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Journal articles on the topic 'Neovascularization'

To see the other types of publications on this topic, follow the link: Neovascularization.

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Chen, Xuanjia, Hongyan Wang, Yuxin Jiang, Jianchu Li, Na Li, Jing Kong, Xiaoyan Zhang, Wei Ye, Dachun Zhao, and Siman Cai. "Neovascularization in carotid atherosclerotic plaques can be effectively evaluated by superb microvascular imaging (SMI): Initial experience." Vascular Medicine 25, no. 4 (April 17, 2020): 328–33. http://dx.doi.org/10.1177/1358863x20909992.

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The objective of this study was to investigate the correlation between the amount of blood flow in the area of neovascularization within a carotid atherosclerotic plaque by superb microvascular imaging (SMI) and the microvessel density (MVD) determined by histopathological staining. Twenty-eight carotid atherosclerotic plaques were detected by SMI in 28 patients who underwent carotid endarterectomy. SMI was graded according to the visual methods as follows: grade I: no appearance of neovascularization within the plaque; grade II: punctate neovascularization; grade III: one or two linear neovascularizations within the plaque; and grade IV: multiple (> 2) linear neovascularizations throughout the plaque. The neovascularization density was determined by the CD31 complex staining method. There was a significant correlation between the density of neovascularization in histopathologic plaques and the blood flow grade found by SMI ( r = 0.788, p < 0.001). A significant difference was observed in SMI blood flow grade between the symptomatic and asymptomatic groups (χ2 = 2.634, p = 0.036). The MVD of plaques in the symptomatic group was significantly higher than that in the asymptomatic group ( t = 2.530, p = 0.018). The SMI-based classification was positively correlated with plaque thickness. SMI, which is a new nonultrasound contrast-enhanced imaging method, can effectively evaluate neovascularization in carotid atherosclerotic plaques and can be used as a novel method for the clinical prediction of stroke risk.

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2

Pasyechnikova, Nataliya V., Volodymyr O. Naumenko, Andrii R. Korol, Oleg S. Zadorozhnyy, Taras B. Kustryn, and Paul B. Henrich. "Intravitreal Ranibizumab for the Treatment of Choroidal Neovascularizations Associated with Pathologic Myopia: A Prospective Study." Ophthalmologica 233, no. 1 (December 6, 2014): 2–7. http://dx.doi.org/10.1159/000369397.

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Purpose: It was the aim of this study to determine the efficacy of intravitreal ranibizumab as treatment of choroidal neovascularizations associated with pathologic myopia. Materials and Methods: In an uncontrolled, prospective time series cohort study, 65 eyes of 64 consecutive patients with choroidal neovascularization associated with pathologic myopia were treated with intravitreal ranibizumab and observed over 12 months. The change in best-corrected visual acuity (BCVA) at 6 and 12 months served as primary end point. Safety, central retinal thickness, neovascularization activity on fluorescein angiography and the number of ranibizumab injections were secondary end points. Results: BCVA improved significantly throughout the follow-up (p = 0.001). The mean BCVA was 0.2 at baseline (SD 0.13) and 0.4 at 12 months (SD 0.21). Improvement was strongest within the first 3 months (p = 0.0001). The mean central retinal thickness showed a reduction from 313 μm (SD 82) to 243.5 μm (SD 31; p = 0.0001). Conclusion: Intravitreal ranibizumab offers a safe and effective treatment for choroidal neovascularizations in pathologic myopia.

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3

Ishida, Susumu, Tomohiko Usui, Kenji Yamashiro, Yuichi Kaji, Shiro Amano, Yuichiro Ogura, Tetsuo Hida, et al. "VEGF164-mediated Inflammation Is Required for Pathological, but Not Physiological, Ischemia-induced Retinal Neovascularization." Journal of Experimental Medicine 198, no. 3 (August 4, 2003): 483–89. http://dx.doi.org/10.1084/jem.20022027.

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Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls. In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte–mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined.

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4

Veríssimo de Mello-Filho, Francisco, Rui Celso Martins Mamede, and Maria A. S. Llorach Velludo. "Tracheal Neovascularization." Laryngoscope 106, no. 1 (January 1996): 81–85. http://dx.doi.org/10.1097/00005537-199601000-00016.

