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• W1966232476 abstract "Purpose: We assessed the characteristic indocyanine green angiographic (ICGA) and spectral domain optical coherence tomographic (SD-OCT) findings of two types of polypoidal choroidal vasculopathy (PCV), distinguishable by different filling patterns on ICGA. Methods: Thirty-one eyes with PCV were classified into types 1 and 2 based on ICGA findings of either the presence or absence of both a feeder and a draining vessel. Characteristic ICGA findings were evaluated for each type of PCV. Spectral domain optical coherence tomographic images of the 31 eyes were also used to compare the two types of PCV. Results: Both a feeder and a draining vessel were observed in 13 eyes (type 1). Eighteen eyes had neither feeder nor draining vessels (type 2). In PCV type 1, a break in the highly reflective line thought to be Bruch’s membrane was detected, corresponding to the feeder vessel in-growth site on SD-OCT. This line was straight. In PCV type 2, the highly reflective line exhibited irregular thickness and had highly reflective substances adhering to its lower portion. It curved downward and became increasingly obscure, ultimately disappearing at a point corresponding to the site at which network vessel filling began. The mean subfoveal choroidal thicknesses in eyes with PCV type 1 and PCV type 2 were 199 ± 65 and 288 ± 98 μm, respectively. Conclusions: Our observations support the existence of two distinct types of PCV. The first type represents choroidal neovascularization, whilst the second type involves choroidal vasculature abnormalities. Polypoidal choroidal vasculopathy (PCV) is now well known to be characterized by a branching vascular network and polypoidal lesions (Spaide et al. 1995) detectable by indocyanine green angiography (ICGA). However, as increasingly advanced genetic studies and imaging technologies become available, our understanding of the pathophysiology of PCV grows. In recent years, spectral domain optical coherence tomography (SD-OCT), including Enhanced Depth Imaging (EDI) OCT, has been used to investigate morphological alterations in eyes with PCV (Ojima et al. 2009; Ozawa et al. 2009; Freund et al. 2010; Chung et al. 2011; Koizumi et al. 2011; Miura et al. 2011). Despite these diagnostic advances, the pathogenesis of PCV remains controversial. Two different histopathological features have been described. One, as we reported previously (Nakashizuka et al. 2008), is related to arteriosclerotic changes of choroidal vessels (Okubo et al. 2002; Nakashizuka et al. 2008).The other corresponds to choroidal neovascularization (CNV) (Lafaut et al. 2000; Rosa et al. 2002; Terasaki et al. 2002). Vascular endothelial growth factor (VEGF) positivity in vascular endothelial cells of PCV was found in some studies (Terasaki et al. 2002; Matsuoka et al. 2004) but not in others (Nakajima et al. 2004; Nakashizuka et al. 2008). The aqueous VEGF level in eyes with PCV is reportedly higher than that in normal eyes but significantly lower than that in eyes with age-related macular degeneration (AMD) (Tong et al. 2006). Thus, uncertainty persists as to the role of humoral growth factors, and the consequences of inhibiting these factors, in PCV. Based on a recent study of the age-related maculopathy susceptibility gene 2 (ARMS-2), Tanaka et al. (2011a,b) suggested that PCV is divisible into two types. They divided their cohort of Japanese patients into 202 with typical PCV, that is, PCV in the narrow sense and 85 with polypoidal CNV. They found one variant of the ARMS-2 gene to be strongly associated with AMD. Typical PCV was not associated with the ARMS-2 variant. We previously reported the characteristic scanning laser ophthalmoscope indocyanine green angiographic (SLO-ICGA) findings of strictly defined PCV, that is, the type of PCV characterized by choroidal vasculature abnormalities (Yuzawa et al. 2005). Taking our SLO-ICGA (Yuzawa et al. 2005) and reported histopathological results (Nakajima et al. 2004) together, along with the findings of other studies (Lafaut et al. 2000; Okubo et al. 2002; Rosa et al. 2002; Terasaki et al. 2002; Matsuoka et al. 2004), we classified PCV into three groups (Yuzawa et al. 2005). The first was the aforementioned PCV in the narrow sense, which is caused by inner choroidal vessel abnormalities, not by CNV. The second, the polypoidal type, is CNV expanding rapidly under the retinal pigment epithelium (RPE), ultimately with polypoidal lesions developing