Retinal ganglion cell dysfunction in patients with coronary microvascular dysfunction

Introduction Glaucoma is an ophthalmic disease characterized by retinal ganglion cell (RGC) degeneration and leading to progressive and irreversible vision loss. Microvascular dysfunction is a risk factor for glaucoma, due to disrupted autoregulation, increased arteriolar resistance, and decreased blood supply to the RGCs. Nocturnal blood pressure (BP) dipping has also been linked to negative glaucomatous outcomes. We hypothesized that patients with coronary microvascular dysfunction (CMD) attributed to microvascular dysfunction may present with RGC degeneration. We compared the retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC) thicknesses between INOCA patients and controls and we examined whether the 24-hour BP profile can explain any observed differences. Materials & Methods All participants underwent functional coronary angiography with coronary physiology assessment and 24-hour BP monitoring. Following ophthalmic screening, we obtained optical coherence tomography scans of the optic nerve and macula from both eyes, if both were found healthy. We extracted the standard peripapillary RNFL (pRNFL) and macular GCC thickness reports. We analyzed all outcomes using multivariable linear mixed models, adjusted for age, sex, optic disc size, axial length, and BP parameters. Results We included 87 eyes from 44 CMD patients and 47 eyes from 26 controls. Inferior pRNFL was thinner in INOCA patients, compared to controls (mean[95% Cl]: 124 [101-145] μm versus 134[109-166] μm, P=0.009). The difference between day and night pulse pressure index (PPi) was a mediator of this association (P=0.002). Higher PPi and increased difference between day and night PPi were independent predictors of thinner total, inferior, and superior pRNFL (all P values <0.05). Higher PPi only correlated with thinner total, inferior, and superior GCC (all P values <0.05). Conclusions CMD patients show early RGC degeneration, associated with less pronounced nocturnal DBP drop, compared to SBP drop. We conjecture that these patients present with a generalized microvascular dysfunction phenotype. Our findings support that vascular damage precede, and not only follow, glaucomatous neurodegeneration.