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5

Chang, Jin-Hong, Eric E. Gabison, Takuji Kato, and Dimitri T. Azar. "Corneal neovascularization." Current Opinion in Ophthalmology 12, no. 4 (August 2001): 242–49. http://dx.doi.org/10.1097/00055735-200108000-00002.

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6

Epstein, Randy J. "Corneal Neovascularization." Cornea 6, no. 1 (1987): 59. http://dx.doi.org/10.1097/00003226-198706010-00029.

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7

Natarajan, Radhika, and Srinivas K. Rao. "Posttraumatic Neovascularization." Journal of Cataract & Refractive Surgery 29, no. 5 (May 2003): 861. http://dx.doi.org/10.1016/s0886-3350(03)00312-2.

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8

Ayachit, Apoorva G., Lakshmipriya Uday Reddy, Shrinivas Joshi, and Guruprasad S. Ayachit. "Epiretinal Neovascularization." Ophthalmology Retina 3, no. 6 (June 2019): 516–22. http://dx.doi.org/10.1016/j.oret.2019.01.022.

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9

Azar, D. T. "Corneal Neovascularization." Ocular Surface 3 (January 2005): S44. http://dx.doi.org/10.1016/s1542-0124(12)70349-x.

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10

Lee, Patricia, Cindy C. Wang, and Anthony P. Adamis. "Ocular Neovascularization." Survey of Ophthalmology 43, no. 3 (November 1998): 245–69. http://dx.doi.org/10.1016/s0039-6257(98)00035-6.

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11

Neely, Kimberly A., and Thomas W. Gardner. "Ocular Neovascularization." American Journal of Pathology 153, no. 3 (September 1998): 665–70. http://dx.doi.org/10.1016/s0002-9440(10)65607-6.

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12

Green, W. Richard, and David J. Wilson. "Choroidal Neovascularization." Ophthalmology 93, no. 9 (September 1986): 1169–76. http://dx.doi.org/10.1016/s0161-6420(86)33609-1.

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13

Nicholas, Matthew P., and Naveen Mysore. "Corneal neovascularization." Experimental Eye Research 202 (January 2021): 108363. http://dx.doi.org/10.1016/j.exer.2020.108363.

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14

Grossniklaus, Hans E., and W. Richard Green. "Choroidal neovascularization." American Journal of Ophthalmology 137, no. 3 (March 2004): 496–503. http://dx.doi.org/10.1016/j.ajo.2003.09.042.

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15

Spaide, Richard F. "Choroidal Neovascularization." Retina 37, no. 4 (April 2017): 609–10. http://dx.doi.org/10.1097/iae.0000000000001575.

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16

Campochiaro, Peter A. "Ocular neovascularization." Journal of Molecular Medicine 91, no. 3 (January 18, 2013): 311–21. http://dx.doi.org/10.1007/s00109-013-0993-5.

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17

Qing, Xun. "Ocular Neovascularization." Archives of Ophthalmology 103, no. 1 (January 1, 1985): 111. http://dx.doi.org/10.1001/archopht.1985.01050010117033.

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18

Deutman, A. F. "Subretinal Neovascularization." Archives of Ophthalmology 104, no. 11 (November 1, 1986): 1588. http://dx.doi.org/10.1001/archopht.1986.01050230026019.

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19

Hayreh, Sohan Singh, and Gene F. Lata. "Ocular neovascularization." International Ophthalmology 9, no. 2-3 (May 1986): 109–20. http://dx.doi.org/10.1007/bf00159839.

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20

Goldberg, Morton F. "Retinal neovascularization." Survey of Ophthalmology 29, no. 4 (January 1985): 309–10. http://dx.doi.org/10.1016/0039-6257(85)90157-2.

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21

Dutheil, Cyril, Jean-François Korobelnik, Marie-Noëlle Delyfer, and Marie-Bénédicte Rougier. "Optical coherence tomography angiography and choroidal neovascularization in multifocal choroiditis: A descriptive study." European Journal of Ophthalmology 28, no. 5 (March 23, 2018): 614–21. http://dx.doi.org/10.1177/1120672118759623.