at vessel termini. The third type, radiation-associated choroidal vasculopathy, is considered to be a complication of radiation (Spaide et al. 1999). Thus, PCV is classified mainly into choroidal vessel abnormalities and polypoidal CNV (Yuzawa 2012). In this study, we used both SLO-ICGA and SD-OCT findings to demonstrate differences between PCV in the narrow sense (hereafter, PCV type 2) and polypoidal CNV (hereafter, PCV type 1). We performed simultaneous SLO-ICGA using eye-tracked Spectralis® HRA + OCT (Heidelberg Retina Angiograph plus OCT; Heidelberg Engineering GmbH, Heidelberg, Germany) in patients with PCV between June of 2008 and November of 2011. Thirty-one eyes of 31 patients which yielded clear images of the early phase of SLO-ICGA were selected. All patients had subretinal haemorrhage and/or serous retinal detachment and/or a haemorrhagic or serous RPE detachment (PED), as demonstrated by slit-lamp fundus examination. Occult CNV involving the macula was also seen on fluorescein angiography (FA) in all cases. Patients who had PCV and other concurrent fundus diseases, or who had undergone prior treatment for PCV, or who exhibited subretinal CNV on FA and/or SD-OCT were excluded from this study. For SLO-ICGA, indocyanine green dye (25 mg in 2 ml balanced saline) was injected into the cubital vein. Video angiography was recorded for 30 seconds starting from the time of dye injection, and consecutive photographs were then taken up to 1 min, and again at approximately 2.5, 5, 10 and 15 min. Indocyanine green angiographic findings in the 31 eyes were divided into two patterns: both a feeder and a draining vessel on SLO-ICGA (PCV type 1), and eyes with neither (PCV type 2). We also obtained simultaneous SD-OCT cross-sectional images, corresponding to either the in-growth site of the feeder vessel or the point at which the network vessel filling began on SLO. In addition, horizontal and vertical cross-sectional SLO-ICGA images were obtained at the fovea. We assessed the sites and filling states of the feeder and draining vessels, and the characteristics of the vessel networks. In eyes with PCV type 2, the filling, number and features of network vessels were evaluated. The subtraction method was employed to assess the images (Spaide et al. 1998). The subtraction image, obtained by subtracting the angiogram taken in the arteriovenous phase from that in the venous phase of SLO-ICGA, allows clear visualization of vessel filling. For both types of PCV, the largest diameter comprising a network of vessels plus polypoidal lesions was measured. We evaluated the pulsation and the presence of plaque, defined as a hyperfluorescent area observed in the late phase of SLO-ICGA (Guyer et al. 1996). For polypoidal lesions, the location and architecture were evaluated. The site on the SD-OCT image corresponding to either feeder vessel in-growth or the point at which the network vessel filling began was identified and subfoveal choroidal thickness was determined as the average of the measured thicknesses in the horizontal and vertical directions. The choroidal thickness under the fovea was scanned 100 times to improve the signal-to-noise ratio and the data obtained were averaged. Enhanced depth imaging was used in cases in which the choroidal thickness could not be measured. The choroidal thickness under the fovea was measured from the outer surface of the hyperreflective line corresponding to the RPE to the inner surface of the sclera. If pigment epithelium detachment was present, the highly reflective line thought to be Bruch’s membrane was used as the inner margin of the choroid instead of the RPE line. If Bruch’s membrane was not identified, the inner margin of the choroid was defined as the boundary. The 31 eyes were classified according to the SLO-ICGA findings. Thirteen eyes had both a feeder and a draining vessel (PCV type 1) whilst 18 eyes lacked both feeder and draining vessels, that is, showed only network vessels with polypoidal lesions (PCV type 2). The PCV type 1 group consisted of 13 eyes of 13 patients (nine males and four females, 55–82 years of age, 69.5 years on average) in which both a feeder and a draining vessel, connecting the network vessels to the polypoidal lesions, were detected. The feeder vessels were visible immediately after filling of the choroidal arterioles in these 13 eyes (1, 2). Fluorescence within the feeder vessels decreased rapidly and was obscured after a short time (1, 2). Very close to the feeder vessel, the draining