Venous Nicking Without Arteriovenous Contact: The Role of the Arteriolar Microenvironment in Arteriovenous Nickings.

IMPORTANCE: Arteriovenous nickings (AVNs) in the retina 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 observed that venous nicking may be observed in the absence of physical contact with an arteriole. OBSERVATIONS: This observational study, conducted from January 2013 to September 2014, included 7 patients showing remodeling of a venous segment close to a retinal arteriole without arteriovenous overlap were imaged by adaptive optics imaging. Affected venous segments showed a variable association of nicking, narrowing, deviation, and opacification. Venous segments were deviated toward the arterioles in 6 of the 7 cases. The degree of venous narrowing ranged from 40% to 77%, while at these sites, the width of the intervascular space ranged from 16 µm to 42 µm. Similar features were identified in typical AVNs. CONCLUSIONS AND RELEVANCE: Arteriovenous nickings do not necessarily involve an arteriovenous compression. Instead, the topology of venous changes suggests a retractile process originating in the intervascular space. These findings have important implications for the understanding of retinal vein occlusions and of cerebrovascular aging.

Morphometric analysis of small arteries in the human retina using adaptive optics imaging: relationship with blood pressure and focal vascular changes.

OBJECTIVES: The wall-to-lumen ratio (WLR) of retinal arteries is a recognized surrogate of end-organ damage due to aging and/or arterial hypertension. However, parietal morphometry remains difficult to assess in vivo. Recently, it was shown that adaptive optics retinal imaging can resolve parietal structures of retinal arterioles in humans in vivo. Here, using adaptive optics retinal imaging, we investigated the variations of parietal thickness of small retinal arteries with blood pressure and focal vascular damage. METHODS: Adaptive optics imaging of the superotemporal retinal artery was done in 49 treatment-naive individuals [mean age (±SD) 44.9 years (±14); mean systolic pressure 132  mmHg (±22)]. Semi-automated segmentation allowed extracting parietal thickness and lumen diameter. In a distinct cohort, adaptive optics images of arteriovenous nicking (AVN; n = 12) and focal arteriolar narrowing (FAN; n = 10) were also analyzed qualitatively and quantitatively. RESULTS: In the cohort of treatment-naive individuals, by multiple regression taking into account age, body mass index, mean, systolic, diastolic and pulse blood pressure, the WLR was found positively correlated to mean blood pressure and age which in combination accounted for 43% of the variability of WLR. In the cohort of patients with focal vascular damage, neither FANs or AVNs showed evidence of parietal growth; instead, at sites of FANs, decreased outer diameter suggestive of vasoconstriction was consistently found, while at sites of AVNs venous narrowing could be seen in the absence of arteriovenous contact. CONCLUSION: High resolution imaging of retinal vessels by adaptive optics allows quantitative microvascular phenotyping, which may contribute to a better understanding and management of hypertensive retinopathy.

Pseudovitelliform Subfoveal Deposit in Waldenström's Macroglobulinemia.

BACKGROUND: Waldenström's macroglobulinemia may be complicated by retinal hemorrhages, retinal vein occlusion, serous macular detachment or macular edema. We report a patient with pseudovitelliform subfoveal deposit complicating Waldenström's macroglobulinemia. CASE REPORT: A 56-year-old man presented with hyperviscosity syndrome due to Waldenström's macroglobulinemia. After systemic therapy, a large serous retinal detachment persisted in the left eye. A pseudovitelliform subfoveal deposit was observed in the right eye. CONCLUSION: Pseudovitelliform subfoveal deposits may be part of the spectrum of ocular complications in Waldenström's macroglobulinemia. They could be due to accumulation of macroglobulins.