Polypoidal Choroidal Vasculopathy (PCV)

Polypoidal choroidal vasculopathy is a disease that affects the layer of blood vessels under the retina, called the choroid. In PCV, a network of new vessels grows under a thin layer called the retinal pigment epithelium (RPE). The network looks like branches that end in round, bubble-like swellings called “polyps.” These polyps can leak fluid and blood. The leaks and bleeding can lift the retina and the RPE and can cause sudden or gradual vision loss. Many experts now describe PCV as “aneurysmal type 1 neovascularization.” This means it is a type of abnormal vessel growth that sits under the RPE (type 1), and it forms balloon-like dilations (aneurysms). The same problem can happen in people with age-related macular degeneration (AMD), but PCV has its own look, behavior, and risks, especially in people with thick choroids (the “pachychoroid” pattern). PCV is diagnosed best when doctors combine the patient’s story, a careful eye exam, and special imaging tests that show the abnormal vessels and polyps clearly. Indocyanine green angiography (ICGA) has long been considered the gold standard test to show the branching network and the polyps. Optical coherence tomography (OCT) can show typical shapes under the RPE, like sharp-peaked or notched RPE detachments, and ring-like shadows that match the polyps. OCT angiography (OCTA) can outline the branching network but is less sensitive for the slow-flow polyps. PMC+2PMC+2EyeWiki

Polypoidal choroidal vasculopathy—often shortened to PCV—is an eye disease where tiny, balloon-like outpouchings (“polyps”) form at the ends of abnormal vessels in the choroid, the blood-rich layer underneath the retina. These fragile, knobby vessels can leak fluid or bleed, causing swelling under the retina and under the retinal pigment epithelium (RPE). Over time, the leakage and bleeding can blur or distort central vision and may leave scars if untreated. PCV is considered a subtype of “wet” (neovascular) age-related macular degeneration (AMD) in many patients, but it behaves a bit differently and is more common in Asian and African populations. Doctors often confirm PCV using a special dye test called indocyanine green angiography (ICGA), which shows the polyp-like bulbs and the branching vessel network that feeds them. Optical coherence tomography (OCT) and OCT-angiography also help, but ICGA remains the gold standard when the diagnosis is uncertain. AAO JournalNCBIScienceDirectNature

Polypoidal choroidal vasculopathy—usually shortened to PCV—is an eye condition that affects the choroid, the rich bed of blood vessels that lies under the retina. In PCV, small, balloon-like outpouchings and a branching network of abnormal vessels grow under the retina. Doctors call these ballooned spots “polyps” and the vessel web a “branching vascular network (BVN).” These changes can leak fluid or bleed, causing blurring, wavy vision, or even sudden vision loss if a big bleed occurs under the center of sight (the macula). PCV is most often found in people with “pachychoroid” features—a thicker-than-usual choroid with enlarged veins—and it partly overlaps with the “wet” form of age-related macular degeneration (nAMD). The current diagnostic gold standard is a dye test called indocyanine green angiography (ICGA), which shows the polyps and the BVN clearly. Non-invasive scanners like OCT and OCTA are very helpful for finding typical signs and for follow-up, but ICGA remains the reference test for a firm diagnosis. PMC+1Nature

Modern retinal imaging has also taught us a lot about how PCV looks on OCT. Doctors look for a “double-layer sign” (a split between the retinal pigment epithelium and Bruch’s membrane), peaked or notched pigment epithelial detachments (PEDs), and thumb-like projections that match the position of polyps. These OCT features can strongly suggest PCV even before ICGA is done, which is helpful in clinics that do not have easy access to ICGA. PMC+1AAO Journal

PCV sits within the pachychoroid disease spectrum, a family of conditions linked to thick choroids and congested choroidal veins. That is why PCV sometimes occurs in eyes that have a past history or signs of central serous chorioretinopathy (CSCR) or other pachychoroid disorders. PMCNatureEyeWiki

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Types of PCV

Doctors describe PCV in several practical ways. You may see more than one label applied to the same eye, because these categories look at different aspects of the disease.