vessel was observed as a gradually brightening fluorescent vessel and was visible for several minutes in all 13 eyes. In the subtraction images, the feeder vessel appeared black due to weakening of the venous phase fluorescence. The draining vessel appeared white due to the venous phase fluorescence in this vessel becoming stronger (1, 2). In these 13 eyes, a large number of vessels branched from the feeder vessels, and these branches constituted the networks (1, 2). Each network vessel was essentially straight and became thinner towards the periphery. The vessels were packed into a thin meshwork between relatively thick vessels branching from the feeder vessel. The shapes of the branching vascular networks were classified into two patterns. One type (eight eyes) was an umbrella-like pattern with vessels radiating from a feeder vessel, that is, spreading outward in a radial configuration (Fig. 1). The other type (five eyes) was a rake-like pattern with vessels extending from a feeder vessel, thereby resembling the teeth of a rake (Fig. 2). No pulsation was detected in the network vessels in any of these 13 eyes. Filling of the network vessels gradually became obscure, and plaque was prominent in the late phase in all 13 eyes (1, 2). All polypoidal lesions were at the termini of the network vessels and consisted of the dilatation of marginal tortuous network vessels. The polypoidal lesions followed the course of the marginal vessel in 11 of the 13 eyes, rather like an irregular string of beads (Fig. 1B). The largest diameters of the networks of vessels together with the polypoidal lesions ranged from 4250 to 7200 μm (mean 5513 ± 976 μm). Scanning Laser Ophthalmoscope Indocyanine Green Angiography (SLO-ICGA) of PCV type 1 showing an umbrella-like configuration of network vessels with 2 pigment epithelial detachments (PED). (A) At 22 seconds, the in-growth site of a feeder vessel is visible (white arrow). Many vessels can be seen to radiate from the feeder vessel. (B) At 29 seconds, a draining vessel is observed very close to the feeder vessel (yellow arrows). The network is composed of a large number of vessels. Polypoidal lesions are dilatations of marginal tortuous vessels (yellow arrowheads). The pattern is similar to that of choroidal neovascularization although there are numerous polyps at the periphery. (C) Subtraction image (A from B). The feeder vessel is black (black arrowheads) because at 29 seconds fluorescence in the feeder vessel has weakened markedly. The draining vessel appears white because only this vessel fluoresces in B (black arrows). (D) At 36 seconds, the draining vessel can still be seen. (E) At 634 seconds, plaque is surrounded by polypoidal lesions. (F) Spectral domain optical coherence tomographic showing a break in Bruch’s membrane and separation between the retinal pigment epithelium (RPE) and Bruch’s membrane. A break (black arrow) is observed in Bruch’s membrane corresponding to the in-growth site of the feeder vessel on SLO-ICGA (yellow arrow). Irregular elevations of the RPE are observed corresponding to network vessels. Bruch’s membrane is straight. (G) Illustration of 1F. Scanning laser ophthalmoscope indocyanine green angiographic (SLO-ICGA) of polypoidal choroidal vasculopathy type 1 showing a rake-like configuration of network vessels with a haemorrhagic PED. (A) At 17 seconds, the in-growth site of a feeder vessel is visible (white arrow). (B) At 24 seconds, a draining vessel is observed very close to the feeder vessel (yellow arrow). The network is composed of a large number of vessels. Polypoidal lesions are dilatations of marginal tortuous vessels (yellow arrowheads). (C) Subtraction image (A from B). The feeder vessel is black (yellow arrow). The draining vessel appears white (yellow arrowheads). (D) At 33 seconds, the draining vessel can still be seen. (E) At 969 seconds, plaque is surrounded by polypoidal lesions. (F) Spectral domain optical coherence tomographic (SD-OCT) showing a break in Bruch’s membrane and separation between the retinal pigment epithelium and Bruch’s membrane. The line is thin and straight. Hypo-reflective substances pass through the break in Bruch’s membrane (black arrow) on SD-OCT. The location of this break corresponds to the in-growth site of the feeder vessel on SLO-ICGA (yellow arrow). (G) Illustration of 2f. The PCV type 2 group, in which feeder vessels do not exist, consisted of 18 eyes of 18 patients (12 males and six females, 46–78 years of age, 64.6 years on average). Filling