Virchow Triad


Vascular thrombi are formed in the setting of low flow and shear stress and mainly consist of fibrin strands, red blood cells, and a few platelets. In 1856, Rudolf Virchow, a renowned Berlin scientist and physician recognized these factors due to his extensive work on venous thrombosis.[1] These concepts evolved over the years and are relevant to developing arterial thrombosis.[2]

Rudolf Virchow is one of the first physicians to describe the concept at a cellular level, believing that most conditions, including pathological thrombosis, were caused by cellular pathology.[3] He is known as the "father of modern pathology," Virchow was a physician, scientist, anthropologist, prehistorian, and biologist in addition to his endeavors in pathology. In addition, he received credit for his work in cellular biology and early cancer research. He theorized the left supraclavicular lymph node (now called Virchow's node), when enlarged and hard on palpation, is associated with gastric cancer.[3] Charles Emile Troisier later recognized the further association of other abdominal cancers and testicular cancer with the presence of Virchow's node.[4]

Virchow sought to explain the causation of pulmonary thromboembolism and theorized that pulmonary arterial embolus arises from peripheral/distant thrombosis. He attempted to explain the mechanism or define the specific conditions necessary to initiate peripheral clotting and how a thrombus may dislodge from a peripheral vein, travel to the right heart, and enter the pulmonary arterial system. The three factors of Virchow's triad include intravascular vessel wall damage, stasis of flow, and the presence of a hypercoagulable state.[1] Understanding these factors involved in thrombus formation and subsequent thromboembolic events enables the clinician to stratify risk, direct clinical decision-making regarding treatment, and establish preventative measures. Virchow died from cardiac disease on September 5, 1902, after sustaining a femur fracture.[3] His main contributions to medicine emanated from his observational skills and abilities to accurately deduce cellular processes contributing to health and disease. Many of his observations remain accurate to this day, and scientists are, in many instances, only beginning to unravel the molecular pathways underlying the observations made by this physician nearly 150 years ago.

In theory, Virchow's triad postulates the presence of three factors that predisposes a person to develop vascular thrombosis. These factors include:

  • Hypercoagulability of blood
  • Alteration in blood flow in the vessels
  • Vessel wall injury/ Endothelial damage

Issues of Concern

Thrombosis, by definition, is the formation of a clot within a blood vessel. As described earlier, Virchow's triad represents three qualities in physiology that can result in thrombosis. These include:

Endothelial Damage

A healthy endothelium provides an anticoagulant and anti-platelet surface with certain cell surface glycoproteins and the release of various molecules, some of which are stored pre-formed in specialized and unique Weibel-Palade bodies.[5][6] Examples of glycoproteins include thrombomodulin, tissue factor, and ectonucleotidase(s) that act as a receptor for thrombin, as an initiator of coagulation by its interaction with coagulation factor VII, and minimize the prothrombotic effects of nucleotides such as ADP.[7] However, various pathological processes can cause the cleavage or shedding of these molecules from the cell surface. The molecules can be measured in the blood using the ELISA technique. Thus, one of the features of a damaged or dysfunctional endothelium is increased plasma levels of various molecules normally present as part of the cell membrane. As membrane thrombomodulin has anticoagulant properties, its loss from the cell surface may tip hemostasis towards pro-coagulation.[8][9] 

Nevertheless, since increased levels of all the plasma forms of cell surface molecules are found in atherothrombotic disease, it may be presumed that they reflect a shift towards thrombosis.[10] The endothelium also secretes/releases various molecules that may be active in thrombosis and hemostasis. Foremost among these are the von Willebrand factor, t-PA antigen factor, and fibrinogen; high levels have repeatedly been shown to predict major cardiovascular events.[11][12][13]

  • Damage to a vessel's endothelial wall alters blood flow dynamics. Endothelial disturbance can result from insults such as smoking, chronically elevated blood pressure, and atherosclerotic disease secondary to hyperlipidemia. When an insult to the wall occurs, flow disruption or "turbulence" occurs. Turbulent flow within a vessel occurs when the blood flow rate becomes too rapid, or blood flow passes over an affected surface; this creates disordered flow and eddy currents, increasing the flow friction within a vessel. Reynold's number can represent the tendency for turbulence to occur.[2][14]
  • Re = (v x d x p) / n
    • Where v = mean velocity, d = diameter (in centimeters), n = viscosity (in poise), and p = density.
  • Turbulence within the vessel may occur due to various factors, such as irregular atheromas from plaque formation, bifurcations in the vessel, and areas of stenosis, most prominent in patients with vascular disease.[2][14]

