Why Carotid and Subclavian Artery Thrombosis Occur in Takayasu Arteritis
Thrombosis in the carotid and subclavian arteries in Takayasu arteritis results from the disease's characteristic inflammatory process that causes concentric wall thickening, intimal proliferation, and stenosis—creating a prothrombotic environment in these preferentially affected vessels.
Pathophysiologic Mechanism of Thrombosis
The fundamental pathology explains why thrombosis develops:
Takayasu arteritis is a T-cell-mediated panarteritis that begins in the adventitial vasa vasorum and progresses inward through all vessel wall layers 1
The inflammatory cascade leads to two primary pathologic outcomes: intimal proliferation with concentric wall thickening causing stenosis, or destruction of elastic and muscular layers leading to aneurysm formation 1, 2
Inflammation and intimal proliferation specifically lead to wall thickening, stenotic lesions, and thrombosis formation within the narrowed lumen 2
The non-specific inflammation causes concentric wall thickening, fibrosis, and direct thrombus formation in diseased arteries 3
Why the Carotid and Subclavian Arteries Are Preferentially Involved
These vessels are anatomically predisposed to involvement:
All patients with Takayasu arteritis have subclavian artery involvement (100% in studied cohorts), and 69% have common carotid artery involvement 4
Bilateral involvement is the rule for common carotid arteries (100% bilateral when affected), while subclavian involvement is bilateral in 33% of cases 4
Left-sided lesions are more prominent, with all internal carotid artery involvement occurring on the left side in studied patients 4
The disease affects the aorta and its major branches as elastic arteries, making the great vessels arising from the aortic arch (carotid and subclavian) primary targets 1, 5
The Stenosis-Thrombosis Sequence
The progression from inflammation to thrombosis follows a predictable pattern:
Homogeneous circumferential intima-media thickening of the common carotid arteries is a highly specific ultrasonographic finding in Takayasu arteritis, particularly in young women 4
This concentric thickening pattern differs fundamentally from ordinary atherosclerosis and creates a narrowed, irregular luminal surface prone to thrombosis 4
Progressive vascular stenosis occurs through concentric thickening rather than longitudinal spreading, further concentrating the prothrombotic risk in focal segments 4
CT and MRI demonstrate circumferential soft tissue thickening of arterial walls with narrowing of the arterial lumen 6
Clinical Implications of This Thrombotic Tendency
The thrombotic complications manifest in specific ways:
Carotid artery tenderness, claudication, ocular disturbances, and central nervous system abnormalities are among the most frequent clinical features, reflecting thrombotic and stenotic complications 2
Diminished or absent peripheral pulses are common physical examination findings resulting from thrombotic occlusion or severe stenosis 1
Blood pressure discrepancy >10 mmHg between arms is a significant finding reflecting asymmetric subclavian involvement and thrombosis 1
Vascular bruits over subclavian arteries or aorta are characteristic findings indicating turbulent flow through stenotic, partially thrombosed segments 1
Why Antiplatelet Therapy Is Recommended
The prothrombotic pathophysiology justifies specific treatment:
Low-dose aspirin or another antiplatelet agent should be added for patients with active disease and critical cranial or vertebrobasilar involvement to prevent ischemic events 1
This recommendation reflects the recognized thrombotic risk in inflamed, stenotic vessels supplying the brain 1
Common Pitfall to Avoid
Do not assume that thrombosis only occurs during active inflammation—stenotic lesions remain prothrombotic even when systemic inflammatory markers normalize, which occurs in 50% of active cases 1, 7
Serial imaging is essential because vascular progression and thrombotic complications can occur unpredictably, even in patients on immunosuppressive therapy 4
Most patients remain clinically stable despite severe stenosis or occlusion of common carotid arteries due to collateral vessel development, but acute thrombotic occlusion can still cause stroke 4