of network vessels was observed even in the choroidal venous phase on ICGA, indicating slow filling within network vessels in all 18 eyes. The networks were composed of a small number of vessels showing focal dilatation and tortuosity (3, 4). Vessels constituting branching networks began to fill simultaneously with the surrounding choroidal arteries (3, 4). In the subtraction images, network vessels were still fluorescing, indicating slow vessel filling (3, 4). Pulsation was detected in network vessels in three eyes. All polypoidal lesions were located at the edges of the networks except for one, which was within the network itself. Thirteen eyes had one polyp, the other five-two polyps. The polypoidal lesions consisted of either a dense cluster of numerous small hyperfluorescent dots representing relatively large aneurysmal dilatations, or large vessels with abnormal courses such as loop-like vessels. Plaque was observed in nine of the 18 eyes (3, 4). Each polypoidal lesion was independent of the others. The largest diameters of a vascular network together with polypoidal lesions ranged from 830 to 3910 μm (mean 2093 ± 799 μm), significantly smaller than that in type 1 PCV (p < 0.01,Wilcoxon signed-rank test). Indocyanine green angiography of polypoidal choroidal vasculopathy type 2 showing network vessels with polyps. (A) At 16 seconds, network vessels (white arrows) and choroidal arteries (yellow arrows) become apparent. (B) At 23 seconds, filling of the network vessels can still be seen (black arrows). Network vessels show tortuosity and numerous microaneurysmal dilatations of small vessels. (C) Subtraction image (A from B). Network vessels are still fluorescing (white arrows), indicating slow vessel filling. (D) At 30 seconds, the network vessel can still be seen. (E) At 913 seconds, no plaque is observed. (F) Spectral domain optical coherence tomographic showing separation between the retinal pigment epithelium (RPE) plus Bruch’s membrane on the one hand, and the inner choroid on the other. The point denoted by the black arrow corresponds to the site at which network filling began on scanning laser ophthalmoscope indocyanine green angiographic (yellow arrow). The line thought to be the inner choroid shows irregular thickness with highly reflective substances adhering to its lower portion (black arrowheads). It curves downward towards the point where network filling began (yellow arrowhead). A vessel appears to invade the space between the RPE plus Bruch’s membrane and the inner choroid and to push the RPE upward. The RPE above the point denoted by the green arrow is dimpled. (G) Illustration of F. Indocyanine green angiography of another case with polypoidal choroidal vasculopathy type 2 showing network vessels. (A) At 19 seconds, network vessels become apparent (white arrows). (B) At 26 seconds, filling of the network vessels can still be seen (white arrows). Network vessels show focal dilatation, constriction and tortuosity. (C) Subtraction image (A from B). Network vessels are still fluorescing (white arrows), indicating slow vessel filling. (D) At 30 seconds, the network vessel can still be seen. (E) At 955 seconds, plaque is observed. (F) Spectral domain optical coherence tomographic (SD-OCT) showing separation between the retinal pigment epithelium (RPE) plus Bruch’s membrane and the inner choroid. The point denoted by the black arrow on SD-OCT corresponds to the point, denoted by the yellow arrow, at which a network vessel started to fill in the early phase of scanning laser ophthalmoscope indocyanine green angiographic. The line thought to be the inner choroid shows irregular thickness with highly reflective substances adhering to its lower portion (black arrowheads). It curves downward towards the point where network filling began (yellow arrowhead). A vessel appears to invade the space between the RPE plus Bruch’s membrane and the inner choroid and to push the RPE upward. (G) Illustration of F. In PCV type 1, a break in the highly reflective line thought to be Bruch’s membrane, corresponding to the in-growth site of the feeder vessel on SD-OCT, was detected (1, 2). The line was thin and straight and lacked highly reflective substances adhering to its lower portion. Irregular elevations of the RPE above thick vessels forming part of the network of vessels were also observed. Prominent elevations of the RPE corresponded to polypoidal lesions. In PCV type 2, the highly reflective line differed markedly from that in PCV type 1. First, the