1. By how active it is

• Active PCV: There is fresh leakage or bleeding, new fluid on OCT, or recent vision changes.

• Quiescent (quiet) PCV: The abnormal vessels are present but not leaking or bleeding right now.

2. By where it sits in the back of the eye

• Macular PCV: The polyps and BVN are under the macula (the center of sharp vision), so symptoms tend to be more obvious.

• Peripapillary PCV: The complex is nearer to the optic nerve head. Vision may be less affected early on.

3. By how it looks on angiography

• BVN with terminal polyps: A branching vessel network that ends in one or several bulb-like polyps (the classic pattern).

• Clustered or isolated polyps: One or a few polyps without an obvious network visible.

4. By the main way it shows itself

• Exudative PCV: Mainly causes fluid leakage, swelling, and multiple PEDs.

• Hemorrhagic PCV: Bleeding is prominent, sometimes with large submacular hemorrhage.

5. By its clinical family

• Pachychoroid-driven PCV: Occurs in thicker choroids with enlarged “pachyvessels,” often in younger patients than typical AMD.

• AMD-associated PCV: Occurs with drusen and other AMD signs, often in older patients.

These type labels help doctors choose the right tests and treatments, but the core point is the same: abnormal choroidal vessels form a network with polyp-like bulbs that can leak or bleed and threaten central vision. PMC+1Nature

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Causes and Contributors

PCV does not usually have a single cause. It is multifactorial, which means several things add up to make it more likely. Below are 20 well-supported contributors—some are ocular factors (changes inside the eye), and some are systemic factors (whole-body influences). Think of them as “risk builders” rather than one-to-one causes.

1. Ageing of the choroid and RPE: With age, support tissues under the retina stiffen and thin in places, making abnormal vessels more likely to grow.

2. Pachychoroid (thick choroid with enlarged veins): Thick, congested choroidal veins can raise local pressure and stress the RPE, encouraging new, fragile vessels. PMCNature

3. Choroidal venous congestion: Poor outflow through vortex veins can trap blood in deeper layers and promote the BVN and polyps. Nature

4. Genetic susceptibility: Risk variants near ARMS2/HTRA1 and CFH (complement factor H) increase the chance of polypoidal disease in some ethnic groups.

5. Asian or African ancestry: PCV is relatively more common in East and Southeast Asian populations and also reported more in people of African descent.

6. Male sex (relative tendency): Some series show a modest male predominance, particularly in pachychoroid-type PCV.

7. Smoking: Tobacco toxins damage choroidal vessels and the RPE, raising the risk for neovascular changes.

8. High blood pressure: Long-term vascular stress injures the micro-circulation and can make choroidal leakage and bleeding more likely.

9. High blood lipids (dyslipidemia): Lipid imbalance is linked to vessel wall damage and can worsen exudation.

10. Metabolic syndrome and higher BMI: Systemic inflammation and vascular strain are higher, which may contribute to choroidal disease.

11. Diabetes: Even when retinopathy is not present, diabetes adds oxidative stress and microvascular vulnerability.

12. Sleep apnea: Repeated nighttime drops in oxygen can damage or remodel choroidal vessels over time.

13. Oxidative stress: Free-radical injury to the RPE and Bruch’s membrane lowers the barrier against abnormal vessel growth.

14. Inflammatory signaling (complement pathway): Over-active complement can inflame the choroid-RPE complex and encourage pathologic vessels.

15. Prior central serous chorioretinopathy (CSCR) features: The pachychoroid traits that drive CSCR can also set the stage for PCV. PMC

16. Sunlight and blue-light exposure (lifetime load): Chronic light stress may contribute to RPE wear-and-tear (a weaker link, but biologically plausible).

17. Vascular endothelial dysfunction: When vessel linings lose their normal “anti-leak” behavior, fluid seeping and micro-bleeds become more likely.

18. Imbalanced VEGF signaling: VEGF is the body’s “grow new vessels” signal; when it is high around the RPE/choroid, fragile vessels can sprout.

