May-Thurner Syndrome (MTS) is a vascular condition often overlooked as a cause of unexplained deep vein thrombosis (DVT), particularly in the left leg. MTS involves a specific anatomical arrangement of major blood vessels in the pelvis that restricts blood flow returning from the lower body. Because its symptoms mimic other common vein issues, diagnosis is frequently delayed until a serious complication, like a blood clot, develops. This delay leads people to question whether the syndrome is inherited or develops later in life.
Understanding the Mechanism of May-Thurner Syndrome
MTS is defined by a physical obstruction in the left common iliac vein, a large vein in the lower abdomen. This vein carries deoxygenated blood from the left leg and pelvis back toward the heart. Compression occurs because the vein is pinched between the right common iliac artery and the underlying fifth lumbar vertebra of the spine.
The artery, which carries high-pressure blood, crosses directly over the left common iliac vein. The constant pulsation of the artery against the vein causes chronic irritation to the vein wall. This mechanical trauma stimulates the formation of fibrous bands or spurs on the inside lining of the vein, which further narrows the channel.
This narrowing, or stenosis, significantly slows blood flow, creating turbulence and pooling in the vein, known as venous stasis. The sluggish blood flow and physical damage to the vein wall create the ideal environment for deep vein thrombosis (DVT) formation. This anatomical arrangement, present in 22% to 24% of the population, is called May-Thurner anatomy, but the development of symptoms defines the syndrome.
Genetic Predisposition vs. Acquired Condition
The medical consensus is that MTS is primarily an anatomical variant and an acquired mechanical condition, not a purely inherited disorder. MTS is not passed directly from a parent to a child like eye color or a specific gene mutation. The compression results from the normal, yet occasionally unfavorable, positioning of the major blood vessels within the pelvis.
While the syndrome is not genetic, inherited factors can significantly influence the risk of developing a serious complication like DVT once compression is present. Individuals with inherited blood clotting disorders, such as Factor V Leiden or Prothrombin G20210A mutations, are more susceptible to forming clots in the already narrowed vein. These genetic predispositions accelerate the progression from asymptomatic anatomical compression to symptomatic MTS.
Certain connective tissue disorders with a genetic component could also contribute by affecting the structure or elasticity of the vein wall. However, compression remains the underlying mechanical cause. A person may inherit factors that make them more likely to clot, but they do not inherit the syndrome itself, which is a structural issue. MTS is largely a result of chronic mechanical stress on the vein and is considered a non-hereditary vascular disorder.
Diagnosis and Management Options
Confirming MTS requires advanced medical imaging, as the condition is deep within the abdomen and often asymptomatic until a DVT occurs. A simple Doppler ultrasound of the leg can detect a blood clot but often cannot visualize the compression high up in the iliac vein. Specialized imaging techniques like CT venography or MR venography are used to map the vascular anatomy and confirm the site of narrowing.
The gold standard for detailed diagnosis is a combination of catheter-based venography and intravascular ultrasound (IVUS). IVUS involves inserting a tiny probe into the vein to provide real-time, three-dimensional images from inside the vessel. This allows the physician to precisely measure the degree of compression and any internal scarring. This internal measurement is more accurate than external imaging for determining obstruction severity.
Management focuses on two primary goals: preventing blood clots and relieving the mechanical obstruction. For patients with a DVT, initial treatment involves anticoagulation therapy (blood thinners) to stop the clot from growing and prevent a pulmonary embolism. If a large, fresh clot is present, thrombolysis may be performed to dissolve the clot before addressing the underlying compression.
The definitive treatment for the compression is typically an endovascular procedure involving angioplasty and stenting. In this minimally invasive procedure, a balloon opens the narrowed vein, and then a dedicated venous stent, usually made of nitinol, is placed to hold the vein open permanently. This restores normal blood flow and significantly reduces the risk of recurrent DVT, offering a long-term solution.