line was of irregular thickness with highly reflective substances adhering to its lower portion. Second, the line was not straight. It curved downward and became increasingly obscure, ultimately disappearing at a point corresponding to the site at which the network vessel filling began. Third, there were no breaks in this line. This pattern was observed in all 18 eyes with PCV type 2. The RPE was pushed upward in these 18 eyes, apparently by a dilated vessel corresponding to the network vessels (3, 4). A dimple in the RPE at the site at which the network vessel filling began was observed in 10 of the 18 eyes. Mean subfoveal choroidal thicknesses in eyes with type 1 and type 2 PCV were 199 ± 65 and 288 ± 98 μm, respectively. Thus, mean subfoveal choroidal thickness was significantly greater in type 2 than in type 1 PCV (p = 0.019, Wilcoxon signed-rank test). Characteristic SLO-ICGA findings of the presence of both a feeder vessel and an accompanying draining vessel were documented in 13 eyes with PCV type 1 in this study. Numerous vessels radiated from the feeder vessel. Costa et al. (2005) advocated that PCV lesions be considered a variety of CNV. They observed in-growth sites of feeder vessels in 95.5% of 22 eyes with PCV. Pathological studies have shown a choroidal arteriole and a vein (El Baba et al. 1986; Bressler et al. 1992; Chang et al. 1994) extending through the break in Bruch’s membrane in CNV associated with AMD. In the present study, vessels branching from the feeder vessel were essentially straight and became thinner towards the periphery on ICGA. The network vessels formed umbrella-like or rake-like configurations. Vessels between these straight vessels showed multiple interconnections and thereby formed dense mesh-like networks. The umbrella-like configuration is similar to the characteristic findings of classic CNV, as demonstrated by FA, whilst the rake-like configuration is similar to retinal neovascularization observed in sickle cell retinopathy (Fadugbagbe et al. 2010). Plaque was reported to be a characteristic finding of CNV within Bruch’s membrane (Guyer et al. 1996). All lesions in the 13 eyes in our PCV type 1 group showed plaque in the late phase. Dye may leak rapidly from numerous network vessels and reveal this plaque on ICGA. Our results indicate that the network vessels described herein have the characteristics of CNV beneath the RPE. Polypoidal lesions appeared to have been caused by the dilatation of marginal tortuous network vessels. Furthermore, Gass (2004) classified subretinal CNV into two types, sea fan and polypoidal. The polypoidal type was described as a peculiar growth pattern of new vessels, not a specific disease, occurring in patients who would ordinarily be relatively resistant to the development of subretinal neovascularization because of their highly pigmented fundi. Characteristic SD-OCT findings in the present study included a break, corresponding to the in-growth site of the feeder vessel, in the line thought to be Bruch’s membrane, separation between the RPE and Bruch’s membrane, and irregular RPE elevations corresponding to network vessels and polypoidal lesions. These SD-OCT findings indicate that network vessels branching from feeder vessels may pass through ruptures in Bruch’s membrane, spread between the RPE and Bruch’s membrane, become deformed polypoidal vessels at the margin, and then drain into the draining vessels close to feeder vessels. Taking the SLO-ICGA results of the present study together with the aforementioned findings in the literature (El Baba et al. 1986; Bressler et al. 1992; Chang et al. 1994; Gass 2004), we hypothesize that the type of PCV which has a feeder vessel and a draining vessel as well as polypoidal lesions at network vessel termini in a string-of-beads configuration represents CNV with polyps under the RPE and is thus polypoidal CNV. On the other hand, the SLO-ICGA findings of PCV in the narrow sense (PCV type 2), as described in our previous report (Yuzawa et al. 2005), are also characteristic. Vessels constituting branching networks begin to fill slowly, but simultaneously, with the surrounding choroidal arteries. Hypofluorescence in and around network vessels is observed in the early phase. The vessels, all of which fill, within a branching network are few in number and show focal dilatation, constriction and tortuosity in the arterial and arteriovenous phases of SLO-ICGA. Vessel abnormalities corresponding to polypoidal lesions include loops similar in