19. Chronic PEDs: Long-standing pigment epithelial detachments can trap fluid and create a space where abnormal vessels and polyps form.

20. Eye biomechanics: Local differences in Bruch’s membrane stiffness and RPE adhesion may create “weak spots” where polyps bulge and leak.

The strongest, reproducible signals point to pachychoroid anatomy, ICGA-visible BVN/polyps, and OCT markers such as the double-layer sign and peaked/notched PEDs; genetics and systemic risks modulate this base. PMCNatureAAO Journal

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Symptoms

Each item below is written in plain language. Not everyone gets all of them. Symptoms can change over time, especially if a fresh leak or bleed happens.

1. Blurry central vision: Words, faces, and small details are not crisp.

2. Wavy or bent lines (metamorphopsia): Straight edges look kinked or ripple-like, especially when you check one eye at a time.

3. A dark or gray spot near the center (central scotoma): A patch in your central view looks missing or dim.

4. Sudden drop in vision: This can happen if a big bleed occurs under the macula.

5. Distortion that seems to come and go: Fluid can build and then partially clear, so the distortion can fluctuate.

6. Colors look faded: Reds and greens may look washed out.

7. Slow reading: Letters swim or seem broken; you lose your place more often.

8. Trouble with small print: You need brighter light or a larger font than before.

9. Glare sensitivity: Strong light scatters more, making detail harder to see.

10. Worse vision in dim rooms: It is harder to adapt to the dark after bright light.

11. Micropsia: Things look slightly smaller than they are.

12. A “shadow” over the center: A hazy veil in the central field, especially after a recent bleed.

13. Floaters: Specks or strands drifting across the vision, sometimes after a small vitreous hemorrhage.

14. Eye feels normal, but sight is off: Most people do not feel pain with PCV.

15. One eye worse than the other: PCV can be in one eye or both, but it often starts or acts up in just one eye at first.

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Diagnostic Tests

Important: In real-world practice, imaging is the heart of PCV diagnosis. ICGA is the reference test. OCT and OCTA provide strong non-invasive clues and are essential for follow-up. Other tests help describe function, rule out look-alike problems, and measure related health risks. PMC+1AAO Journal

A) Physical Exam

1. Best-corrected visual acuity (VA)
   You read letters on a chart with the best glasses correction. This tells the doctor how sharp your central vision is today and becomes a baseline to see if treatment helps.

2. Pupil exam for a relative afferent pupillary defect (RAPD)
   The doctor swings a light between your eyes to see if one optic pathway responds more weakly. A strong RAPD is uncommon in PCV but, if present, pushes the doctor to look for additional issues.

3. Intraocular pressure (IOP) measurement
   A gentle tonometer touches or blows on the eye to check pressure. PCV does not raise pressure directly, but the measurement is part of a complete retinal assessment.

4. Dilated fundus examination
   With your pupil widened by drops, the doctor inspects the retina and choroid. In PCV, they may see orange-red polyp-like bumps, patches of blood, lipid deposits, or dome-shaped pigment epithelial detachments.

B) Manual (Clinic Room) Functional Tests

5. Amsler grid
   You look at a small grid to check if lines bend or if boxes vanish. New wavy areas or missing squares suggest fresh leakage or bleeding affecting the macula.

6. Photostress recovery test
   A bright light bleaches your photoreceptors. The doctor times how quickly your reading vision recovers. Slow recovery suggests macular dysfunction from fluid under the center.

7. Contrast sensitivity chart (e.g., Pelli–Robson)
   This measures how well you can see faint letters, not just high-contrast black-on-white. PCV can reduce contrast even when the standard letter score looks fair.

8. Color vision screening (e.g., Ishihara plates)
   Not a primary PCV test, but it can show subtle macular impact and helps rule out optic nerve problems.

C) Laboratory / Pathological (Systemic Work-up)

These tests do not diagnose PCV. They look for whole-body risks that can worsen choroidal disease or bleeding and help tailor safe care.

