The origins of polypoidal choroidal vasculopathy

Abstract

Background/aim: There are two theories on the pathogenesis of polypoidal choroidal vasculopathy (PCV): variants in choroidal neovascularisation (CNV) and inner choroidal vessel abnormalities. On indocyanine green angiography (IGA) with a video camera system, PCV has a characteristic appearance, but inadequate image quality has made detailed interpretation difficult. This study aims to improve imaging, using confocal scanning laser ophthalmoscopy (SLO), to elucidate the pathogenesis of PCV.

Methods: High speed IGA with confocal SLO of 45 eyes (44 patients) showed typical PCV findings of a branching vascular network and polypoidal lesions.

Results: Vessels comprising branching networks began to fill simultaneously with the surrounding choroidal arteries in 38 eyes. Small numbers of vessels filling within a branching network, in the arterial and arteriovenous phases of IGA, showed focal dilatation, constriction, and tortuousity. Vessel abnormalities, corresponding to polypoidal lesions, existed within a network in eight eyes and included loops similar in calibre to network vessels, and numerous microaneurysmal dilatations of small vessels. Vessel pulsation was seen in 24 eyes.

Conclusion: PCV is caused by inner choroidal vessel abnormalities, not CNV.

Figures

Figure 1

Indocyanine green angiography. Few arteries follow tortuous courses (A, 25 seconds). Large calibre vessels, apparently veins, hyperfluoresce (B, 32 seconds).

Figure 2

Indocyanine green angiography. Arteries follow tortuous paths, flowing towards the macula. Large branching vessels radiate upwards (A, 28 seconds). An abnormal course of a vessel shows a vascular loop (arrow) (B, 36 seconds). Looped vessel showing leakage, apparently constituting a large polypoidal lesion (C, 73 seconds). Area corresponding to abnormal vessels and polypoidal lesion hyperfluoresces (D, 1566 seconds).

Figure 3

Indocyanine green angiography. Few hyperfluorescent vessels are surrounded by hypofluorescence (arrow). Area in and around arteries hypofluoresces because of vessel paucity (A, 23 seconds). Vessel, with constriction and dilatation, filled slowly (arrow) (B, 29 seconds). Dilatation is more prominent (arrows) (C, 32 seconds).

Figure 4

Indocyanine green angiography. Vessels with abnormal courses appear to be arteries (arrows) (A, 17 seconds), other vessels veins (B, 28 seconds).

Figure 5

Indocyanine green angiography. Large vessel branching into smaller vessels, with large loops (arrow) (A, 20 seconds); more numerous within hypofluorescent area (B, 24 seconds). Numerous hyperfluorescent dots apparently represent cluster of polypoidal lesions. Area corresponding to large vessel also hyperfluoresces (C, 36 seconds).

Figure 6

Indocyanine green angiography. Faint discernible network vessels (A, 24 seconds); hyperfluorescence corresponds to network and polypoidal lesions (B, 533 seconds).

Figure 7

Indocyanine green angiography. A polypoidal lesion is seen within abnormal vessel area comprising a vascular network (arrows) (A, 81 seconds, B, 631 seconds).

Figure 8

(A–C) Internal polypoidal lesion structure.

Figure 9

Internal polypoidal lesion structure. Two large vessels, within a polypoidal lesion, show dilatation and constriction. Small vessels apparently form bridge between the two large vessels (A, 14 seconds). Dye leaked from dilated portions of large vessels (B, 27 seconds) accumulates in upper half of the polypoidal lesion (C, 208 seconds).

Figure 10

Four months after fundus photographs in figure 9. Indocyanine green angiography shows disappearance of small bridging vessels (A, 33 seconds). Leakage from dilated portions of looped vessels (B, 35 seconds); consists of ring of hyperfluorescence (C, 1680 seconds).