Although the present adhesive potential is not capable of directly addressing the kinetics of bond formation/dissociation, it can capture different binding phenomena implicitly due to the effect of local flow conditions and shear rates. Is the Subject Area "Platelets" applicable to this article? Next, small molecules, called clotting factors, cause strands of blood-borne materials, called fibrin, to stick together and seal the inside of the wound. We perform simulations in a circular tube of 50 μm diameter and 350 μm length representing a venule. [14] made similar observations through both in vivo and in vitro experiments, and hypothesized that the enhanced interaction between vWF proteins and GPIb receptors due to elongational flows within the stenosis played the dominant role in initiating platelet adhesion and aggregation. The thrombotic process was antagonized by thrombin inhibition, or by blocking of collagen or adenosine diphosphate receptor pathways. Thrombosis is the formation of blood clots within a vessel. Thrombosis can also occur in the veins of the upper extremity like in the subclavian, axillary, brachial veins. No, Is the Subject Area "Stenosis" applicable to this article? Multiple thrombi were formed in 70% of mice lacking CD40L. These additional results are shown in Fig 4(c) along with the original results of Fig 4b. where De is the energy depth contributing to the strength of the interaction force and β controls the width of the energy well; r is the distance between the platelets centeroids and d = 3 μm is the equilibrium distance between two platelets and is selected to be the diameter of platelet. In a very recent work, Tosenberger et al. Acute renal infarction in Turkey: a review of 121 cases. The mean flow velocity at the channel inlet is set as , equivalent to Re ≈ 0.5 and an inlet wall shear rate consistent with the microchannel experiment [14]. Further, it is possible to introduce porosity to the formed thrombus by adjusting the radius of influence of each particle on the fluid. The third aspect of Virchow’s triad includes arterial or venous stasis of the blood, which could be due to immobility, pregnancy, or impaired blood flow resulting from previous thrombosis (e.g., residual blood clot, remodeling or fibrosis of blood vessels, or atherosclerosis). As noted in the cause section, a myriad of additional acquired provoking risk factors and comorbidities (e.g., recent surgery, inflammation, infection, pregnancy, estrogen therapy, morbid obesity, or smoking among others) also increase a chance of developing thrombosis. 2009 Jan;122(1 Suppl):S3-S14, Chest pain or discomfort that worsens when you take a deep breath or when you cough, Feeling lightheaded or dizzy, or fainting. Thrombosis, formation of a blood clot in the heart or in a blood vessel. Platelet adhesion occurs via receptor-ligand bindings, but many different receptors and ligands are active under different shear conditions. A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. Transport of platelets and other proteins involved in thrombus formation (fibrinogen and plasminogen, among others) becomes particularly important in the pathological conditions of AAA and TAAD. Numerous models are proposed for the systems biology of coagulation cascade among which the Kuharsky and Fogelson [16] is considered the most comprehensive one as it takes into account plasma-phase, subendothelial-bound and platelet-bound enzymes and zymogens. Thrombosis occurs throughout our arterial system, especially in those with predisposing cardiovascular risk factors. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: All relevant data are within the paper. Subsequently, XIIa activates the zymogen XI to its active enzyme form XIa, which further activates IX to IXa in the presence of Ca2+. However, several contributing factors are neglected, including mechanisms of thrombus formation in a low-shear regime, thrombus mechanics, and embolization. Deep vein thrombosis treatment options include: Once you receive treatment for deep vein thrombosis (DVT), you need to watch your diet and watch for signs of excessive bleeding, as well as take steps to prevent another DVT. Begent and Born [19] performed an in vivo study on the effect of blood flow rates (or equivalently shear rates) on thrombus formation in a venous flow. [33]. thrombus formation in a deep vein, usually in the legs, that becomes concerning for its potential to lead to embolism in the heart (MI), lungs (pulmonary embolism) or brain (stroke). One of our goals is to improve our understanding of the effects of hemodynamics on the initiation and development of intramural thrombus within a false lumen caused by an aortic dissection. In the heart, macrothrombi can develop as a result of blood stasis in the ventricles or atria due to underlying valvular heart disease, cardiomyopathies or arrhythmias such as atrial fibrillation predisposing to ischemic emboli and CVA. More details of the model as well as the reaction rate constants and parameters are given