Alteration in Blood Flow

In streamlined (laminar) flow, endothelial cell morphology and function are affected by the shear stresses, and accordingly, to minimize this, they elongate and align in the direction of flow.[15] The secretion and release of endothelial defenses such as nitric oxide (NO), prostacyclin (PGI2), and tissue plasminogen activator (t-PA) are dependent on the stressors on the vessel wall. Thereby, in the event of an endothelial injury, the blood flow regulates vascular reactivity and confines platelet adhesion, aggregation as well as fibrin formation to sites of endothelial injury.[16] Additionally, the synthesis and release of prothrombotic and proinflammatory endothelial mediators such as tissue factor (TF), von Willebrand factor (vWF), endothelin, ICAM-1, and VCAM-1 are also dependent on the vessel wall stress.[17] There is evidence that some endothelial mediators influencing vessel wall reactivity are under genetic control.[16] As the central (axial) flow is disrupted, numerous red blood cells, leucocytes, and platelets get strategically concentrated near the vessel wall for adhesion and activation.[17] High shear forces at the vessel wall further activate platelets via the release of vWF and promote their adhesion to the exposed subendothelium. Hence stasis (induced by internal or external pressure) is required to allow fibrin formation and secondary hemostasis.

Atherogenesis occurs preferentially at arterial bifurcations and bends; at these sites, flow separation results in areas of low-flow, low-shear recirculation of blood cells and proteins in contact with the vessel wall. Such flow conditions favor the adhesion of platelets and monocytes, as well as infiltration of plasma components such as low-density lipoprotein (LDL) cholesterol and fibrinogen causing the development of a plague.[18] This mechanical blockade in the arterial vessel wall leads to high intravascular shear stress at the site of the stenotic lesion.

Arterial thrombosis usually follows the rupture of atherosclerotic plaques and is the commonest pathophysiological process in acute coronary syndromes, ischaemic stroke, and critical leg ischemia.[19] High intra-stenotic shear stresses may be one factor in promoting arterial plaque rupture. High-shear activation of blood platelets may promote the initial platelet-rich "white head" of arterial thrombi. Distal to the atherothrombotic stenosis, low-shear stresses may promote the subsequent, fibrin-and-red-cell-rich "red tail." [19]

 Some examples of blood flow alteration include atrial fibrillation, LV wall akinesis, valvular heart disease, prolonged immobility such as bedridden patients or prolonged travel, surgery, and trauma.[2][20] 

  •  When an insult to the wall occurs, flow disruption or "turbulence" occurs. Turbulent flow within a vessel occurs when the blood flow rate becomes too rapid, or blood flow passes over an affected surface; this creates disordered flow and eddy currents, increasing the flow friction within a vessel. Reynold's number can represent the tendency for turbulence to occur.[2][14]
  • Re = (v x d x p) / n
    • Where v = mean velocity, d = diameter (in centimeters), n = viscosity (in poise), and p = density.
  • Turbulence within the vessel may occur due to various factors, such as irregular atheromas from plaque formation, bifurcations in the vessel, and areas of stenosis, most prominent in patients with vascular disease.[2][14]

Hypercoagulability of Blood 

The constituents of blood are many and varied, but soluble coagulation factors (such as fibrinogen and tissue factor) and cells (such as platelets) are implicated in the process of thrombosis. Understandably a continuum exists between healthy and hemostatic abnormalities in prothrombotic or hypercoagulable states and 'overtly' increased clotting in acute thrombosis. 


The role of platelets in the pathogenesis of atherosclerosis and as a constituent of atheroma is well elucidated. Platelet function can be quantified by its tendency to aggregate and measure its levels in urine and plasma. The alpha granule constituents (beta thromboglobulin, platelet factor 4 (PF-4)) and the adhesion molecule P-selectin can be measured in the plasma. The PF-4 competes with antithrombin III for binding to heparan glycosaminoglycans, thereby impairing heparan-catalyzed inhibition of thrombin. Raised levels of various platelet molecules are abnormal in cancer, peripheral disease, acute myocardial infarction, diabetes, and hypertension.[21][22]

The adhesion molecule P-selectin (CD62P) is of particular interest because of its role in modulating interactions between blood cells and the endothelium and the possible use of the soluble form as a plasma predictor of adverse cardiovascular events. For example, it is known that thrombin induces surface expression of P-selection on platelets.[23] Although present on the external cell surface of both activated endothelium and activated platelets, it now seems clear that most, if not all, of the measured plasma P-selectin is of platelet origin.[23] P-selectin is also partially responsible for the adhesion of certain leukocytes and platelets to the endothelium. Increased P-selectin expression has been demonstrated on active atherosclerotic plaques.[24]


Thrombogenesis is finely balanced between coagulation and fibrinolytic pathways. The fibrinolytic system is primarily influenced by the interaction between plasminogen activators (such as tissue plasminogen activators) and inhibitors that modulate this activity (e.g., plasminogen activator inhibitor, PAI-1). Plasma fibrinogen is the primary determinant of blood viscosity and blood flow. It affects the aggregation of platelets, interacts with plasminogen binding, and mediates the final steps of clot formation after it combines with thrombi. 

