TY - JOUR T1 - Update of the vascular model of AMD JF - British Journal of Ophthalmology JO - Br J Ophthalmol SP - 161 LP - 163 DO - 10.1136/bjo.2003.036277 VL - 88 IS - 2 AU - E Friedman Y1 - 2004/02/01 UR - http://bjo.bmj.com/content/88/2/161.abstract N2 - Are statins or antihypertensives protective? The observation that age related macular degeneration (AMD) and atherosclerosis share risk factors and pathogenetic mechanisms1 has led to the development of a hypothesis that is identified as a haemodynamic2 or vascular1 model of the pathogenesis of AMD. It holds that AMD is a vascular disorder characterised by impairment of choroidal perfusion of the retinal pigment epithelium (RPE). This model, evolved over four decades,3 is now updated to incorporate recently reported evidence4 that the changes affecting Bruch’s membrane in age and AMD involve lipoproteins processed by the RPE. The model proposes that these lipoproteins accumulate in drusen and in Bruch’s membrane because the choriocapillaris does not clear them.Theoretical models of disease are evaluated by how much they explain and by their success in making useful predictions. As the vascular model, by emphasising the pathogenetic importance of atherosclerotic processes and increased intravascular pressure, essentially predicts that statins and antihypertensive agents should have a protective effect on AMD, it is instructive to review the evidence to date. Figure 1 Schematic representation of the vascular model of the pathogenesis of age related macular degeneration. This model asserts that choroidal vascular resistance is increased by decreased compliance of ocular tissues,5 as a result of progressive infiltration with lipid. It is likely that progressive narrowing of the macular choriocapillaris with age3 also contributes to the increased resistance.6 While the systemic circulation is the source of the lipid in the sclera7 and choroidal vasculature, there is evidence that the RPE is the source of lipids in drusen and in Bruch’s … ER -