9. Fasting lipid profile
   Checks cholesterol and triglycerides; abnormal results can tie into vascular fragility and exudation.

10. Fasting glucose and/or HbA1c
    Looks for diabetes or poor glucose control, which increases oxidative and vascular stress.

11. Complete blood count and coagulation profile
    Reviews platelets and clotting; helpful if there has been bleeding or if treatment choices could affect bleeding risk.

12. Targeted genetic testing (ARMS2/HTRA1/CFH) in research-level cases
    Seldom needed clinically, but in selected centers it can clarify risk background where research protocols exist.

D) Electrodiagnostic (retinal and visual pathway function)

13. Multifocal electroretinogram (mfERG)
    A gentle contact lens measures tiny electrical signals from many spots across the macula while you watch a flickering pattern. It maps localized macular function loss that fluid or blood may cause.

14. Full-field electroretinogram (ffERG)
    Measures the overall electrical response of the retina to flashes of light. It is usually normal in PCV but helps rule out widespread retinal disease.

15. Electro-oculography (EOG)
    Assesses the health of the retinal pigment epithelium (RPE), the support layer often lifted by PEDs in PCV.

16. Visual evoked potential (VEP)
    Measures signals reaching the visual brain. It is rarely needed in straightforward PCV but can be useful if the clinical picture is mixed.

E) Imaging (the key tests)

17. Indocyanine green angiography (ICGA)
    A green dye is injected into a vein while specialized cameras take images of the back of the eye. ICGA is the gold standard for PCV. It shows early, bright, nodular spots (polyps), and often the branching vascular network that feeds them. Doctors may even see pulsation in a polyp on the movie sequence. PMCNature

18. Optical coherence tomography (OCT)
    This painless scan uses light waves to make cross-section pictures through the retina. In PCV, doctors look for peaked or notched PEDs, sub-RPE “thumb-like” projections, subretinal fluid, intraretinal fluid, and the “double-layer sign.” These OCT clues can flag PCV with good accuracy in many clinics. PMC+1AAO Journal

19. Optical coherence tomography angiography (OCTA)
    OCTA maps blood flow without any dye. It can outline the BVN and sometimes hints of polyps, and it is excellent for regular follow-up. Newer swept-source OCTA units penetrate deeper and show “tangled vasculature” patterns linked to polyp areas, but OCTA has not fully replaced ICGA for diagnosis. PMC

20. Fluorescein angiography (FA / FFA)
    A yellow dye is injected and photos are taken quickly. FA shows leakage patterns and helps rule in or out other causes of macular swelling. It does not show polyps as reliably as ICGA does, but it adds useful context.

Non-pharmacological (non-drug) treatments and supports

(what they are, why they’re used, and how they help)

1. Observation with close monitoring
   What: Careful watching with scheduled OCT scans and eye exams when disease activity is low.
   Why: Some eyes stay quiet for long periods. Treat only when activity (fluid/bleed) appears.
   How it helps: Reduces unnecessary procedures and focuses care when there’s proof of leakage or active polyps. AAO Journal

2. Patient education & self-monitoring (Amsler grid / home OCT if available)
   What: Learn warning signs (new distortion, gray spots) and check at home.
   Why: Early relapse detection improves outcomes.
   How: A crooked line on a grid or a dark patch means call the retina clinic promptly. AAO Journal

3. Lifestyle: stop smoking
   What: Structured smoking-cessation support (counseling, local programs).
   Why: Smoking strongly raises the odds of AMD/PCV and hemorrhagic events.
   How: Quitting lowers inflammation and vascular stress that aggravate macular disease. PMCPubMed

4. Sun/bright-light protection
   What: Sunglasses with UV/HEV protection outdoors.
   Why: Limits light-induced retinal stress; recommended in AMD care.
   How: Reduces photo-oxidative load on macular tissues over time. National Eye Institute