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Purpose: To analyze the ability of optical coherence tomography angiography to identify choroidal neovascularization in multifocal choroiditis and to describe active and inactive choroidal neovascularization findings. Methods: Retrospective study of consecutive patients with multifocal choroiditis and choroidal neovascularization examined between January and November 2016. In addition to usual exams, optical coherence tomography angiography (AngioPlex™ CIRRUS™ HD-OCT model 5000; Carl Zeiss Meditec, Inc., Dublin, CA, USA) images were assessed for morphological analysis: choroidal neovascularization size, choroidal neovascularization margin (well or poorly circumscribed), choroidal neovascularization shape (tangled or interlacing), choroidal neovascularization core (feeder vessel) and dark ring around the choroidal neovascularization. Results: A total of 10 eyes were included. Optical coherence tomography angiography identified all choroidal neovascularization. Active choroidal neovascularization had well-circumscribed margins (67%), interlacing shape (83%), and a surrounding dark ring (83%). Inactive choroidal neovascularization had rather poorly circumscribed margins (75%), tangled shape, and “dead tree” appearance (50%) with less frequently a surrounding dark ring (50%). Conclusion: Optical coherence tomography angiography is adapted to confirm the diagnosis of choroidal neovascularization complicating multifocal choroiditis, but it is still insufficient to differentiate active and inactive lesions.

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22

Kwak, Jae Hyuck, Woo Kyung Park, Rae Young Kim, Mirinae Kim, Young-Gun Park, and Young-Hoon Park. "Unaffected fellow eye neovascularization in patients with type 3 neovascularization: Incidence and risk factors." PLOS ONE 16, no. 7 (July 19, 2021): e0254186. http://dx.doi.org/10.1371/journal.pone.0254186.

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Purpose To evaluate the incidence and risk factors of neovascularization in unaffected fellow eyes of patients diagnosed with type 3 neovascularization in Korea. Methods This retrospective study included 93 unaffected fellow eyes of 93 patients diagnosed with type 3 neovascularization. For initial type 3 neovascularization diagnosis, optical coherence tomography and angiography were conducted. These baseline data were compared between patients with and without neovascularization in their fellow eyes during the follow-up period. Results The mean follow-up period was 66.1±31.1 months. Neovascularization developed in 49 (52.8%) fellow eyes after a mean period of 29.5±19.6 months. In the fellow eye neovascularization group, the incidence of soft drusen and reticular pseudodrusen was significantly higher than that in the non-neovascularization group (83.7% vs. 36.5%, p<0.001; 67.3% vs. 40.9%, p = 0.017, respectively), but the choroidal vascularity index (CVI) showed a significantly lower value (60.7±2.0% vs. 61.7±2.5%; p = 0.047). The presence of reticular pseudodrusen was related with the duration from baseline to development of fellow eye neovascularization (p = 0.038). Conclusion Neovascularization developed in 52.8% of unaffected fellow eyes. The presence of soft drusen, reticular pseudodrusen, and lower CVI values can be considered risk factors of neovascularization in unaffected fellow eyes of patients with type 3 neovascularization. The lower CVI values suggest that choroidal ischemic change may affect the development of choroidal neovascularization in these patients.

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23

Ergul, Adviye, Mohammed Abdelsaid, Abdelrahman Y. Fouda, and Susan C. Fagan. "Cerebral Neovascularization in Diabetes: Implications for Stroke Recovery and beyond." Journal of Cerebral Blood Flow & Metabolism 34, no. 4 (February 5, 2014): 553–63. http://dx.doi.org/10.1038/jcbfm.2014.18.

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Neovascularization is an innate physiologic response by which tissues respond to various stimuli through collateral remodeling (arteriogenesis) and new vessel formation from existing vessels (angiogenesis) or from endothelial progenitor cells (vasculogenesis). Diabetes has a major impact on the neovascularization process but the response varies between different organ systems. While excessive angiogenesis complicates diabetic retinopathy, impaired neovascularization contributes to coronary and peripheral complications of diabetes. How diabetes influences cerebral neovascularization remained unresolved until recently. Diabetes is also a major risk factor for stroke and poor recovery after stroke. In this review, we discuss the impact of diabetes, stroke, and diabetic stroke on cerebral neovascularization, explore potential mechanisms involved in diabetes-mediated neovascularization as well as the effects of the diabetic milieu on poststroke neovascularization and recovery, and finally discuss the clinical implications of these effects.

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24

Di Staso, Federico, Mariachiara Di Pippo, and Solmaz Abdolrahimzadeh. "Choroidal Neovascular Membranes in Retinal and Choroidal Tumors: Origins, Mechanisms, and Effects." International Journal of Molecular Sciences 24, no. 2 (January 5, 2023): 1064. http://dx.doi.org/10.3390/ijms24021064.