Fibrin D-dimer Levels

Raised levels of fibrin D-dimer are fibrin degradation products, an index of intravascular thrombogenesis, and fibrin turnover.

Clinical Significance

The function of Virchow's triad is to demonstrate the underlying physiology that drives the formation of a thrombus. Clots within the vasculature place the patient at risk for thromboembolic events such as CVA, pulmonary arterial embolus or organ infarction, ischemia, and cell death. Understanding physiology enables clinicians to understand better the risk factors for developing deep vein thrombosis. 

Thrombogenesis in Deep Vein Thrombosis (DVT)

The simultaneous presence of venous stasis, hypercoagulability and vascular injury increases the risk for clot formation, as described in Virchow's triad. Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow, such as the pockets adjacent to valves in the leg's deep veins.[25] While valves help to promote blood flow through the venous circulation, they are also potential locations for venous stasis and hypoxia. Multiple postmortem studies have demonstrated the propensity for venous thrombi to form in the sinuses adjacent to venous valves.[26][27] The hypercoagulable micro-environment may downregulate certain antithrombotic proteins preferentially expressed on venous valves, including thrombomodulin and endothelial protein C receptor (EPCR).[28] In addition to reducing important anticoagulant proteins, hypoxia drives the expression of certain procoagulants. Among these is P-selectin, an adhesion molecule that attracts immunologic cells containing tissue factors to the endothelium.[29][30]

A venous thrombus has two components, an inner platelet-rich white thrombus forming the so-called lines of Zahn surrounded by an outer red cell dense fibrin clot. Fibrin and extracellular DNA complexed with histone proteins forms the outer scaffold, which may be important in determining thrombus susceptibility to tissue plasminogen activator (TPA) and thrombolysis.[30] As the ratio of procoagulants to anticoagulants increases, so does the risk of thrombus formation. The proportion of proteins is partly determined by the ratio of the endothelial cell surface to blood volume. A decreased cell surface-to-blood volume ratio (i.e., large vessels) favors procoagulants.[31] Factor VIII, von Willebrand factor, factor VII and prothrombin seem to be particularly influential in tipping the scale towards coagulation.[32]

In addition to promoting thrombin generation, prothrombin inhibits the anticoagulant properties of activated protein C, thereby dampening a natural anticoagulant pathway. There are three pathways: the protein C anticoagulant pathway (protein C, protein S, thrombomodulin, and perhaps EPCR), the heparin-antithrombin pathway, and the tissue factor inhibitor pathway. Defects in these pathways are associated with an increased risk for thrombus formation. In humans, less is known regarding the role of the tissue factor inhibitor pathway.[32][33] 

Several familial variants predispose to thrombus formation by increasing the levels of factors VII, VIII, IX, von Willebrand factor, and prothrombin. Other risk factors for clot formation include cancer, oral contraceptives, obesity, and advancing age. Malignancy can exert a compressive effect on veins contributing to stasis. It also leads to shedding procoagulants, such as tissue factor on membrane particles that promotes thrombosis.[34] Obesity and oral contraceptive use are independent risk factors for thrombosis. Together, they increase thrombosis risk synergistically.[35]

Finally, advancing age is associated with an increased risk for thrombosis. While the cause for this remains unsettled, several factors related to aging have been observed: greater prevalence of obesity, increased frequency of illness and periods of prolonged immobility, comorbid medical conditions, and an increase in the level of procoagulants without a commensurate increase in anticoagulants such as protein C.[27] Thrombosis formation is a dynamic, multicausal process that hinges on a fine balance of physical and biochemical factors.

Thrombogenesis in Pregnancy 

- Progesterone causes systemic venous dilation.[36] Consequently, renal vasodilatation leads to an increase in systemic volume and Na retention. This rise in venous blood volume and pressure, along with resulting distension of the vessels, led to stasis and increased lower extremity edema.[37] However, it has been proposed that, unlike VTE in the general population, VTE in pregnancy may start in the pelvis [38] rather than the lower extremities, as the percentage of isolated pelvic deep venous thrombosis is significantly higher in pregnancy. There are also circulating cytokines and growth factors that may contribute to the breakdown of the endothelial monolayer.[39] In addition, the increase in blood volume and diameter of vessels cause sheer stress on the vessels. This can cause vascular dysfunction and injury by degrading or removing cell junctional proteins.[39]

