An Update on the Hemodynamic Model of Age-Related Macular Degeneration

Abstract

To provide an update on the hemodynamic model of age-related macular degeneration (AMD). Evidence-based perspective. Review of the literature and experience of the authors. Choroidal hemodynamics are not the primary cause of AMD as proposed by Ephraim Friedman in 1997. However, evidence is accumulating to suggest that choroidal perfusion is an important environmental influence that contributes to our understanding of disease progression in this complex genetic disorder. Although early and intermediate AMD seem to be influenced to a large extent by the underlying genetics, the asymmetry of disease progression to the later stages of AMD cannot be explained by genetics alone. The progression of disease and the asymmetry of this progression seem to correlate with abnormalities in choroidal perfusion that can be documented by optical coherence tomography. These perfusion abnormalities in the setting of a thickened Bruch's membrane are thought to exacerbate the impaired nutritional exchange between the retinal pigment epithelium and the choriocapillaris. We propose that the genetic susceptibility to develop AMD combined with age-related changes in macular choroidal hemodynamics, such as increasing choriocapillaris perfusion deficits and decreasing choroidal vascular densities, play an important role in disease progression and may help to explain the asymmetry between eyes, particularly in the later stages of AMD. This updated hemodynamic model of AMD focuses on disease progression and highlights the importance of age-related changes in the choroidal circulation as a major environmental influence on disease severity in eyes that are genetically susceptible to develop AMD.