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Choroidal neovascularizations are historically associated with exudative macular degeneration, nonetheless, they have been observed in nevus, melanoma, osteoma, and hemangioma involving the choroid and retina. This review aimed to elucidate the possible origins of neovascular membranes by examining in vivo and in vitro models compared to real clinical cases. Among the several potential mechanisms examined, particular attention was paid to histologic alterations and molecular cascades. Physical or biochemical resistance to vascular invasion from the choroid offered by Bruch’s membrane, the role of fibroblast growth factor 2 and vascular endothelial growth factor, resident or recruited stem-like/progenitor cells, and other angiogenic promoters were taken into account. Even if the exact mechanisms are still partially obscure, experimental models are progressively enhancing our understanding of neovascularization etiology. Choroidal neovascularization (CNV) over melanoma, osteoma, and other tumors is not rare and is not contraindicative of malignancy as previously believed. In addition, CNV may represent a late complication of either benign or malignant choroidal tumors, stressing the importance of a long follow-up.

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25

Temkar, Shreyas, Geeta Behera, Hemanth Ramachandar, Disha Agarwal, Mary Stephen, and Amit Kumar Deb. "Expeditious resolution of disc and iris neovascularization." Indian Journal of Ophthalmology - Case Reports 4, no. 2 (April 2024): 425–27. http://dx.doi.org/10.4103/ijo.ijo_3203_23.

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Intraocular neovascularization is seen commonly as a response to retinal ischemia or less commonly due to inflammation. Inflammatory iris neovascularization responds well to topical steroids, whereas retinal neovascularization associated with uveitic conditions responds to systemic steroids or periocular depot injections. This case highlights an unusually rapid resolution of disc neovascularization along with iris neovascularization just with topical steroids in a middle-aged lady diagnosed with bilateral panuveitis and retinal vasculitis. We presume it may be due to a spontaneous decrease in posterior segment inflammation or due to systemic vascular remodeling.

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26

Averbukh, Edward, Michael Halpert, Ravit Yanko, Lutza Yanko, Jacob Peèr, Samuel Levinger, Allan Flyvbjerg, and Itamar Raz. "Octreotide, a Somatostatin Analogue, Fails to Inhibit Hypoxia-induced Retinal Neovascularization in the Neonatal Rat." International Journal of Experimental Diabetes Research 1, no. 1 (2000): 39–47. http://dx.doi.org/10.1155/edr.2000.39.

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Objective:Octreotide, a somatostatin analogue, has been shown to prevent angiogenesis in diversein vitromodels. We evaluated its effect on retinal neovascularizationin vivo, using a neonatal rat retinopathy model.Methods:We used, on alternating days, hypoxia (10%O2) and hyperoxia (50%O2) during the first 14 days of neonatal rats, to induce retinal neovascularization. Half of the rats were injected subcutaneously with octreotide 0.7 μg/g BW twice daily. At day 18 the eyes were evaluated for the presence of epiretinal and vitreal hemorrhage, neovascularization and epiretinal proliferation. Octreotide pharmacokinetics and its effect on serum growth hormone (GH) and insulin-like growth factor I (IGF-I) were examined in 28 rats.Results:Serum octreotide levels were 667 μg/1 two hours after injection, 26.4 μg/1 after nine hours and 3.2 μg/1 after 14 hours. GH levels were decreased by 40% (p= 0.002) two hours after injection but thereafter returned to baseline. IGF-I levels were unchanged two hours after injection and were elevated by 26% 14 hours after injection (p= 0.02). Epiretinal membranes were highly associated with epiretinal hemorrhages (p< 0.001), while retinal neovascularization was notably associated with vitreal hemorrhages (p< 0.001).Conclusions:Twice-daily injections of octreotide failed to produce sustained decrease in serum GH, but produced rebound elevation of serum IGF-I. Accordingly, no statistically significant effect of injections on retinal pathology was noted. This finding, however, does not contradict our assumption that GH suppression may decrease the severity of retinopathy.

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27

Saita, Norio, Nagatoshi Fujiwara, Ikuya Yano, Kazuhiko Soejima, and Kazuo Kobayashi. "Trehalose 6,6′-Dimycolate (Cord Factor) of Mycobacterium tuberculosis Induces Corneal Angiogenesis in Rats." Infection and Immunity 68, no. 10 (October 1, 2000): 5991–97. http://dx.doi.org/10.1128/iai.68.10.5991-5997.2000.