5. Heart-healthy diet pattern
   What: Leafy greens, colorful vegetables, fish, nuts, whole grains.
   Why: The AREDS evidence base for AMD supports antioxidant and carotenoid intake for macular health (see supplements below).
   How: Lowers oxidative stress and supports photoreceptor/RPE metabolism. National Eye Institute

6. Weight, blood pressure, and lipid control
   What: Work with your primary-care team.
   Why: Healthier vessels = less leak/bleed risk overall; standard advice in macular disease.
   How: Reduces systemic vascular risk that can amplify choroidal congestion. Retina Specialists

7. Manage anticoagulants/antiplatelets carefully (doctor-guided)
   What: Do not stop prescribed blood thinners on your own; discuss with your doctors.
   Why: Eyes with PCV can bleed; decisions about these drugs must balance stroke/heart risk versus eye bleeding risk.
   How: Shared decision-making between retina specialist and the clinician who prescribed the blood thinner. AAO Journal

8. Prompt care for new symptoms
   What: Same-day or next-day retina evaluation for sudden distortion, dark spots, or a shower of new floaters.
   Why: Early treatment of a fresh bleed or fluid episode preserves vision.
   How: Triage pathways and emergency slots in many retina clinics exist for this. AAO Journal

9. Low-vision rehabilitation (when needed)
   What: Magnifiers, high-contrast lighting, reading strategies, device accessibility settings.
   Why: Maximizes remaining vision and independence if damage has occurred.
   How: Trains you to use healthier retinal areas and adaptive tools effectively. AAO Journal

10. Adherence coaching & reminders
    What: Calendar alerts and ride planning for injection/PDT visits.
    Why: Missed treatments can let PCV flare and scar.
    How: Simple systems improve real-world outcomes with anti-VEGF care. Lippincott Journals

11. Nutritional counseling
    What: Practical meal plans to hit carotenoid/antioxidant targets safely.
    Why: Supplements help specific AMD stages; diet supports overall retinal health.
    How: Boosts intake of lutein/zeaxanthin, vitamin C/E, and zinc-rich foods. National Eye Institute

12. Protect the other eye
    What: Regular exams and early imaging in the fellow eye.
    Why: PCV can be bilateral or the other eye can develop wet AMD.
    How: Early detection → earlier treatment → better vision. AAO Journal

13. Home blood-pressure and glucose awareness (if diabetic)
    What: Keep systemic health on target.
    Why: Microvascular stability benefits the macula.
    How: Daily/weekly checks and primary-care follow-up. Retina Specialists

14. Falls and injury prevention
    What: Good lighting, contrast strips on steps.
    Why: Central vision fluctuation can increase fall risk.
    How: Simple home safety tweaks preserve independence. AAO Journal

15. Counseling for anxiety/depression
    What: Support groups or therapy if vision changes cause stress.
    Why: Quality-of-life is part of treatment success.
    How: Emotional support improves adherence and outcomes. PMC

16. Vaccination & infection prevention around eye procedures
    What: Follow clinic hygiene instructions before and after injections.
    Why: Lowers rare but serious risk of endophthalmitis.
    How: Don’t touch the lid margin; heed post-injection warning signs. AAO Journal

17. Reading ergonomics
    What: Bigger fonts, higher contrast, more light, e-readers.
    Why: Reduces eye strain when macular sensitivity is variable.
    How: Sustains reading comfort during treatment phases. AAO Journal

18. Driving safety review
    What: Periodic legal-vision checks and cautious night driving.
    Why: PCV flare-ups can transiently reduce acuity and contrast.
    How: Discuss with your clinician; adapt routes and timing. AAO Journal

19. Regular scheduled imaging
    What: OCT monthly initially, then every 1–3 months depending on stability.
    Why: Detects tiny fluid changes before symptoms.
    How: OCT thickness and sub-RPE fluid guide treatment intervals. AAO Journal

20. Shared decision-making
    What: Understand options (injections vs PDT vs combined).
    Why: PCV responds differently from typical wet AMD; choices matter.
    How: Discuss EVEREST II and PLANET-informed strategies with your retina specialist. PubMedPMC

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Evidence-based drug treatments

(class, typical dose/timing, purpose, mechanism, key side effects)

Important: Doses/routes below are typical; your specialist tailors them to your eye and responds to imaging.

