Choroidal Neovascularization

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An integral part of choroidal neovascularization (CNV) is blood flow. We often use the term CNV to describe a disease process that not only has blood vessels with their associated flow but also has invasion of macrophages, myofibroblasts, fibroblasts, and retinal pigment epithelium in an organized attack. Blood vessels offer an efficient means to transport cells and required building blocks as part of this assault on the macular region. However, the blood flow aspect of CNV may have its own importance. Grossniklaus and Green1 proposed that CNV also may be an attempt at recapitulating the perfusion offered by the choriocapillaris, which can be compromised in patients with late age-related macular degeneration.2 In that sense, CNV is not necessarily a disease but may be a compensatory response.
So there is a dichotomy in meanings for the term CNV: the first being a disease, the second an integral component that may actually have merit. Choroidal neovascularization, the disease, emulates a localized autoimmune disease involved in an orchestrated onslaught against some undefined foe in the macula. Once this foe is vanquished, coincidentally destroying the macula in the process, the attack abates, leaving a scar. At one time, seeing a scar starting to develop was sometimes interpreted as a good thing; the war was nearly over in the eye.
Fortuitously, we can alter the disease, CNV, by targeting the new vessel growth. Earlier attempts included burning with laser and surgical extirpation, both attempts at eradicating the blood vessels at nearly any cost. At one time, intentional photocoagulation of the central fovea was a recommended treatment.3,4 Photodynamic therapy was a strategy to kill, or at least significantly harm, the newly growing vessels, but the treatment caused collateral photochemical damage to neighboring vessels and secondary inflammation. The greatest advance was the introduction of effective treatments targeting vascular endothelial growth factor, a key initiator of angiogenesis and a principal cause of vascular leakage.5,6 With treatment, regression of the most recently formed vascular elements was possible, but more established vessels did not regress. In addition, eyes treated monthly with the anti–vascular endothelial growth factor agent ranibizumab still showed some growth of their vascular lesions after 1 year.6 Even though the CNV vessels were present, control of CNV, the disease, resulted in improved outcomes for treated patients. This implied that the vessels were not necessarily bad, reinforcing the Grossniklaus–Green axiom of years earlier. Physicians are taught to eradicate disease, in this case CNV disease, but CNV, the vessels, may not be so bad.
The interesting study by Ichiyama et al7 highlights this issue. In the study, 20 eyes with treated CNV in remission were analyzed with optical coherence tomography (OCT) angiography. Remission phase for CNV was considered to be achieved if the patient had no subretinal hemorrhage, sign of fluid in or under the retina, and had no treatment for at least 6 months. The patients were treated by a variety of methods to include 10 with anti–vascular endothelial growth factor injections, 1 with photodynamic therapy, and in 9 both. The vascular density of the neovascular lesions was evaluated. Multivariate analysis showed that best-corrected visual acuity was correlated with central retinal thickness and also with vessel density; those with higher amounts of vascularity of their CNV lesion had better acuity. Best-corrected visual acuity was not correlated with duration of disease, vascular area, or use of photodynamic therapy. Obviously, the study was extremely small and several eyes were treated with a method, photodynamic therapy, which is considered inferior to anti–vascular endothelial growth factor therapy for CNV. The type of CNV and how the patients were selected was not specified by the authors.
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