Treatment of subfoveal choroidal neovascularisation in age related macular degeneration: focus on clinical application of verteporfin photodynamic therapy.

Age related macular degeneration (AMD) is a degenerative disease usually occurring in people over the age of 50 years. Macular involvement can cause vision impairment and result in legal blindness due to atrophic or neovascular complications. The definition of specific lesions associated with AMD has led to classifications of the condition and its severity. The “dry” or non-neovascular form of AMD is characterised by drusen or abnormalities of the retinal pigment epithelium (RPE) such as atrophy, or hypopigmentation or hyperpigmentation. “Wet” or neovascular AMD is manifested by choroidal neovascularisation (CNV). The prevalence of non-neovascular AMD is greater than that of neovascular AMD. However, 10–20% of patients with non-neovascular AMD progress to neovascular AMD. 4 Severe vision loss usually occurs when CNV extends under the centre of the foveal avascular zone (subfoveal CNV). Neovascular proliferation from the choriocapillaris extends through Bruch’s membrane, invades the space under the RPE and leaks serous fluid, including lipid or blood, into this space. This neovascular process is associated with the development of fibrous tissue which replaces the normal architecture of the outer retina, often leading to severe, irreversible loss of central vision. Neovascular AMD, although present in less than 20% of all patients with AMD, is responsible for approximately 90% of cases with severe vision loss. It occurs in up to 200 000 individuals in the USA each year, with approximately 500 000 new cases throughout the world. Without treatment, most aVected eyes have poor central vision (<20/200) within 2 years. The prevalence of AMD has been estimated in several epidemiological studies and ranges from 2% to over 10%, depending on the working definition of AMD, the grading system used, and the age and environment of the study population. All the studies, however, point to the association between AMD prevalence and age. AMD occurs most frequently in people above 50 years of age, with a strong increase in prevalence in people over 65 years of age. This rapid increase in AMD prevalence with age will probably pose a growing health problem for developed countries because of the increasing proportion of the population in older age groups. By 2020, as many as 7.5 million people over 65 years of age may suVer from vision loss due to AMD. Data from the UK have shown that the number of new registrations of blindness due to AMD has increased by 30–40% in the past 50 years. Untreated CNV secondary to AMD is usually associated with a poor vision outcome. The risk of severe visual acuity loss in untreated cases, for which photocoagulation would have been beneficial, can be at least twice that of cases treated with laser photocoagulation. However, photocoagulation is indicated in only a small proportion of cases. Until now, no eVective treatment was available for most patients presenting with neovascular AMD. 23 Patients with CNV secondary to AMD in one eye are at high risk of severe vision loss in the fellow eye, which, when it occurs, will result in a significant adverse impact on the patient’s quality of life. About 50% of patients presenting with bilateral CNV are legally blind within 5 years, compared with 12% of patients with unilateral CNV. In the latter group, however, CNV can develop in the fellow eye. Recent studies have also indicated that the prognosis of the fellow eye is strongly aVected by four risk factors: three characteristics of the macula (presence of five or more drusen, focal hyperpigmentation, and one or more large drusen) and systemic hypertension. The 5 year incidence of CNV in the fellow eye has been estimated to be 87% in patients with all four factors, compared with 7% in patients with none of these risk factors. Thus, the four CNV risk factors are important for the identification of patients who are at risk of developing CNV in the fellow eye. The ideal treatment for neovascular AMD should stabilise visual acuity or prevent the development of severe visual acuity loss, as well as preserve or limit the destruction of the retina overlying the choroidal neovascular lesion while destroying the pathological choroidal neovasculature. Such treatment would benefit most patients with CNV, without causing side eVects, and would improve the patient’s quality of life. Given the public health impact of neovascular AMD, many therapies are under investigation for this condition, leading to an explosion of information in this field. This paper reviews current and experimental treatments for neovascular AMD, focusing on the impact of verteporfin therapy (Visudyne; Novartis Ophtalmia, Bülach, Switzerland).