1. Aflibercept (Eylea®) — anti-VEGF biologic
   Dose/Timing: 2 mg intravitreal injection. Often 3 monthly “loading” doses, then every 8 weeks, with treat-and-extend to 8–12(–16) weeks if stable.
   Purpose: Dry up fluid, stabilize or improve vision; in PCV, many eyes do well with aflibercept alone.
   Mechanism: “VEGF-trap” that binds VEGF-A/VEGF-B and PlGF, blocking leaky vessel growth.
   Side effects: Transient eye discomfort, small subconjunctival bleed, very rare infection; systemic events are rare.
   Evidence: PLANET showed aflibercept monotherapy preserved vision in most PCV patients and many did not need rescue PDT at 1–2 years. PMCIOVSAAO

2. Ranibizumab (Lucentis®) — anti-VEGF biologic
   Dose/Timing: 0.5 mg intravitreal; often monthly at first, then treat-and-extend.
   Purpose: Control exudation and improve vision.
   Mechanism: Antibody fragment neutralizing VEGF-A.
   Side effects: Similar to other anti-VEGF agents.
   Evidence: EVEREST II—ranibizumab + verteporfin PDT delivered better visual gains, higher polyp regression, and fewer injections than ranibizumab alone at 12–24 months in PCV. JAMA NetworkPubMed

3. Bevacizumab (Avastin®; off-label) — anti-VEGF biologic
   Dose/Timing: 1.25 mg intravitreal; monthly then PRN/treat-and-extend.
   Purpose/Mechanism/Side effects: Similar to ranibizumab; used off-label for cost reasons; evidence in PCV is supportive but less robust than aflibercept/ranibizumab RCTs. AAO Journal

4. Faricimab (Vabysmo®) — bispecific anti-VEGF-A/anti-Ang-2
   Dose/Timing: 6 mg intravitreal; 4 monthly loading injections, then extend to 8–16 weeks if stable.
   Purpose: Reduce treatment burden while maintaining disease control; emerging evidence shows polyp regression and anatomical gains in PCV cohorts.
   Mechanism: Blocks VEGF-A and Ang-2, stabilizing leaky vessels and improving barrier function.
   Side effects: As with other injections; rare intraocular inflammation events reported across the class.
   Evidence: Real-world PCV series and early trial readouts (e.g., SALWEEN week-16) show robust improvements and polyp effects; randomized PCV-specific trials are ongoing. PMC+1IOVSClinicalTrials.gov

5. Brolucizumab (Beovu®) — anti-VEGF biologic
   Dose/Timing: 6 mg intravitreal; intended for longer intervals after loading (where used).
   Purpose: Potent fluid control with potential for extended dosing; PCV-specific high-quality RCTs are limited.
   Mechanism: Small scFv that binds VEGF-A.
   Safety note: Post-marketing signals of intraocular inflammation and retinal vasculitis/occlusion led to risk-mitigation guidance; use is cautious and individualized.
   Evidence: Multiple safety analyses and society updates outline the risk profile; some centers avoid use in PCV. AAO Journalophthalmologyretina.orgAAO

6. Verteporfin (Visudyne®) for Photodynamic Therapy (PDT) — photosensitizer drug used with laser light
   Dose/Timing: 6 mg/m² IV over ~10 minutes; 689-nm laser delivered 15 minutes after infusion start at 50 J/cm² for 83 seconds (standard fluence). Reduced-fluence protocols are sometimes used.
   Purpose: Close the polyps and shrink the branching network, especially when combined with anti-VEGF.
   Mechanism: Light-activated verteporfin generates reactive oxygen species that occlude abnormal choroidal vessels selectively.
   Side effects: Temporary photosensitivity—avoid strong light for 48 hours; rare hemorrhage or RPE changes.
   Evidence: EVEREST protocols and procedural references; EVEREST II confirms the benefit of adding PDT to ranibizumab in PCV. www.amdbook.orgNCBIJAMA Network