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ABSTRACT Neovascularization or angiogenesis is required for the progression of chronic inflammation. The mechanism of inflammatory neovascularization in tuberculosis remains unknown. Trehalose 6,6′-dimycolate (TDM) purified from Mycobacterium tuberculosis was injected into rat corneas. TDM challenge provoked a local granulomatous response in association with neovascularization. Neovascularization was seen within a few days after the challenge, with the extent of neovascularization being dose dependent, although granulomatous lesions developed 14 days after the challenge. Cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8), IL-1β, and vascular endothelial growth factor (VEGF), were found in lesions at the early stage (within a few days after the challenge) and were detectable until day 21. Neovascularization was inhibited substantially by neutralizing antibodies to VEGF and IL-8 but not IL-1β. Treatment with anti-TNF-α antibodies resulted in partial inhibition. TDM possesses pleiotropic activities, and the cytokine network plays an important role in the process of neovascularization.

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28

Glotzbach, Jason P., Victor W. Wong, and Geoffrey C. Gurtner. "Neovascularization in diabetes." Expert Review of Endocrinology & Metabolism 5, no. 1 (January 2010): 99–111. http://dx.doi.org/10.1586/eem.09.57.

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29

Nagiel, Aaron, David Sarraf, Srinivas R. Sadda, Richard F. Spaide, Jesse J. Jung, Kavita V. Bhavsar, Hossein Ameri, Giuseppe Querques, and K. Bailey Freund. "TYPE 3 NEOVASCULARIZATION." Retina 35, no. 4 (April 2015): 638–47. http://dx.doi.org/10.1097/iae.0000000000000488.

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30

Burger, Peter C., David B. Chandler, and Gordon K. Klintworth. "Experimental Corneal Neovascularization." Cornea 4, no. 1 (January 1985): 35???41. http://dx.doi.org/10.1097/00003226-198501000-00008.

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31

Sasisekharan, R., M. A. Moses, M. A. Nugent, C. L. Cooney, and R. Langer. "Heparinase inhibits neovascularization." Proceedings of the National Academy of Sciences 91, no. 4 (February 15, 1994): 1524–28. http://dx.doi.org/10.1073/pnas.91.4.1524.

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32

Cunningham, Emmett T., Francesco Pichi, Rosa Dolz-Marco, K. Bailey Freund, and Manfred Zierhut. "Inflammatory Choroidal Neovascularization." Ocular Immunology and Inflammation 28, no. 1 (January 2, 2020): 2–6. http://dx.doi.org/10.1080/09273948.2019.1704153.

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33

Blinder, Kevin J., Scott M. Friedman, and Robert N. Mames. "Diabetic Iris Neovascularization." American Journal of Ophthalmology 120, no. 3 (September 1995): 393–95. http://dx.doi.org/10.1016/s0002-9394(14)72173-7.

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34

Epstein, Randy J., Robert L. Hendricks, and Richard M. Lipman. "Cyclosporine and neovascularization." Ophthalmology 106, no. 1 (January 1999): 3. http://dx.doi.org/10.1016/s0161-6420(99)90035-0.

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35

Yoshida, Takeshi, Kyoko Ohno-Matsui, Kenjiro Yasuzumi, Ariko Kojima, Noriaki Shimada, Soh Futagami, Takashi Tokoro, and Manabu Mochizuki. "Myopic choroidal neovascularization." Ophthalmology 110, no. 7 (July 2003): 1297–305. http://dx.doi.org/10.1016/s0161-6420(03)00461-5.

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36

Cheung, Chui Ming Gemmy, Jennifer J. Arnold, Frank G. Holz, Kyu Hyung Park, Timothy Y. Y. Lai, Michael Larsen, Paul Mitchell, et al. "Myopic Choroidal Neovascularization." Ophthalmology 124, no. 11 (November 2017): 1690–711. http://dx.doi.org/10.1016/j.ophtha.2017.04.028.

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37

Ruiz-Moreno, Jose M., María I. López-Gálvez, Juan Donate, Francisco Gomez-Ulla, José García-Arumí, Alfredo García-Layana, Inmaculada Sellés, et al. "Myopic Choroidal Neovascularization." Ophthalmology 118, no. 12 (December 2011): 2521–23. http://dx.doi.org/10.1016/j.ophtha.2011.07.029.