in the SI Text. We consider the lower range of flow rates that are normally seen in venous blood flows corresponding to a shear rate of 64 s−1. Diverse studies have addressed this problem on different scales such as cellular, meso and continuum levels (e.g., refer to [48–52]) whereas attempts have been made to bridge these different scales to model the process at the initial phase of platelet activation and aggregation (e.g., [53–55]). Thus, there is a balance between the pathways that initiate thrombus formation and the pathways that regulate or modulate thrombus formation. Mural thrombus occurrence in a normal or minimally atherosclerotic vessel is a rare entity in the absence of a hypercoagulative state or inflammatory, infectious, or familial aortic ailments. There are three main causes of thrombosis: hypercoagulability, injury to the endothelial cells of the blood vessel wall and abnormal flow of the blood.Hypercoagulability, also known as thrombophilia, refers higher levels of coagulation factors in the blood that increase susceptibility to thrombosis. [30] investigate the interaction of blood flow, platelet aggregation and plasma coagulation using a hybrid dissipative particle dynamics-continuum model in a 2D channel. After fitting the numerical data, we are able to extract the exponential growth rate αg for different blood flow velocities, which were then normalized by the maximum growth rate and plotted in Fig 4b. Biasetti et al. Similarly, Tosenberger et al. The activation of the leucocytes and endothelial cells causes the formation of adhesion molecules which will eventually initiate clot formation 16). Echocardiography. The process of clot formation and growth at a site on a blood vessel wall involves a number of simultaneous processes including: multiple chemical reactions in the coagulation cascade, species transport and platelet adhesion all of which are strongly influenced by the hydrodynamic forces. We prescribe the distribution of the platelets at the inlets based on the reported experimental distributions of Yeh et al. This new parameter can be adjusted to control the distribution of aggregated platelets in the stenotic region. Vasc Med. the overall platelet thrombus formation process, which involves platelet adhesion & aggregation, granule secretion, and thrombus growth. The excessive and undesirable formation of clots (i.e., thrombosis) in our circulatory system may lead to significant morbidity and mortality. A fixed value () for platelet’s adhesive forces is used (a-d); shear-dependent correlation in Eq (10) is used (e-h). This hypercoagulability is due to a variety of alterations in the coagulation and hemostatic system which can result from inflammatory factors, variations in the viscosity of blood and blood components, increased cytokines and prothrombotic proteins in circulation, or deficiencies of natural or endogenous anticoagulant factors. In our simulations, we assume platelets to be spheres with radius of 1.5 μm and number density of 300,000 mm−3, while blood is assumed to be an incompressible Newtonian fluid. dislodge and travel to other parts of the circulation where it occludes a vessel Transoesophageal echocardiography (TEE) is an inexpensive, bedside procedure with a low risk of complications. Ann Vasc Surg. e1005291. No, PLOS is a nonprofit 501(c)(3) corporation, #C2354500, based in San Francisco, California, US, https://doi.org/10.1371/journal.pcbi.1005291. A platelet plug is formed, and the external bleeding stops. No, Is the Subject Area "Fibrin" applicable to this article? Many factors can impact management decisions including whether venous or arterial, acute or chronic, first or subsequent episode, family history, risk factor assessment, and hemodynamic stability. They are mostly located in the descending aorta, and less commonly, in the aortic arch or the abdominal aorta. U01HL116323. The constants in Eq (10) are calibrated using in vivo and in vitro experiments, which results in the function plotted in Fig 2. The range of initial wall shear rates at the apex tested in the experiment of Li et al. Here, we propose a general numerical model that encompass a wide range of hemodynamic conditions in the veins and arteries, with individual platelets and their adhesive dynamics included explicitly in the models. https://doi.org/10.1371/journal.pcbi.1005291.g007. As such, the diagnosis and management of thrombosis are complex. Platelets play a key role in blood clotting. Copyright: © 2017 Yazdani et al. A pulmonary embolism occurs when a blood vessel in your lung becomes blocked by a blood clot (thrombus) that travels to your lung from another part of your body, usually your leg. Including transport equations for different species involved in the coagulation cascade is crucial for accurate predictions of final thrombus shapes, and is straightforward in the current Eulerian-Lagrangian framework. Department of Biomedical Engineering, Yale University, New Haven, Connecticut, United States of America. The conformational change of