7. Intravitreal triamcinolone acetonide (off-label, adjunct) — corticosteroid
   Dose/Timing: Often 2–4 mg intravitreal in select cases as an adjunct to reduce refractory edema; not a first-line PCV drug.
   Purpose/Mechanism: Anti-inflammatory and anti-permeability effects can quiet stubborn exudation.
   Risks: Cataract acceleration, eye-pressure rise; used sparingly by specialists. AAO Journal

8. Dexamethasone implant (Ozurdex®; adjunct in select cases) — corticosteroid implant
   Dose/Timing: 0.7 mg biodegradable implant; not standard for PCV but occasionally used off-label in mixed pathology with heavy inflammation/edema.
   Purpose/Mechanism/Risks: As above; individualized specialist use only. AAO Journal

9. Tissue plasminogen activator (tPA) with gas (for large submacular hemorrhage)
   Dose/Timing: Very small intravitreal or subretinal doses during a procedure, combined with pneumatic displacement and often anti-VEGF afterward.
   Purpose: Dissolve and move thick blood away from the fovea to protect photoreceptors.
   Mechanism: Enzymatically breaks down clot; gas bubble floats the blood off the center.
   Risks: Procedure-related complications; used urgently for big bleeds.
   Evidence: Contemporary series support PD + tPA (and sometimes vitrectomy) for blood displacement. PMCScienceDirect

10. Topical/systemic therapies
    There is no proven pill or eye drop that treats PCV itself. Avoid internet “cures.” Medical therapy centers on injections ± PDT by a retina specialist. AAO Journal

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Dietary molecular supplements

(typical dosage, function, mechanism—evidence refers to AMD risk reduction; supplements do not treat active PCV)

The AREDS2 formula helps people with intermediate AMD reduce the risk of progression by about 25%. It does not cure PCV or replace injections, but many retina doctors consider AREDS2 in appropriate AMD-stage patients (especially if the other eye has AMD). Smokers should avoid beta-carotene and use AREDS2 (with lutein/zeaxanthin). Always discuss with your doctor. National Eye Institute+1

1. Vitamin C — 500 mg/day
   Function: Antioxidant support for the macula.
   Mechanism: Scavenges free radicals to reduce oxidative stress in RPE/photoreceptors. BrightFocus Foundation

2. Vitamin E — 400 IU/day
   Function: Lipid-phase antioxidant protection.
   Mechanism: Stabilizes cell membranes; safe at AREDS2 dosing. National Eye Institute

3. Zinc (as zinc oxide) — 80 mg/day
   Function: Cofactor for retinal enzymes; supports RPE function.
   Mechanism: Antioxidant/immune modulation; must be paired with copper to prevent deficiency anemia. BrightFocus Foundation

4. Copper (as cupric oxide) — 2 mg/day
   Function: Prevents copper-deficiency anemia from high-dose zinc.
   Mechanism: Restores enzyme balance. BrightFocus Foundation

5. Lutein — 10 mg/day
   Function: Macular pigment carotenoid.
   Mechanism: Filters blue light; antioxidant action in the fovea. BrightFocus Foundation

6. Zeaxanthin — 2 mg/day
   Function/Mechanism: As with lutein; concentrates at foveal center. BrightFocus Foundation

7. Omega-3 fatty acids (from diet; supplements not proven for AMD)
   Function: Anti-inflammatory lipid profile.
   Mechanism: DHA/EPA support photoreceptor membranes; dietary fish intake is preferred. National Eye Institute

8. Dark leafy greens (food source of lutein/zeaxanthin)
   Function: Natural carotenoid supply.
   Mechanism: Nutrient synergy with other antioxidants. National Eye Institute

9. Vitamin-rich fruits (vitamin C sources)
   Function: Support AREDS pattern through diet.
   Mechanism: Antioxidant network with vitamin E and carotenoids. National Eye Institute

10. Nuts/legumes (natural vitamin E, minerals)
    Function: Complement AREDS nutrients via food.
    Mechanism: Stabilizes oxidative balance; heart-healthy fats support vascular health. National Eye Institute

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Regenerative / advanced therapies

These options aim to reduce injection burden or replace/support damaged cells. They are in clinical trials mainly for neovascular or dry AMD—not specifically approved for PCV. If interested, ask your specialist about trial eligibility.

