Investigating the impact of atrial fibrillation on the vascular onset of glaucoma via multiscale cardiovascular modeling

Background and objective:

Atrial fibrillation (AF) is the most common tachyarrhythmia, exhibiting faster and irregular beating. Although there is growing evidence of the impact of AF on the cerebral hemodynamics, ocular hemodynamic alterations induced by AF are still poorly investigated to date. The objective of this study is to computationally inquire into the role of AF on the ocular hemodynamics as one of the possible vascular triggers of glaucoma, which is the leading cause of blindness due to the damage of the optic nerve.

Methods:

A validated 0D–1D multiscale cardiovascular model is exploited to compute the hemodynamic response of AF against sinus rhythm (SR), by simulating 2000 beats for each condition. To mimic AF rhythm, its main features are accounted for: (i) accelerated, variable and uncorrelated beating; (ii) absence of atrial kick; (iii) ventricular systolic dysfunction.

Results:

We focused on intraocular pressure ($IOP$), ocular perfusion pressure ($OPP$), and translaminar pressure ($TLP$). Apart from a modest $OPP$ decrease, beat-averaged values of $IOP$ and $TLP$ barely vary in AF with respect to SR. Instead, during AF a significant reduction and dispersion of pulsatile values (i.e., maximum minus minimum values reached in a beat), as well as wave amplitude damping, is observed for $IOP$, $OPP$ and $TLP$. The marked variability of pulsatile values, which are hardly measured due to clinical difficulties, can induce transient hypoperfusions and hypo-pulsatility events (for $OPP$) as well as hypertensive episodes (for $TLP$).

Conclusions:

Awaiting necessary clinical data which are to date lacking, the present study can enrich – through hemodynamic-driven hints in the AF framework – the vascular theory, which associates reduced ocular perfusion (by means of decreased $OPP$ and increased $TLP$) to an augmented risk of glaucoma. In this context, present modeling findings suggest a possible mechanistic link between AF-induced hemodynamic alterations and the increased risk of glaucoma development.