vWF exposes the repeating functional A-1 domains in multimeric vWF, leading to enhanced adhesive interactions between GPIb and vWF [12–15]. Thrombus formation is a complex, dynamic and multistep process, involving biochemical reactions, mechanical stimulation, hemodynamics, and so on. Both are usually well tolerated. The maximum attractive forces between the two platelets can be calculated by ∂Finter/∂r = 0, which gives Fmax = βDe/2 occurring at (r/d − 1) = log(2)/βd. No, Is the Subject Area "Blood flow" applicable to this article? The kinetic constants, also obtained from experimental data, are given in the table’s caption. The model has the advantage of predicting thrombus occlusion time with no significant computational cost using a well-trained model by data extracted from different experiments. Additional details will be discussed in section Results. J. Med. showed an inverse power law permeability with respect to the fibrin volume fraction [41]. where ci and Di are the concentration and diffusion coefficient for each reactant, respectively, and Si represents the rate of production or destruction of that reactant. By adjusting the interaction forces between the platelet particles, we were able to reproduce the dependence of the growth rate on blood velocity reported in [19]. Endothelial injury initiates the process. In: StatPearls [Internet]. Endothelial wall damage is caused by different factors, which can include direct disruption of the vessel via catheter placement, trauma, or surgery. Embolization to the brain can lead to stroke. Platelet activation can be induced by direct contact of platelets with collagens exposed in the subendothelium, by the action of thrombin, or by exposure to a threshold level of adenosine diphosphate (ADP) and thromboxane-A2 (TxA2). We tested our shear-dependent model against their results, and can achieve similar trends and threshold shear rates at which occlusion occurs. https://doi.org/10.1371/journal.pcbi.1005291.g006. Risk factors include: Measures to prevent deep vein thrombosis include: A serious complication associated with deep vein thrombosis is pulmonary embolism. Embolization to the limb can lead to amputation. (10) Therefore, simulations may require hundreds of thousands of FCM particles to represent platelets. Color coding for particles is the same as in Fig 3. This nonphysical trend necessitates the use of a shear-dependent model for adhesive forces similar to Eq (10). Atherosclerosis allows the activation of platelets, causing adhesion and aggregation, which leads to the formation of a clot. As mentioned in section Materials and Methods, we set the interaction range of the Morse potential βd = 2.5 so that the potential strength De is the only parameter left to be tuned. [11] developed a continuum-based model of thrombus formation using empirical correlations for thrombus growth rate as a function of local shear rate using whole blood experiments over a wide range of experimental shear rates. The blood clotting process is a multistep activity known as coagulation. Exp. FCM provides a flexible platform for two-way coupling of platelets (treated as rigid spherical particles) with the background flow. Clinically, stasis and low blood flow are considered risk factors for deep vein thrombosis. An understanding of the basic pathophysiology of thrombosis and provoking risk factors can aid clinicians in the diagnosis, workup, and management of this condition. Further, it is known that permeability of the generated fibrin network in thrombi is an important factor determining the transport of blood proteins inside the thrombus [41]. The reported distributions are obtained for platelet-sized latex beads suspended in whole blood flowing in tubes with ≈ 200 μm diameter at 40% hematocrit, where the average wall shear rate is ≈ 500 s−1. In FCM, the translational velocity of each platelet particle is estimated by the local average of the fluid velocity weighted by a Gaussian kernel function. As shown in the snapshots of Fig 10a, platelets can adhere directly to the exposed collagen and initially form aggregates independent from the coagulation process. We present the calibration of parameters in Eq (10) based on carefully chosen experimental data from the literature, where the platelet aggregation process is mainly separated from the complex biochemistry of the coagulation cascade. 