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38

Lim, Jennifer I. "Iatrogenic Choroidal Neovascularization." Survey of Ophthalmology 44, no. 2 (September 1999): 95–111. http://dx.doi.org/10.1016/s0039-6257(99)00077-6.

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39

Sorenson, John A., Lawrence A. Yannuzzi, and Jeffrey L. Shakin. "Recurrent Subretinal Neovascularization." Ophthalmology 92, no. 8 (August 1985): 1059–74. http://dx.doi.org/10.1016/s0161-6420(85)33922-2.

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40

Bene, Catherine, Robert Hutchins, and George Kranias. "Cataract Wound Neovascularization." Ophthalmology 96, no. 1 (January 1989): 50–53. http://dx.doi.org/10.1016/s0161-6420(89)32948-4.

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41

Sorenson, John A., Lawrence A. Yannuzzi, and Jeffrey L. Shakin. "Recurrent Subretinal Neovascularization." Retina 32 (February 2012): 1059. http://dx.doi.org/10.1097/iae.0b013e3182431cf0.

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42

Lai, Timothy Y. Y., and Chui Ming Gemmy Cheung. "MYOPIC CHOROIDAL NEOVASCULARIZATION." Retina 36, no. 9 (September 2016): 1614–21. http://dx.doi.org/10.1097/iae.0000000000001227.

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43

FREUND, K. BAILEY, I. -VAN HO, IRENE A. BARBAZETTO, HIDEKI KOIZUMI, KETAN LAUD, DANIELA FERRARA, YOKO MATSUMOTO, JOHN A. SORENSON, and LAWRENCE YANNUZZI. "TYPE 3 NEOVASCULARIZATION." Retina 28, no. 2 (February 2008): 201–11. http://dx.doi.org/10.1097/iae.0b013e3181669504.

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44

HEIER, JEFFREY S. "PATHOLOGY BEYOND NEOVASCULARIZATION." Retina 29, Supplement (June 2009): S39—S41. http://dx.doi.org/10.1097/iae.0b013e3181ad26c1.

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45

Vine, A. K., and M. W. Johnson. "Peripheral Choroidal Neovascularization." European Journal of Ophthalmology 6, no. 1 (January 1996): 44–49. http://dx.doi.org/10.1177/112067219600600110.

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Peripheral choroidal neovascularization can result in an elevated subretinal lesion which can simulate a choroidal tumor. We reviewed 8 eyes with 11 peripheral areas of subretinal fluid and exudate which were subsequently determined to be secondary to peripheral choroidal neovascularization. Previous reports of peripheral choroidal neovascularization have emphasized the hemorrhagic nature of these lesions which can simulate a choroidal melanoma. In contrast, turbid subretinal fluid and exudate characterized the majority of peripheral lesions in this series and the majority of these patients were referred with a diagnosis of choroidal metastasis. Clinical examination with fluorescein angiography and echography can effectively distinguish these areas of peripheral choroidal neovascularization from choroidal metastasis.

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46

Pels, Klaus, Marino Labinaz, and Edward R. O'Brien. "Arterial Wall Neovascularization." Japanese Circulation Journal 61, no. 11 (1997): 893–904. http://dx.doi.org/10.1253/jcj.61.893.

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47

Schatz, H., and S. N. Trimble. "Subretinal Neovascularization-Reply." Archives of Ophthalmology 104, no. 11 (November 1, 1986): 1588. http://dx.doi.org/10.1001/archopht.1986.01050230026020.

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48

Sorenson, J. A., L. A. Yannuzzi, and J. L. Shakin. "Recurrent Subretinal Neovascularization." Archives of Ophthalmology 105, no. 1 (January 1, 1987): 22. http://dx.doi.org/10.1001/archopht.1987.01060010024008.

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49

Sood, Gitanjli, and Ramanuj Samanta. "‘Sea-fan’ neovascularization." Indian Journal of Medical Research 157, no. 1 (January 2023): 110. http://dx.doi.org/10.4103/ijmr.ijmr_3242_20.

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50

Neri, Piergiorgio, Marta Lettieri, Cinzia Fortuna, Mara Manoni, and Alfonso Giovannini. "Inflammatory choroidal neovascularization." Middle East African Journal of Ophthalmology 16, no. 4 (2009): 245. http://dx.doi.org/10.4103/0974-9233.58422.

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