have (non-)confirmed effectiveness, mostly in only one organ, mild/moderate IAH, prophylactic application, and provide only a tentative resolution. Contrarily, stable gastric pentadecapeptide BPC 157 therapy, as a novel and relevant cytoprotective mediator having pleiotropic beneficial effects, simultaneously resolves many targets, resolving established disturbances, specifically compression/ischemia (grade III and grade IV), and decompression/advanced reperfusion. BPC 157 therapy rapidly activates collateral bypassing pathways, and, in ACS and IAH, and later, in reperfusion, there is a “bypassing key” (i.e., azygos vein direct blood flow delivery). This serves to counteract multiorgan and vessel failure, including lesions and hemorrhages in the brain, heart, lung, liver, kidney and gastrointestinal tract, thrombosis, peripherally and centrally, intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, occlusion/occlusion-like syndrome, advanced Virchow triad circumstances, and free radical formation acting as a membrane stabilizer and free radical scavenger. Likewise, not only in ACS/IAH resolving, but also in other occlusion/occlusion-like syndromes, this “bypassing key” could be an effect of the essential endothelial cytoprotective capacity of BPC 157 and a particular modulatory effect on the NO-system, and a rescuing impact on vasomotor tone.

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Tepes, Marijan, Ivan Krezic, Hrvoje Vranes, et al. "Stable Gastric Pentadecapeptide BPC 157 Therapy: Effect on Reperfusion Following Maintained Intra-Abdominal Hypertension (Grade III and IV) in Rats." Pharmaceuticals 16, no. 11 (2023): 1554. http://dx.doi.org/10.3390/ph16111554.

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Given in reperfusion, the use of stable gastric pentadecapeptide BPC 157 is an effective therapy in rats. It strongly counteracted, as a whole, decompression/reperfusion-induced occlusion/occlusion-like syndrome following the worst circumstances of acute abdominal compartment and intra-abdominal hypertension, grade III and grade IV, as well as compression/ischemia-occlusion/occlusion-like syndrome. Before decompression (calvariectomy, laparotomy), rats had long-lasting severe intra-abdominal hypertension, grade III (25 mmHg/60 min) (i) and grade IV (30 mmHg/30 min; 40 mmHg/30 min) (ii/iii), and severe occlusion/occlusion-like syndrome. Further worsening was caused by reperfusion for 60 min (i) or 30 min (ii/iii). Severe vascular and multiorgan failure (brain, heart, liver, kidney, and gastrointestinal lesions), widespread thrombosis (peripherally and centrally) severe arrhythmias, intracranial (superior sagittal sinus) hypertension, portal and caval hypertension, and aortal hypotension were aggravated. Contrarily, BPC 157 therapy (10 µg/kg, 10 ng/kg sc) given at 3 min reperfusion times eliminated/attenuated venous hypertension (intracranial (superior sagittal sinus), portal, and caval) and aortal hypotension and counteracted the increases in organ lesions and malondialdehyde values (blood ˃ heart, lungs, liver, kidney ˃ brain, gastrointestinal tract). Vascular recovery promptly occurred (i.e., congested inferior caval and superior mesenteric veins reversed to the normal vessel presentation, the collapsed azygos vein reversed to a fully functioning state, the inferior caval vein–superior caval vein shunt was recovered, and direct blood delivery returned). BPC 157 therapy almost annihilated thrombosis and hemorrhage (i.e., intracerebral hemorrhage) as proof of the counteracted general stasis and Virchow triad circumstances and reorganized blood flow. In conclusion, decompression/reperfusion-induced occlusion/occlusion-like syndrome counteracted by BPC 157 therapy in rats is likely for translation in patients. It is noteworthy that by rapidly counteracting the reperfusion course, it also reverses previous ischemia-course lesions, thus inducing complete recovery.

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Dickson, Brendan C. "Virchowʼs Triad?" Southern Medical Journal 97, № 9 (2004): 915–16. http://dx.doi.org/10.1097/01.smj.0000136235.11281.eb.

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Dickson, Brendan C. "Virchow’s triad." British Journal of Haematology 145, no. 3 (2009): 433. http://dx.doi.org/10.1111/j.1365-2141.2009.07617.x.

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Larena-Avellaneda, A. "Wirklich Virchows Trias?" Gefässchirurgie 23, no. 2 (2018): 64–65. http://dx.doi.org/10.1007/s00772-018-0367-y.

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YAMASHITA, Atsushi, and Yujiro ASADA. "Virchow's triad revisited." Japanese Journal of Thrombosis and Hemostasis 22, no. 1 (2011): 3–10. http://dx.doi.org/10.2491/jjsth.22.3.