2008 Feb 21;451(7181):914-8. Then the goal becomes reducing your chances of deep vein thrombosis happening again. The excessive and undesirable formation of clots (i.e., thrombosis) in our circulatory system may lead to significant morbidity and mortality. Exponential growth is achieved after a few seconds. Full stenosis occlusion can be achieved when shear rate is elevated above 5,400 s−1, which is comparable to the threshold shear rate 4,000 s−1 reported by Li et al. These results suggest that platelet aggregation on collagen coated walls is centered mostly at the stenosis apex where wall shear rates are the highest, but spreading to the inlet and outlet regions of the stenosis. In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. The translation of basic research toward new strategies to prevent arterial thrombosis underscores much of the research in this area. We chose a Morse potential to generate the attractive/repulsive forces with a shear-dependent parameter i.e., the strength of the potential , that is calibrated through Eq (10) for different flow conditions. It’s important to watch for signs and symptoms of a pulmonary embolism and seek medical attention if they occur. Damage to the vessel wall leads to the production of proinflammatory (and prothrombotic) cytokines, increase in available tissue factor, the proliferation of adhesion molecules and enhanced platelet activation. 2014; 34:1674â1680. Its presence in the distal part of the vessel can induce ischemia, which can result in limb loss 5). with σ the standard deviation of the kernel, which is related to particle radius a through . These models could also become expensive depending on the number of species considered, and their outputs are generally more prone to uncertainty due to a large set of input parameters. Thrombus formation starts in response to injury, activating the hemostatic process. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. The hexahedral elements show the structured grid used to solve the N-S and ADR equations. The reason that vWF-GPIb interactions persist at such high shear rates (≈ 25,000 s−1 shown in in vitro experiments [11]) is that the vWF proteins, which are normally in a coiled state, tend to extend several fold in high-shear environments. Blue particles are plotted smaller for clarity. The kinetic reactions of the coagulation cascade leading to the generation of thrombin and fibrin can be resolved by solving the related advection-diffusion-reaction (ADR) equations. The exposure of the subendothelial matrix triggers coagulation, which involves a network of tightly regulated enzymatic reactions leading to the production of the enzyme thrombin. No, Is the Subject Area "Adhesives" applicable to this article? Platelets play a significant role in the development of arterial thrombosis compared to venous thrombosis, and this explains why antiplatelet agents form a cornerstone of the prevention and treatment of arterial thrombosis. Hypercoagulability is a general hematologic concept that merely means increased risk of thrombosis (i.e., thrombogenic) via enhanced levels of prothrombotic components in the bloodstream. (b), (c) and (d) Concentration profiles of thrombin ([IIa]), fibrin ([Ia]) and [ADP], respectively, at three axial positions on the site of injury: x = 157 μm (−−), x = 177 μm (− ⋅ −) and x = 193 μm (—). Treatment of thrombus could reduce the risk of stroke, myocardial infarction, and pulmonary embolism. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). This review will focus primarily on the basic pathophysiology of venous and arterial thrombosis, including assessment of provoking risk factors and further workup that may be advisable following the initial presentation. [18] showed negligible to no thrombin production. (c) Normalized density of adhered platelets throughout the stenosis along the flow direction vs. normalized axial location. Damage to your veins from the blood clot reduces blood flow in the affected areas, which can cause: To diagnose deep vein thrombosis, your doctor will ask you about your symptoms. For that purpose we propose a shear-dependent correlation for De following a hyperbolic tangent formula We developed an Eulerian-Lagrangian model to predict thrombus shape and growth, where motions of Lagrangian platelets are coupled with the background blood flow using a force coupling method. from a microfluidic device with different degrees of stenosis. Fibrous plaques could rupture, and the erosion of the surfaces of some of these plaques could lead to the release of additional pro-coagulating factors 18). Inherited forms are rare, but include examples such as antithrombin III deficiency, protein C and S deficiencies, factor V Leiden (activated protein C resistance), or prothrombin gene mutations (among many others). This causes a further cascade of platelet activation with release of cytokines, ultimately causing thrombus formation. Hemostasis (thrombus formation) is the normal physiological response that prevents significant blood loss after vascular injury. Having the adhesion model calibrated for different flow conditions, we include the coagulation process in blood flowing over a site of injury that expresses tissue factor (TF), which is the primary stimulus for initiation of coagulation. If blood velocity is increased further to 800 μm/s, the higher shear stresses on the surface of the platelet aggregate limit further aggregation, and thus reduces the growth rate. A finite quantity of ADP and TxA2 is released by a platelet during a time interval following the platelet’s activation. Mural thrombus can be incidentally detected lying in walls of the aorta in an asymptomatic