## 2 Retinal Vascular Diseases
### Retinal Vein Occlusion  
Retinal vein occlusion (RVO) is ranked the second most common vascular disorder in retina after DR with significant visual impairment. Hypertension, open-angle glaucoma,smoking, thrombophilic disorders and diabetes are among the basic risk factors of RVO [105]. Macular ischemia or macular edema is the leading cause of central vision loss [106] in addition to its neovascular complications, including neovascular glaucoma and vitreous hemorrhage [107]. Figure 5 presents the capillary non-perfusion in DCP and SCP of RVO patient. Almost all clinical and fluorescein angiographic findings that characterize retinal vein occlusions and its later sequelae are demonstrated by OCTA. The principal characteristics include collateral vessels formation, FAZ enlargement, decrease in capillary perfusion and venous dilation [108; 109]. OCTA is actually superior in detecting irregularities of the FAZ and changes in DCP [110]. FA's one advantage is that it shows physiologic leakage and has a wider field of view of the peripheral retina [111; 1]. In general, visual acuity in BRVO correlates with macular edema, and vision improves as edema is reduced [112; 113]. Reduction of ME alone, however, is not sufficient to produce good vision. The recovery of VA may be limited after ME resolution because of foveal photoreceptor damage secondary to macular ischemia, as concluded by OCT research [113; 114]. Microvascular abnormalities, such as FAZ enlargement, microaneurysms, and capillary telangiectasia, in patients with RVO are seen more so in the DCP than in SCP [115; 116; 117; 118]. The vessels' architectural organization in the two plexuses could explain these findings. Transverse venules connect the SCP large venules directly to the DCP. The DCP in turn drains into the large superficial veins. Hence, in RVO patients, the intravascular pressure increase in large veins results in hydrostatic pressure elevation with retinal perfusion reduction in DCP. A direct connection exists between the SCP and arterioles with high perfusion pressure and oxygenation in the retina. This probably helps to protect against the ischemic insult incurred by increased venous pressure in RVO [119]. Many studies ([PERSON] et al. [120], [PERSON] et al. [121], [PERSON] et al. [122], [PERSON] et al. [123]) compared microvascular changes in the eye affected with RVO versus the fellow unaffected eye versus controls. They found reduction of the density of vessels in the DCP and SCP, reduction of choriocapillaris density, thickened subfoveal choroidal thickness, increased central macular thickness, and enlargement of the FAZ in eyes affected with RVO versus fellow unaffected eyes. They also found a reduction of the density of vessels in the DCP and SCP in the fellow unaffected eyes versus healthy controls. OCTA images of RVO eyes have been analyzed by [PERSON] et al. [124], who concluded that the formation of cystoid spaces occurs at areas of disturbed vascular flow in the SCP. However, these cystoid spaces are absent or only present in areas of severely disturbed vascular flow in the DCP. No observed alterations in the pattern of the DCP or SCP occurred after resolution of cystoid spaces with treatment. [PERSON] et al. [117] concluded that in the SCP, cystoid spaces are more common in eyes with central retinal vein occlusion (CRVO), whereas in the DCP, they are more common in eyes with BRVO. Several groups ([PERSON] et al. [125], [PERSON] et al. [40], [PERSON] et al. [126]) have reported enlargement of FAZ in eyes with CRVO. [PERSON] et al. [125] reported enlargement of the mean FAZ area in the SCP from 0.25 in controls to 0.76 in patients with CRVO and enlargement of the mean FAZ area in the DCP from 0.49 in healthy controls to 1.12 in patients with CRVO. [PERSON] et al. [126] reported enlargement of the mean FAZ area in the SCP from 0.28 in the fellow eye to 0.31 in the BRVO eye and enlargement of the mean FAZ area in the DCP from 0.41 in the fellow eye to 0.51 in the eye affected with BRVO. Clinical studies ([PERSON] et al. [125], [PERSON] et al.