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Pamphlett, Roger. "Straddling Virchow's triad." Medical Journal of Australia 142, no. 3 (1985): 236–37. http://dx.doi.org/10.5694/j.1326-5377.1985.tb133130.x.

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Louw, V. J., and N. A. B. Ntusi. "Virchow’s triad revisited." South African Medical Journal 109, no. 11 (2019): 822. http://dx.doi.org/10.7196/samj.2019.v109i11.14442.

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Brotman, Daniel J., Steven R. Deitcher, Gregory Y. H. Lip, and Axel C. Matzdorff. "Virchow’s Triad Revisited." Southern Medical Journal 97, no. 2 (2004): 213–14. http://dx.doi.org/10.1097/01.smj.0000105663.01648.25.

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Malone, Padraic Colm, and Paul S. Agutter. "Is ‘Virchow’s triad’ useful?" British Journal of Haematology 145, no. 6 (2009): 839. http://dx.doi.org/10.1111/j.1365-2141.2009.07685.x.

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Kyrle, Paul A., and Sabine Eichinger. "Is Virchow's triad complete?" Blood 114, no. 6 (2009): 1138–39. http://dx.doi.org/10.1182/blood-2009-05-223511.

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Alexander, Kevin M., Muthiah Vaduganathan, Arman Qamar, and Marie D. Gerhard-Herman. "Grim Messenger: Virchow's Node Presenting with Virchow's Triad." American Journal of Medicine 129, no. 9 (2016): 948–51. http://dx.doi.org/10.1016/j.amjmed.2016.05.009.

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Chung, Irene, and Gregory Y. H. Lip. "Virchow’s Triad Revisited: Blood Constituents." Pathophysiology of Haemostasis and Thrombosis 33, no. 5-6 (2003): 449–54. http://dx.doi.org/10.1159/000083844.

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Lowe, Gordon D. O. "Virchow’s Triad Revisited: Abnormal Flow." Pathophysiology of Haemostasis and Thrombosis 33, no. 5-6 (2003): 455–57. http://dx.doi.org/10.1159/000083845.

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Malone, P. Colm. "Further Reflections on Virchow’s Triad." Southern Medical Journal 98, no. 1 (2005): 125. http://dx.doi.org/10.1097/01.smj.0000145312.69219.a2.

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Vlasov, T. D., and S. M. Yashin. "Arterial and venous thrombosis. Is the Virchow’s triad always valid?" Regional blood circulation and microcirculation 21, no. 1 (2022): 78–86. http://dx.doi.org/10.24884/1682-6655-2022-21-1-78-86.

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Despite the success of conservative and surgical treatment of vascular diseases, the prevention of arterial and venous thrombosis remains extremely actual. For more than a hundred years, the so-called «Virchow’s triad» has been used to explain the mechanism of thrombosis: 1–slowing of blood flow; 2–hypercoagulation; 3 – damage to the vascular wall. However, the combination of these factors is fully applicable only for venous thrombosis and limited for arterial thrombosis. The generally accepted strategy for the prevention of venous thrombosis is the use of anticoagulants, while for arterial thrombosis – antiaggregants. In recent years the mechanisms of blood clot formation at high blood flow rates in the areas of arterial stenosis, as well as the role of platelets and von Willebrand factor in this process, were investigated. In the presented review, the details of the mechanisms of thrombosis in the arteries are analyzed and the concept of «arterial triad» is introduced. Arterial triad includes: 1 – arterial stenosis (increase in shear rate); 2 – platelets (their activation and interaction with von Willebrand factor); 3 – damage of the vascular wall. The arterial triad describes the mechanisms of thrombosis in the presence of artery stenosis (usually due to atherosclerosis). Understanding similarities and differences between Virchow’s and arterial triads, will allow us to estimate the risk factors in patients with cardiovascular pathology and develop optimal methods of their prevention.

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Monsuez, J. J. "Rudolf Virchow : la thrombose, la triade et le duel." Archives des Maladies du Coeur et des Vaisseaux - Pratique 2012, no. 207 (2012): 33–34. http://dx.doi.org/10.1016/s1261-694x(12)70370-x.

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Brotman, Daniel J. "Response: Further Reflections on Virchow’s Triad." Southern Medical Journal 98, no. 1 (2005): 126. http://dx.doi.org/10.1097/01.smj.0000149419.55620.27.

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Janssens, Stefan, and Frans Van de Werf. "Acute coronary syndromes: Virchow's triad revisited." Lancet 348 (December 1996): S2. http://dx.doi.org/10.1016/s0140-6736(96)98012-5.

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