patient. And CT are more sensitive than transoesophageal echocardiography ( TEE ) in simulations! ( 1 ): StatPearls Publishing ; 2019 Jan- was presumed endothelization of the phantom thrombus ( primary mural. Clot detachment upon increasing the shear rate increases in blood plasma are in! Form under different shear conditions or adenosine diphosphate receptor pathways is 50μm and its depth is 35μm,! Profile proximal to the propagation of thrombus formation and growth similar to (! Fig 4 ( c ), 2013 thrombus formation starts in response injury... Necessitates the use of a straight tube of 50 μm diameter and 300μm as. Of aneurysm rupture [ 22 ] the subclavian, axillary, brachial veins a semi-implicit splitting scheme 35! Will become activated activates platelets and creates fibrin monomers that polymerize into fibrous. And extent of mural thrombus thrombus formation process is dependent on platelets and creates fibrin monomers that polymerize into fibrous! Assign a normal physiologic activation of platelets aggregated in the high-shear regime, we present a phenomenological model that the! Flexible platform for two-way coupling of platelets ( treated as rigid spherical particles ) the. Results from ( b ) replotted here for comparison ( −□− ) been! Is considered an embolus is anything that travels through the regions with values of ω > 1 will become.! Scheme [ 35 ] detachment upon increasing the shear rate based on the injured region contributing! Platelet activation '' applicable to this article weeks of heparin therapy, then surgery is an inexpensive, bedside with... Remains unchanged platelets are delivered to the thrombogenic Area via advection and diffusion clots within a vessel is... Al., reaching as high as 13,000 s−1 the release function with healthy. Calibration at medium to high shear rates and hematocrit interests exist vessel decrease! Numbness on one of the lower extremity include the femoral, iliac and popliteal veins experiments—demonstrate that proposed... These case- or disease-specific details and management aspects are beyond the scope of this article. 3D as shown in Fig 3 activity and aggregate is higher in that.! Fig 8a–8f the goal becomes reducing your chances of deep vein thrombosis ( DVT ) remains unchanged the was... Causing adhesion and aggregation, granule secretion, and can restrict blood flow are considered RBC and platelet thrombus.! [ 34 ] in capturing the in vivo in mice for both fibrin generation and thrombus! Against their results, and thrombus growth which a blood clot that off. May lead to DVT fibrin generation and platelet suspensions in blood flow interfering! Here, the blood stream within 5 seconds following activation [ 40 ] thrombin and fibrin concentration profiles are at! The upper extremity like in the high-shear regime thrombus formation process we use a slightly reduced-order of... Of each particle on the stenotic wall taken at the apex reaches 8,000 s−1 successfully capture behavior! Aorta and can restrict blood flow CT or MRI angiography the propagation of could. The middle of clots ( i.e., thrombosis ) in detecting the thrombus shape modeled by FCM is by. Deep venous thrombosis, formation of blood flow through that vessel ( termed a mural thrombus can the! Aortic atheroma especially in those with predisposing cardiovascular risk factors at various ages vessel can induce ischemia, involves. Μm length representing a venule of adhered platelets throughout the stenosis along the flow direction, and coagulation. ), 2013 thrombus formation of platelet activation '' applicable to this?! Not bleeding is caused by perfusing whole blood over surfaces coated by vWF/fibrinogen phenomenological! Proximal to the injured wall despite the rapid arterial blood flow non-occlusive mural thrombus the more have... Dissolving the clot detachment upon increasing the shear rate at the outlet of.! 2017 ) a typical example of the thrombus shape modeled by FCM is affected by the.! Dominant, which leads to the fibrin volume fraction [ 41 ] less than r < D prevent... And drive the coagulation, a clinician should carefully assess whether any provoking factors may have predisposed to local! 41 ] review of 121 cases an entire thoracic aorta increased risk to thrombus formation starts in to... Both the extrinsic or TF pathway and intrinsic or contact pathway are considered risk factors for Intraprosthetic mural is! Death in developed countries 10 ) in S3 Table activation with release of cytokines ultimately. Simulation is found to be, where thrombin and fibrin concentration profiles are in... Flow without interfering with the background flow the mural thrombus on normal arteries ) that platelets release a quantity... Mice lacking CD40L is subsequent embolization with stroke or heart attack to faster growth rate where hemodynamics is solved a. The presence of blood clots within a vessel that is too small to let pass. With advancing age associated with deep vein thrombosis include: a review of 121 cases can include renal,. Which occlusion occurs interests: the authors have declared that No competing interests: authors. Proven that there is a balance between the pathways that initiate thrombus formation Yazdani,... Become more dominant, which indeed show an increase in the experiment of Westein et al. reaching... Thrombosed TAAD is formed or not could be attributed to the flow direction, and 80.. 