Is the arteriolar microenvironment the cause of venous nickings?

Abstract

Purpose: Arteriovenous nickings (AVNs) are the cause of retinal vein occlusions and are also surrogates of cerebrovascular aging. The prevalent mechanistic model of AVNs stating that arteries crush veins remains somewhat unchallenged despite the lack of evidence other than fundus photographs. Here, we report that the microenvironement of arterioles may elicit phenotypic changes in adjacent venules in the absence of physical contact.

Methods: Multimodal high resolution imaging of the arteriovenous interface was done in 7 patients showing focal remodelling of a venous segment proximal to a retinal arteriole, in the absence of arteriovenous overlap.

Results: A variable association of nicking, narrowing, deviation and opacification of affected venous segments was noted. The venous segment was deviated toward the arteriole in 6 out of the 7 cases. An arteriovenous gap up to 40µm was measured at sites of focal venous narrowings; the latter reduced the venous lumen diameter by 43% to 77%. Similar features were retrospectively identified in a series of AVNs.

Conclusions: Our results suggest that the microenvironment of arterioles may elicit venous nicking, in the absence of detectable arteriovenous contact. The topology of such changes suggests a retractile and/or constrictive process. Identifying the factors involved in this arteriovenous interaction may have implications for the understanding of retinal vein occlusions and more generally of cerebrovascular aging.