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

Abstract

PURPOSE\nTo provide an update on the hemodynamic model of age-related macular degeneration (AMD).\n\n\nDESIGN\nEvidence-based perspective.\n\n\nMETHODS\nReview of literature and experience of authors.\n\n\nRESULTS\nChoroidal 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 disease progression in this complex genetic disease. While early and intermediate AMD appear 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 appear 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 explain the asymmetry between eyes, particularly in the later stages of AMD.\n\n\nCONCLUSIONS\nThis 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.