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Henri Bounameaux is a known clinical faculty and Professor of Medicine (hon), specialized in internal and vascular medicine (angiology), and general medicine. [1]
Professor Bounameaux served as the Dean of Faculty of medicine at the University of Geneva, Switzerland. Presently, Professor Bounameaux is a distinguished professor of the University of Geneva and the President of the Swiss Academy of Medical Sciences (SAMS). [2]
Professor Bounameaux has authored numerous research papers and several review papers. His research interests cover all aspects related to the prevention, diagnosis, and treatment of venous thromboembolism. [3] His main contribution to the field relates to the non-invasive work-up of suspected pulmonary embolism, particularly the use of fibrin D-dimer. He was among the first scientists in the late eighties to suggest that this dosage in the patient plasma allowed to safely rule out venous thromboembolism, which was demonstrated in subsequent publications of the Geneva research group. [4] [5] He was among the first scientists in the late eighties to suggest that this dosage in the patient plasma allowed to safely rule out venous thromboembolism, which was demonstrated in the subsequent publications of the Geneva research group. [6]
Henri Bounameaux completed his primary and secondary education at Lubumbashi (Belgian Congo, Zaïre) and Baccalaureate type C from St.-Louis, France in 1971. [7]
He received his medical degree and post-graduate specialization from the Faculty of medicine, University of Basel , and is board-certified in internal and vascular medicine (angiology). He completed the post-doctoral education from Center for Thrombosis and Vascular Research, Belgium. [8]
He is now an emeritus professor of the University of Geneva.
Professor Bounameaux research interests are broad and include studies on Non-invasive vascular diagnosis, venous thromboembolism and pulmonary embolism & Cardiology, Angiology, Hemostasis. [3] [9] His main contribution to the field relates to the non-invasive work-up of suspected pulmonary embolism, particularly the use of fibrin D-dimer. He was among the first scientists in the late eighties to suggest that this dosage in the patient plasma allowed to safely rule out venous thromboembolism, which was demonstrated in subsequent publications of the Geneva research group. [10]
During his career, Professor Bounameaux has received the following awards and honors:
Thrombosis is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. A clot, or a piece of the clot, that breaks free and begins to travel around the body is known as an embolus.
Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism). Symptoms of a PE may include shortness of breath, chest pain particularly upon breathing in, and coughing up blood. Symptoms of a blood clot in the leg may also be present, such as a red, warm, swollen, and painful leg. Signs of a PE include low blood oxygen levels, rapid breathing, rapid heart rate, and sometimes a mild fever. Severe cases can lead to passing out, abnormally low blood pressure, obstructive shock, and sudden death.
Venous thrombosis is the blockage of a vein caused by a thrombus. A common form of venous thrombosis is deep vein thrombosis (DVT), when a blood clot forms in the deep veins. If a thrombus breaks off (embolizes) and flows to the lungs to lodge there, it becomes a pulmonary embolism (PE), a blood clot in the lungs. The conditions of DVT only, DVT with PE, and PE only, are all captured by the term venous thromboembolism (VTE).
Factor V Leiden is a variant of human factor V, which causes an increase in blood clotting (hypercoagulability). Due to this mutation, protein C, an anticoagulant protein that normally inhibits the pro-clotting activity of factor V, is not able to bind normally to factor V, leading to a hypercoagulable state, i.e., an increased tendency for the patient to form abnormal and potentially harmful blood clots. Factor V Leiden is the most common hereditary hypercoagulability disorder amongst ethnic Europeans. It is named after the Dutch city of Leiden, where it was first identified in 1994 by Rogier Maria Bertina under the direction of Pieter Hendrick Reitsma. Despite the increased risk of venous thromboembolisms, people with one copy of this gene have not been found to have shorter lives than the general population. It is an autosomal dominant genetic disorder with incomplete penetrance.
Fibrinogen is a glycoprotein complex, produced in the liver, that circulates in the blood of all vertebrates. During tissue and vascular injury, it is converted enzymatically by thrombin to fibrin and then to a fibrin-based blood clot. Fibrin clots function primarily to occlude blood vessels to stop bleeding. Fibrin also binds and reduces the activity of thrombin. This activity, sometimes referred to as antithrombin I, limits clotting. Fibrin also mediates blood platelet and endothelial cell spreading, tissue fibroblast proliferation, capillary tube formation, and angiogenesis and thereby promotes revascularization and wound healing.