calibre to network vessels and numerous microaneurysmal dilatations of small vessels. Vessel pulsation is sometimes seen in both the network and polypoidal lesions. Plaque has also been observed in several, though not all, eyes with PCV in the narrow sense (PCV type 2). In our prior study (Nakashizuka et al. 2008), characteristic pathological features of PCV type 2 were shown to include abnormally dilated vessels located beneath Bruch’s membrane. These vessels are occasionally observed above the RPE. Another characteristic feature is hyalinization. Hyalinization is thought to result from an increase in intravascular pressure and is an essentially arteriosclerotic change, so-called hyalinized arteriosclerosis, not neovascularization. Vascular endothelial cells were negative for VEGF in our previous study (Nakashizuka et al. 2008). Judging from the present SLO-ICGA findings and the results of earlier pathological studies (Okubo et al. 2002; Yuzawa et al. 2005), we speculate that the aetiology of this type of PCV is choroidal vascular abnormalities. Spectral domain optical coherence tomographic (SD-OCT) findings in PCV type 2 also appear to differ from those of PCV type 1. Nakashizuka et al. (2008) from our research group used immunohistochemical techniques to stain for CD34 and demonstrated discontinuous vascular endothelium in hyalinized vessels, indicating massive exudation. Furthermore, α-SMA (smooth muscle actin) staining was negative in hyalinized vessels in the same study. Disappearance of smooth muscle cells from vessel walls results in vessel dilatation. Judging from the results of histopathological studies, abnormally dilated vessels may push the RPE upward secondary to an increase in intravascular pressure due to the presence of several dilated vessels and in response to massive exudation from these vessels within the choroid. In fact, we found mean subfoveal choroidal thickness to be significantly greater in eyes with PCV type 2 than in those with type 1. The choroid is reportedly thick in PCV whilst being relatively thin in exudative AMD (Chung et al. 2011; Koizumi et al. 2011). The presence of dilated vessels and the massive exudation documented in our studies is thought to result from the thickened choroid in PCV type 2. RPE dimpling in type 2 PCV might be attributable to intrachoroidal pressure being decreased at the point at which network vessel filling begins. An issue awaiting resolution is the discrepancy in the highly reflective line in cases of PCV type 2, observed on SD-OCT, which we initially believed to be Bruch’s membrane. The line is straight in PCV type 1. In marked contrast, the line in PCV type 2 is of irregular thickness with highly reflective substances adhering to its lower portion, and it curves downward and becomes increasingly obscure, ultimately disappearing at a point corresponding to the site at which network vessel filling begins. There are no breaks in this line. The aforementioned pathological studies showed abnormally dilated vessels to be present beneath Bruch’s membrane in PCV type 2. Our pathological investigation revealed that collagenous membranes with plasma protein appear to be present beneath polypoidal lesions. These membranes may extend beneath the network vessels and represent collagenous materials which result from the accumulation of plasma constituents secondary to the excessive endothelial permeability of dilated choroidal vessels. These findings may correspond to the line showing irregular thickness with highly reflective substances adhering to its lower portion. The vessels and exudation from them may push the RPE plus Bruch’s membrane upward on SD-OCT. Therefore, the line which we initially believed to be Bruch’s membrane may not in fact be Bruch’s membrane at all, instead possibly being the inner choroid, in PCV type 2. Kahn et al. (2012) recently reported that PCV corresponds to polypoidal CNV (PCV type 1) in our classification. The ICGA and SD-OCT findings of polypoidal CNV classified according to our system are indeed similar to those reported by Kahn et al. (2012). Lesions are located between the hyperreflective RPE band and Bruch’s membrane plus the inner choroid. In some cases, they observed three highly reflective layers (triple-layer sign), that is, the choroid, detached from Bruch’s membrane, and inner choroid was seen as a highly reflective, independent layer. Our histopathological results have proven the lesion to be located under Bruch’s membrane in PCV type 2 (Nakashizuka et al. 