Glaucoma is a multifactorial optic neuropathy that affects more than 50 million people and is the second leading cause of blindness worldwide.1 The role of IOP has been well documented as a major modifiable risk factor for glaucoma, but decreasing IOP does not always stop the progression of the disease.2 Additionally, many glaucoma patients have a relatively low IOP, while some healthy individuals have a relatively high IOP.2
Vascular impairment as a risk for glaucoma has also been well established, especially over the past 2 decades. In 1953, Duke-Elder suggested vascular risk factors in the pathogenesis of open-angle glaucoma.3 Hundreds of prospective studies have since determined that impaired vascular regulation, lower blood flow in ocular vessels, and lower ocular perfusion pressure (OPP) are some of the main hemodynamic issues contributing to primary openangle glaucoma. In 2009, the World Glaucoma Association reached a consensus that vascular dysregulation may contribute to the pathogenesis of glaucoma and that impaired OPP is an independent risk factor for glaucoma.
Despite this wealth of evidence, ophthalmologists’ understanding of vascular considerations in glaucoma management remains limited. No gold standard for measuring all relevant ocular vascular beds exists, imaging devices have inherent limitations and assumptions, and experienced technicians are in short supply. Furthermore, vascular contributions as risk factors for glaucoma have largely been studied for disease incidence and prevalence but not fully explored in terms of the risk of disease progression.