Deep vein thrombosis (DVT) is a type of venous thrombosis involving the formation of a blood clot in a deep vein, most commonly in the legs or pelvis. A minority of DVTs occur in the arms. Symptoms can include pain, swelling, redness, and enlarged veins in the affected area, but some DVTs have no symptoms.
Low-molecular-weight heparin (LMWH) is a class of anticoagulant medications. They are used in the prevention of blood clots and, in the treatment of venous thromboembolism, and the treatment of myocardial infarction.
D-dimer is a dimer that is a fibrin degradation product, a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it contains two D fragments of the fibrin protein joined by a cross-link, hence forming a protein dimer.
Ximelagatran is an anticoagulant that has been investigated extensively as a replacement for warfarin that would overcome the problematic dietary, drug interaction, and monitoring issues associated with warfarin therapy. In 2006, its manufacturer AstraZeneca announced that it would withdraw pending applications for marketing approval after reports of hepatotoxicity during trials, and discontinue its distribution in countries where the drug had been approved.
Paget–Schroetter disease is a form of upper extremity deep vein thrombosis (DVT), a medical condition in which blood clots form in the deep veins of the arms. These DVTs typically occur in the axillary and/or subclavian veins.
In medicine, Homans' sign is considered by some physicians to be a sign of deep vein thrombosis (DVT). It was defined by John Homans in 1941 as discomfort behind the knee upon forced dorsiflexion of the foot. After many examples of false-positive Homans' signs were reported, Homans redefined it in 1944, stating that "discomfort need have no part in the reaction", and that increased resistance, involuntary flexure of the knee or pain in the calf upon forced dorsiflexion should be considered positive responses.
Activated protein C resistance (APCR) is a hypercoagulability characterized by a lack of a response to activated protein C (APC), which normally helps prevent blood from clotting excessively. This results in an increased risk of venous thrombosis, which resulting in medical conditions such as deep vein thrombosis and pulmonary embolism. The most common cause of hereditary APC resistance is factor V Leiden mutation.
Post-thrombotic syndrome (PTS), also called postphlebitic syndrome and venous stress disorder is a medical condition that may occur as a long-term complication of deep vein thrombosis (DVT).
Hyperprothrombinemia is a state of high of prothrombin levels in the blood which leads to hypercoagulability. An example of a genetic cause includes the mutation prothrombin G20210A. Hyperprothrombinemia is a risk factor for venous thromboembolism.
The Geneva score is a clinical prediction rule used in determining the pre-test probability of pulmonary embolism (PE) based on a patient's risk factors and clinical findings. It has been shown to be as accurate as the Wells Score, and is less reliant on the experience of the doctor applying the rule. The Geneva score has been revised and simplified from its original version. The simplified Geneva score is the newest version for the general population, and predicted to have the same diagnostic utility as the original Geneva score. A version of the revised score was modified to be applicable to pregnant patients.
Superficial thrombophlebitis is a thrombosis and inflammation of superficial veins presenting as a painful induration (thickening) with erythema, often in a linear or branching configuration with a cordlike appearance.
Prothrombin G20210A is a genetic condition that increases the risk of blood clots including from deep vein thrombosis, and of pulmonary embolism. One copy of the mutation increases the risk of a blood clot from 1 in 1,000 per year to 2.5 in 1,000. Two copies increases the risk to up to 20 in 1,000 per year. Most people never develop a blood clot in their lifetimes.
Kazi Mobin-Uddin was an American surgeon specializing in vascular surgery research.
Ultrasonography in suspected deep vein thrombosis focuses primarily on the femoral vein and the popliteal vein, because thrombi in these veins are associated with the greatest risk of harmful pulmonary embolism.
The Wells score is a clinical prediction rule used to classify patients suspected of having pulmonary embolism (PE) into risk groups by quantifying the pre-test probability. It is different than Wells score for DVT. It was originally described by Wells et al. in 1998, using their experience from creating Wells score for DVT in 1995. Today, there are multiple versions of the rule, which may lead to ambiguity.