Deep venous thrombosis: The valve cusp hypoxia thesis and its incompatibility with modern orthodoxy |
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| Affiliation: | 1. Clinical Hospital Centre Zagreb, Department of Orthopaedic Surgery, Zagreb, Croatia;2. University of Zagreb School of Medicine, Clinical Hospital Centre Zagreb, Department of Orthopaedic Surgery, Zagreb, Croatia;1. Division of Medical Oncology, School of Medicine, Karadeniz Technical University, 61080 Trabzon, Turkey;2. Division of Radiation oncology, School of Medicine, Karadeniz Technical University, Trabzon, Turkey;3. Department of Biochemistry, School of Medicine, Karadeniz Technical University, Trabzon, Turkey;1. Department of Neurosurgery, Yiwu Central Hospital, Wenzhou Medical College, Yiwu 32200, Zhejiang Province, People’s Republic of China;2. Department of Neurosurgery, Renji Hospital, School of Medicine, Shanghai Jiao-Tong University, No. 1630, Dongfang Road, Pudong New District, Shanghai 200127, People’s Republic of China;1. Department of Child and Adolescent Psychiatry, School of Paediatrics and Child Health & School of Psychiatry and Clinical Neurosciences, Faculty of Medicine, Dentistry and Health Sciences, The University of Western Australia (M561), Perth, WA, Australia;2. Specialised Child and Adolescent Mental Health Services (CAMHS), Department of Health in Western Australia, Perth, WA, Australia;3. Community Child and Adolescent Mental Health Services, Department of Health in Western Australia, Perth, WA, Australia;4. Paediatric Consultation-Liaison Program, Child and Adolescent Mental Health Services, Department of Health in Western Australia, Perth, WA, Australia;5. Centre for Neonatal Research and Education, The University of Western Australia (M551), Perth, WA, Australia;6. The Perron Rotary Express Milk Bank, King Edward Memorial Hospital, Subiaco, WA, Australia |
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| Abstract: | The valve cusp hypoxia thesis (VCHT) of the aetiology of deep venous thrombosis (DVT) was adumbrated in this journal in 1977 and fully articulated in 2008, the original hypothesis having been strongly corroborated by experiments published in 1981 and 1984. It presents a unitary account of the pathogenesis of venous thrombosis and embolism that is rooted in the pathophysiological tradition of Hunter, Virchow, Lister, Welch and Aschoff, a tradition traceable back to Harvey. In this paper we summarise the thesis in its mature form, consider its compatibility with recent advances in the DVT field, and ask why it has not yet been assimilated into the mainstream literature, which during the past half century has been dominated by a haematology-orientated ‘consensus model’. We identify and discuss seven ways in which the VCHT is incompatible with these mainstream beliefs about the aetiology of venous thrombosis, drawing attention to: (1) the spurious nature of ‘Virchow’s triad’; (2) the crucial differences between ‘venous thrombus’ and ‘clot’; the facts that (3) venous thrombi form in the valve pockets (VVPs), (4) DVT is not a primarily haematological condition, (5) the so-called ‘thrombophilias’ are not thrombogenic per se; (6) the conflict between the single unitary aetiology of DVT and the tacit assumption that the condition is ‘multicausal’; (7) the inability of anticoagulants to prevent the initiation of venous thrombogenesis, though they do prevent the growth of thrombi to clinically significant size. In discussing point (7), we show that the VCHT indicates new approaches to mechanical prophylaxis against DVT. These approaches are then formulated as experimentally testable hypotheses, and we suggest methods for testing them preclinically using animal trials. |
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