Chronic depression symptoms and salivary NOx are associated with retinal vascular dysregulation: the SABPA study.

Background Depression has been associated with impaired nitric oxide (NO)-mediated vasodilation and vascular dysregulation (VD). Whether depression and NO levels will disturb retinal hemodynamics is not clear. Objectives and methods Associations between the retinal vasculature, diastolic ocular perfusion pressure (DOPP) as measure of hypoperfusion, NO metabolites (NOx) and depression symptoms were assessed. Chronic VD risk markers [depression symptoms (Patient Health Questionnaire/PHQ-9 ≥ 10) and 24h pulse pressure] were determined in a bi-ethnic cohort (n=313; 48.6 ± 9 years; 53.9% men). At 3 year follow-up, retinal vessel calibre and retinopathy signs were quantified from digital images. Salivary NOx, a novel approach, was obtained pre- and post-flicker light-induced provocation (FLIP). DOPP was defined as diastolic blood pressure minus intraocular pressure. Results Chronic VD risk was evident in Blacks opposed to acute risk in Whites (P<0.05). At follow-up, retinopathy (Blacks 60.4%/Whites 39.6%), lower pre-FLIP (µM) and higher post-FLIP NOx (%), arteriolar narrowing and wider venular calibre values were evident in Blacks compared to Whites, independent of confounders. A wider venular calibre, an index of stroke risk, was associated with chronic depression symptoms [cut point 248 MU: Area under the curve 0·61 (95% CI: 0·51, 0·72); 71% sensitivity; 55% specificity] as well as with hypoperfusion in the Blacks. In this group, arteriolar narrowing was associated with hypoperfusion; and attenuated arteriolar dilation with increased FLIP NOx responses (%). Conclusions Higher NOx increased arteriolar vasoconstriction, presumably impeded perfusion and facilitated VD. Chronic depression symptoms may trigger disturbed NOx and retinal hemodynamics in Blacks and thereby potentiate stroke ris

Retinal vessel response to flicker-light for all groups.

<p>The response to flicker-light is depicted for all groups. A trend towards a less pronounced primary vasodilation (A) and secondary vasoconstriction (B) is observed, but no significant difference is found late after SAH. Quality assessment of vasodilation (C) and vasoconstriction (D) as judged by amplitude and shape (absent/diminished/intact) illustrates an initial disturbance in the acute phase compared to the healthy control group, with gradual improvement over time (aSAH, late).</p

Demography and outcome data of all patients.

<p>Demography and outcome data of all patients.</p

Retinal arterial diameter SAH patients compared to healthy controls.

<p>Baseline arterial diameter is determined in a representative vessel segment at a prespecified distance to the papilla (A: white arrow/dark-grey annular segment). For longitudinal investigation in the same patient, the identical position is detected automatically via RVA-software algorithm. In our cohort, arterial diameter is significantly increased in patients with acute SAH when compared to healthy controls (p<0.01); this significance is also present, but to a lesser extent, at the time of follow-up in the late phase after SAH (p<0.05).</p

Arterial diameter of two exemplary patients in relation to nimodipine therapy.

<p>The longitudinal development of arterial diameter of two exemplary patients (GO, BK) is depicted over time. Increase, decrease and preservation of arterial diameter are observed at initiation or continuation of oral nimodipine therapy.</p