Polypoidal choroidal vasculopathy and central serous chorioretinopathy: author’s reply

Abstract

I was pleased to learn that Doctors Ahuga, et al, have also had experience with “polypoidal choroidal vasculopathy” (PCV) in association with central serous chorioretinopathy (CSC). Their cases, although predominantly white, are not dissimilar from those in our report. They do stress two features to this alleged association that are also in agreement with our observations. First, two of their patients had CSC in the fellow eye without evidence of PCV. We, too, have noticed this peculiar relationship in a few patients. It suggests that the PCV may be a secondary rather than a primary factor in the evolution of exudative changes. Clinicians should keep in mind that ICG angiography will be helpful in discriminating this causal versus coincidental relationship by detection of one or more islands of inner choroidal hyperfluorescence reported to be seen bilaterally in patients with CSC in as many as 98.6% of these patients.1Spaide R.F. Hall L. Haas A. et al.Indocyanine green videoangiography of older patients with central serous chorioretinopathy.Retina. 1996; 16: 203-213Crossref PubMed Scopus (320) Google Scholar With respect to the nature of the PCV, primary or secondary, in patients with CC, we should keep in mind two points. The first is that choroidal neovascularization (CNV) of any type may evolve from nonspecific disturbance of the retinal pigment epithelium.2Yannuzzi L.A. Shakin J.L. Fisher Y.L. Altomonte M.A. Peripheral retinal detachments and retinal pigment epithelial atrophic tracts secondary to central serous pigment epitheliopathy.Ophthalmology. 1984; 91: 1554-1572Abstract Full Text PDF PubMed Scopus (215) Google Scholar Polypoidal-CNV does not appear to be an exception. However, polypoidal CNV tends to regress spontaneously more predictably and dramatically than other forms of neovascularization without evidence of fibrovascular scarring. Furthermore, the regression may be so pronounced that ICG angiographic evidence of preexisting PCV virtually vanishes. We believe that this is due to regression, or possibly even infarction, of the membrane and by reconstitution of its endothelial structures so that the leakage disappears, and consequently, the affinity for the ICG dye to conjugate with tissue or pool into associated exudative spaces no longer exists. I thank the authors for their appropriate and valuable comments, and I join them in suggesting that PCV should be considered in any patient with CSC when the clinical manifestations are unusual.3Yannuzzi L.A. Ciardella A. Spaide R.F. et al.The expanding clinical spectrum of idiopathic polypoidal choroidal vasculopathy.Arch Ophthalmol. 1997; 115: 478-485Crossref PubMed Scopus (389) Google Scholar