2008). Bruch’s membrane becomes detached from the inner choroid. We believe that the hyperreflective line which we initially considered to be Bruch’s membrane may in fact be the inner choroid on SD-OCT in PCV type 2. The study of Kahn et al. showed that the inner choroid alone can appear as a hyperreflective line. This assumption on our part is based on Bruch’s membrane becoming detached, due to elevation of dilated choroidal vessels, whilst the inner choroid remains in place. Our SD-OCT images show the PCV lesion to be located between a band, comprised of the RPE plus Bruch’s membrane, and the inner choroid. Further detailed investigation is needed to interpret our present SD-OCT findings. The largest diameter of a vascular network together with polypoidal lesions in eyes with type 2 PCV was significantly smaller than that in type 1 PCV. Tsujikawa et al. (2011) assert that PCV with small vascular lesions shows minimal progression. Type 2 PCV may also show limited progression. Okubo et al. (2008) classified PCV into two groups based on lesion size and disease duration and showed that eyes with small lesions of short duration had atrophic changes in the RPE, hyperpermeablility and pulsation. This group of eyes may represent the same aetiology as our type 2 PCV. Tanaka et al. (2011a) showed the ARMS2 A69S gene, which is a causative candidate gene for AMD, to be closely related to polypoidal CNV but not to PCV in the narrow sense (PCV type 2). The same investigators subsequently showed single-nucleotide polymorphisms (SNPs) of the ARMS2 gene to potentially be strong genetic markers for retinal angiomatous proliferation whilst SNPs of two other genes (elastin; ELN and methyltetrahydrofolate reductase; MTFHR) were associated with the neovascular form of AMD (Tanaka et al. 2011b). Neither ELN nor MTFHR was associated with PCV in the narrow sense. In another recent study, Bessho et al. (2011) suggested ARMS2 variants to be associated with both the phenotypic features and responses to photodynamic therapy of AMD and typical PCV. In a very recent study, the same authors investigated the associations of cluster of differentiation 36 (CD36) variants with PCV and AMD (Bessho et al. 2012). They found the allelic frequencies of two SNPs to differ between PCV and AMD. They concluded that CD36, a multi-functional molecule, may be associated with differences in genetic susceptibility to PCV versus typical AMD, as well as also explaining the better response of PCV to photodynamic therapy. These genetic differences may reflect pathogenic differences between PCV types 1 and 2. Although PCV reported in Caucasians is generally considered to be polypoidal CNV, PCV in the narrow sense (PCV type 2) is very important in studies of Asian populations, because the number of patients with PCV is high (Maruko et al. 2007). In recent years, photodynamic therapy and anti-VEGF drugs, alone or in combination, have been used for the treatment of PCV. However, efficacies may differ depending on the type of PCV. Differentiation of the two types of PCV described herein is anticipated to be useful for determining both optimal treatments and visual prognosis. It is also hoped that distinguishing amongst the types of PCV and other, possibly related, choroidal disorders will allow patients who would not benefit from certain treatments to be identified, an important medical economic consideration in our ageing society. Polypoidal choroidal vasculopathy has been the focus of various reclassification efforts because it was first identified three decades ago (Freund et al. 2010). Ever more sophisticated diagnostic and treatment techniques are anticipated to allow refinement of the classification of this group of disorders. As our knowledge of the aetiology and prognosis of different types of PCV grows, we will be able to provide our patients with optimal, individualized treatments. These results were presented orally at a scientific programme of the 27th Asian Pacific Academy of Ophthalmology Congress, Busan Korea, April 13–16 2012. This study was funded in part by the Research Committee on Chorioretinal Degenerations and Optic Atrophy, The Ministry of Health, Welfare and Labor of Japan (Mitsuko Yuzawa)." @default.
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• W1966232476 title "Indocyanine green angiographic and optical coherence tomographic findings support classification of polypoidal choroidal vasculopathy into two types" @default.
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