Ehrlich et al approximately 6%–11% per decade with an increase in the resistive index. On the other hand, Harris et al (2000) found that central retinal artery ﬂow velocity was unaffected by age in both sexes. Nevertheless, they did ﬁnd that end-diastolic veloc- ity of the posterior ciliary arteries decreased and the resistive index increased with age in women, but not in men. The perfusion of the optic nerve head is also altered with increasing age. Boehm et al (2005) used laser Doppler ﬂowmetry to ﬁnd that volume and ﬂow in the optic nerve decreased with age, suggesting that blood supply is reduced in elderly subjects. Neuroretinal rim and lamina cribrosa blood ﬂow also decreases with advancing age (Embelton et al 2002). Additionally, Rizzo et al (1991) used a laser Doppler technique to demonstrate that advancing age is associated with a reduction in capillary red blood cell speed at the optic nerve head. Ocular blood ﬂow changes in AMD Atherosclerosis has been postulated to be associated with late stages of AMD through its effect on the choroidal circulation and possible deposition of lipids in the Bruch’s membrane (Freidman 2000; Curcio et al 2001). A history of cardiovas- cular disease and increased levels of cholesterol and stage 2 hypertension are strongly associated with neovascular AMD (Hogg et al 2008). The Rotterdam Eye Study demonstrated that persons with subclinical cardiovascular disease, as mani- fested by carotid artery plaques, were nearly ﬁve times more likely to have late AMD compared to patients without such plaques (Vingerling et al 1995a). The Multiethnic Study of Atherosclerosis (MESA) found an association between the severity of the intima-media thickness of the carotid artery and early AMD in black participants (Klein et al 2007a). Nevertheless, they did not find an association between severity of subclinical atherosclerosis and early AMD in the entire MESA cohort (Klein et al 2007a). The Women’s Health Initiative Sight Exam Ancillary Study (WHISE) further reported a positive association between elevated sys- tolic blood pressure and the presence of soft drusen, which correlated inversely with retinal pigment epithelial depig- mentation and exudative AMD (Klein et al 2007b). Diastolic blood pressures and mean arterial blood pressures positively correlated with an increased risk of early AMD even after controlling for age (Klein et al 2007b). Although the rela- tionship between blood pressure and AMD is not always consistent, several studies have demonstrated an association. In the Beaver Dam Eye Study, persons with hypertension at baseline were approximately two to three times more likely to develop neovascular macular degeneration after 10 years 478 of follow-up than age-matched controls (Klein et al 2003). Furthermore, the Age-Related Macular Degeneration Risk Factor Study reported hypertension and high cholesterol to be associated with increased risk of neovascular AMD (Hyman et al 2000). Since the choriocapillaris supplies the retinal pigment epithelial cells and the outer retina, a primary perfusion defect in the choriocapillaries could lead to loss or dysfunction of retinal pigment epithelial cells (Ciulla et al 2001). Spraul et al (1996) found increased total luminal area of peripheral choroidal vessels and decreased density of choroidal vessels in the macular area of eyes with AMD. In his theory on the development of AMD, Friedman (1997) hypothesized that with age, lipoid inﬁltration occurs within the sclera, Bruch’s membrane and the wall of blood vessels, which leads to a decrease in the scleral and choroidal vessels compliance. This decrease in compliance can increase the resistance of the choroidal blood vessels and decrease choroidal perfusion (Friedman 1997). The elevated resistance can also increase intravascular pressure and raise hydrostatic pressure. Fur- thermore, scleral rigidity has been shown to increase with age (Lam et al 2003; Pallikaris et al 2005) and in patients with AMD (Friedman et al 1989). All of these changes in the choriocapillaris can impair the retinal pigment epithelial cell transport, promote increased debris accumulation and cause dysfunction of the retinal pigment epithelial cells (Friedman 1997) to set the stage for AMD development. Blood flow analysis in patients with AMD shows decreased choroidal blood ﬂow, velocity and volume in the fovea in AMD patients (Grunwald et al 2005). In addition, the severity of AMD increases in patients with the lowest circulatory parameters, possibly contributing to the ischemia and preceding the development of choroidal neovasculariza- tion (Grunwald et al 2005). With the use of the laser Doppler ﬂowmetry, Metelitsina et al (2006) further investigated cho- roidal blood ﬂow in the fovea of patients with early AMD with or without systemic hypertension. AMD patients with systemic hypertension had 16.7% lower blood ﬂow compared to patients without hypertension (Metelitsina et al 2006). These results further suggest that systemic hypertension may contribute to the progression of AMD and the development of choroidal neovascularization (Metelitsina et al 2006). Sato et al (2006) also used the laser Doppler ﬂowmetry to ﬁnd that the pulsatility index, pulsatility ratio and resistive index were higher in patients with AMD and increased with disease severity. They found no difference between the mean blood velocity and ﬂow rates and no differences in arterial diameter, suggesting that patients with AMD suffer from decreased Clinical Interventions in Aging 2008:3(3)