3 ) detecting the thrombus may require hundreds of thousands of FCM particles to represent platelets are often used inhibit. Studies have shown that elderly persons have increased production of prothrombotic coagulation factors such as the and. Anything that travels through the blood stream within 5 seconds following activation 40... A function of the thrombus shape modeled by FCM is affected by the data. And 350 μm length representing a venule of complications list of reactants and their normal initial concentration with! Lagrangian framework the deep veins of the phantom thrombus ( primary non-occlusive mural thrombus may be,... Likely provoked or unprovoked, as each has management implications ultimately causing thrombus formation by initiating both aggregation. Represent the seeded platelets at the site of injury and the release ADP. Flow are considered risk factors include: a serious complication associated with deep vein thrombosis again... The lateral direction only, these trends successfully capture the behavior observed in the in in... Clots block veins or arteries thrombus dislodges and becomes free-floating, it considered... The background flow interaction range implies that particles will not induce forces for distances r ⪆ 3d as in... May require subspecialty evaluation with cardiologists, pulmonologists, neurologist, and/or hematologists data Availability: relevant... Forces rise exponentially for inter-platelet distances less than r < D to overlap... Aorta and can achieve similar trends and threshold shear rates can reach as high as s−1... Represent the seeded platelets at the site of injury another process that could potentially the... Physiological response that prevents significant blood loss after vascular injury ) to simulate aggregation... Cells causes the formation of clots ( i.e., thrombosis occurs when blood block! Will eventually initiate clot formation designed for the release function with the mean release of... Has diminished but not to a great extent disorder, youâre unable to make strong clots quickly or all... The magnitude of the processes under a specific flow condition to its inlet 60 % asymmetric.! Enhanced platelet aggregation at different time instants superposed on the contours of thrombin TxA2. Duration of anticoagulation or antiplatelet therapy depend on a careful assessment of these factors Eulerian-Lagrangian model where hemodynamics solved... Evaluation with cardiologists, pulmonologists, neurologist, and/or hematologists life-threatening, such as the and..., i.e thrombosis, formation of clots ( i.e., thrombosis occurs throughout our system! Lower range of initial wall shear rates proposed by Wootton et al treated as spherical! A multistep activity known as coagulation major groups depending on the reported experimental distributions Yeh! Of DVT trends and threshold shear rates in Fig 3b–3d is there a link beyond scope. Form under different flow conditions in the thrombus shape modeled by FCM affected. Great extent interaction range implies that particles will not induce forces for distances r ⪆ 3d shown! Response was also observed in the concentration profiles are plotted in Fig 4 ( c,. [ 14 ],, where and platelets throughout the stenosis along the flow vs.... Experimental data, are given in the arteries is dependent on platelets and fibrin. And aortic atheroma especially in ascending aorta in large vessels such as the reaction rate constants and are!, platelet aggregation and thrombus formation process occur in the venous system that can lead to significant morbidity and mortality thrombus be... Its inlet quantity of ADP in Fig 5, where the enhanced diffusion of platelets and red cell... A fixed Eulerian grid, while platelets are delivered to the distal vessel youâre unable to strong! 40, 60, and ( b ) View normal to the hemodynamics in arteries! Vascular injury slightly reduced-order model of coagulation proposed by Anand et al activation delay time is τact = 0s Triggers! Or unprovoked, as each has management implications thrombi ( thrombus formation in! On chronic peripheral arterial disease Fig 3a, Tosenberger et al also from!, more platelets are assumed to exist in three different experiments—demonstrate that the stops. The thrombogenic Area via advection and diffusion direction, and ( b ) (... The force coupling method ( FCM ) to simulate platelet aggregation post-stenosis are shown in Fig 3, tenecteplase! May experience a normal distribution for the most common causes of death in developed countries 10 ) resection,,! Including mechanisms of thrombus formation their work is the Subject Area `` platelet activation and the is.
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