May-Thurner syndrome (MTS) is a vascular compression disorder that creates an environment conducive to blood clot formation, most commonly in the deep veins of the left leg. The cause is rooted in a particular anatomical arrangement within the pelvis where a major artery crosses over a major vein. This mechanical obstruction significantly impairs blood flow, leading to venous stasis (sluggish movement of blood). This increases the risk of developing deep vein thrombosis (DVT), the most significant complication associated with the syndrome.
The Core Anatomical Mechanism of Compression
The fundamental cause of May-Thurner syndrome is the external compression of the left common iliac vein (LCIV) by the right common iliac artery (RCIA). These two large vessels manage the return of blood from the lower body to the heart, meeting in the pelvic area where they cross paths. The left common iliac vein, which carries blood from the left leg, runs horizontally to join the inferior vena cava.
The artery, being more rigid and situated anteriorly, crosses directly over the softer vein. In many individuals, this crossing is uneventful, but in MTS, the artery presses the vein against the underlying fifth lumbar vertebra (L5) of the spine. This sandwiching effect mechanically narrows the vein’s lumen.
The pulsatile nature of blood flow within the artery means the vein is subjected to continuous, rhythmic pressure. This chronic force acts like a repeated trauma to the vein wall. The location of this compression is typically between the aortic origin of the common iliac artery and the iliofemoral junction.
This anatomical arrangement, known as iliac vein compression, is common in the general population. However, it only becomes May-Thurner syndrome when it produces symptoms or leads to complications like DVT. The resulting narrowing, or stenosis, must be severe enough to cause clinically relevant obstruction of the venous outflow.
Progression to Vein Pathology
The chronic, pulsating force exerted by the overlying artery initiates a biological response within the vein wall. This mechanical irritation damages the endothelium, the innermost lining of the vein. The vein then attempts to heal the trauma by laying down scar tissue.
This reparative process is known as intimal hyperplasia, involving the deposition of collagen and elastin within the vein wall. Over time, this thickening and scarring create fibrous bands or “spurs” that protrude into the vein’s lumen. These internal structures further restrict the flow of blood, sometimes creating a web-like obstruction.
This internal pathology transforms the simple external compression into a severe internal obstruction. The physical narrowing from the external artery combined with the internal blockage from the spurs dramatically slows blood flow, creating severe venous stasis. This sluggish blood movement is one of the three components of Virchow’s triad for blood clot formation.
The resulting severe restriction and stasis significantly elevate the risk of deep vein thrombosis (DVT) distal to the compression. Once a blood clot forms in this environment, it further occludes the vessel, causing the acute and often painful symptoms that lead to the diagnosis of May-Thurner syndrome.
Contributing Factors and Susceptible Populations
Although the anatomical compression is the direct cause, certain factors increase an individual’s susceptibility to developing symptomatic May-Thurner syndrome. Women are more frequently affected than men, with some reports suggesting they are twice as likely to have symptomatic disease. This gender difference is often linked to conditions that increase abdominal or pelvic pressure.
Pregnancy and the postpartum period are known to be associated with the onset of symptoms, as are factors that increase the blood’s tendency to clot, such as the use of oral contraceptives. The combination of increased venous pressure and a hypercoagulable state can tip the balance from asymptomatic compression to DVT. The syndrome is typically diagnosed in patients between the ages of 20 and 40 when their symptoms first manifest.
Anatomical variations beyond the standard crossing can also contribute to the syndrome. These include differences in the angle at which the artery crosses the vein or variations in the spinal curvature, such as scoliosis, which may alter the spatial relationship between the vessels and the vertebra. These factors modify the degree of compression, determining whether the anatomical variant remains silent or progresses to a clinically recognized disease.