During pregnancy, the blood becomes hypercoagulable with increases in pro-coagulation factors V, VII, VIII, IX, X, and XII and von Willebrand factor.[40] Factor VII increases up to 10-fold, whereas fibrinogen rises 2-fold. There is also a decrease in anticoagulant activity with a reduction in protein S with gestational age, whereas protein C activity remains unchanged.[40] Fibrinolysis is reduced in pregnancy due to enhanced activity of plasminogen activator inhibitor type I and II and a decreased activity of tissue plasminogen activator. All these factors mentioned above predispose the patient to venous thromboembolism.[41]

Thrombogenesis in Atrial Fibrillation 

Atrial fibrillation (AF) is the most common supraventricular arrhythmia associated with a high risk of stroke and thromboembolism.[42] There is an increased risk of pathological thrombus formation due to disruption of physiological hemostatic mechanisms, as understood with the help of Virchow's triad.[43] Anatomically, the left atrial appendage (LAA) is the most common site of intra-atrial thrombus formation in patients with AF. Disruption/denudation of the extracellular matrix leads to conduction defects (perpetuating atrial fibrillation).[42] It further induces fibrosis and infiltration of the endocardium, thereby promoting thrombogenesis. Abnormal changes in flow are evident by stasis in the left atrium and are seen as spontaneous echo contrast.[44] Some structural changes include progressive atrial dilatation, endocardial denudation, and extracellular matrix fibroblastic infiltration. Additionally, the coagulation cascade increased activation, platelet reactivity, and impaired fibrinolysis due to AF. This process has implicated several prothrombotic biomarkers, including platelet factor 4, von Willebrand factor, fibrinogen, B-thromboglobulin, and D-dimer.[45][46] In summary, These structural changes promote further atrial remodeling and provide a platform for clot formation and subsequent embolization. 

Thrombogenesis in LV Thrombus Post-MI 

The mechanism involving LV thrombus formation following AMI involves the principle of Virchow's triad. Mechanically, infarct expansion with regional thinning and dilation of the damaged endothelium in the infarct zone begins almost immediately, increases wall stress, and may lead to ventricular aneurysm formation.[47] Blood stasis is primarily driven by LV dysfunction with a reduced ejection fraction and large apical or anterior LV akinesis.[48] Additionally, abnormal flow patterns resulting from regional LV dysfunction are closely associated with thrombus formation compared with normal flow patterns. In combination with the low shear rate in the infarct zone, local tissue injury activates the coagulation system, accumulating fibrin via cross-linking (common pathway), platelets (intrinsic pathway), and erythrocytes, which collectively form the fresh thrombus.[49] Endothelial injury in AMI triggers an inflammatory and prothrombotic state (i.e., hypercoagulability) by exposing subendothelial tissue and collagen to the circulating blood.[50]  

Larger infarcts, evidenced by higher levels of cardiac enzymes, have also been associated with increased rates of LV thrombus formation compared with patients with smaller infarcts. Baseline C-reactive protein, fibrinogen, and the neutrophil-lymphocyte ratio are independent predictors of early LV thrombus formation after AMI. In this context, the propagation and growth of small thrombi into larger thrombi protruding into the ventricular cavity and exposed to circulating blood flow may lead to embolism.[51] The hypercoagulable state following AMI appears to persist for six months or longer. A fresh thrombus may contribute to a persistent inflammatory reaction in the underlying myocardium and is itself thrombogenic. In contrast, a chronic thrombus is less prone to embolism once it becomes more firmly anchored to the endocardium, more laminar and less protruding, and isolated from the dynamic forces of circulating blood.[51][49] The physical characteristics of the thrombus (i.e., its size, shape, mural [sessile] or protruding morphology, mobility, and age relative to the acute event) may influence its consequences. 

Nursing, Allied Health, and Interprofessional Team Interventions

Given the serious nature of thrombosis, an interprofessional healthcare team, including clinicians, nurses, mid-level providers, and specialists, should be familiar with Virchow's triad and recognize the presentation when examining or interacting with patients. Prompt recognition can lead to further testing and specialized intervention, resulting in better patient outcomes.

Multiple studies show regular exercise reduces the risk of arterial and venous thrombotic events. One mechanism may be that regular exercise reduces circulating levels of viscosity and hemostatic and inflammatory variables.[52] Encouraging regular exercise and minimizing immobility may reduce the risk of cardiovascular thrombotic events through systemic effects that maintain blood flow.

Article Details

Article Author

Abigail Kushner

Article Author

William P. West

Article Author

Mahammed Z. Khan Suheb

Article Editor:

Leela Sharath Pillarisetty


12/10/2022 3:24:12 PM



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