1. RGX-314 (gene therapy, AAV8 anti-VEGF)
   Dose/Route: One-time subretinal or suprachoroidal injection in trials.
   Function: Eye makes its own anti-VEGF protein continuously.
   Mechanism: Delivers DNA encoding a ranibizumab-like Fab to retinal cells. AAONature

2. ADVM-022 / Ixo-vec (gene therapy, aflibercept expression)
   Dose/Route: One intravitreal gene-therapy injection in trials.
   Function/Mechanism: Sustained intraocular aflibercept production to suppress VEGF long-term. PMCBMJ Open

3. RPE cell suspensions (hESC-RPE/iPSC-RPE)
   Dose/Route: Surgical subretinal delivery of RPE cells.
   Function: Replace/support diseased RPE so photoreceptors survive longer.
   Mechanism: Cell replacement + trophic support. Oxford AcademicPMC

4. RPE monolayer patches (e.g., CPCB-RPE1)
   Dose/Route: Pre-grown cell sheet implanted under the macula.
   Function/Mechanism: Organized RPE layer may integrate better than scattered cells. ScienceDirect

5. OpRegen® (RPE therapy for geographic atrophy)
   Dose/Route: Subretinal implantation in GA trials (dry AMD).
   Function/Mechanism: RPE replacement to slow degeneration; not for PCV, but illustrates direction of regenerative medicine. ClinicalTrials.gov

6. Next-generation gene/cell platforms
   Dose/Route: Various vectors and cell sources in early trials.
   Function/Mechanism: Longer-lasting VEGF suppression or cell rescue; future-facing options. BioMed CentralReview of Ophthalmology

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Procedures/surgeries

(what happens and why it’s done)

1. Photodynamic therapy (PDT) with verteporfin
   What happens: Verteporfin is infused IV (6 mg/m²). 15 minutes after starting infusion, a 689-nm laser delivers 50 J/cm² over 83 seconds to the lesion zone (standard fluence). Reduced-fluence strategies exist.
   Why: To shut down polyps and shrink the feeding network; often combined with anti-VEGF for stronger, more durable control. www.amdbook.orgNCBIJAMA Network

2. Thermal laser photocoagulation (for extrafoveal PCV)
   What happens: A focal laser spot seals feeder vessels/polyps that are safely away from the fovea.
   Why: Useful when lesions are peripheral/extrafoveal or when PDT access is limited. MDPIPubMed

3. Pneumatic displacement for large submacular hemorrhage (often with tPA)
   What happens: A gas bubble (and sometimes tPA) is used to float blood off the fovea, sometimes combined with vitrectomy or subretinal tPA if blood is thick.
   Why: Thick blood is toxic to photoreceptors; moving it away quickly can preserve vision. PMCophthalmologyretina.org

4. Pars plana vitrectomy (PPV) for non-clearing vitreous hemorrhage
   What happens: The vitreous gel and blood are removed; anti-VEGF can be given at the end.
   Why: When a big bleed spills into the vitreous and obscures vision, PPV clears the media and may improve outcomes. PMCNature

5. Rescue/combination approaches
   What happens: Tailored mixes of anti-VEGF + PDT ± laser based on OCT/ICGA findings.
   Why: EVEREST II shows combination therapy can drive higher polyp closure and stronger visual gains in many PCV eyes than anti-VEGF alone. PubMed

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Prevention pointers

1. Don’t smoke; get help to quit. (Strongest modifiable risk.) PMC

2. Keep regular retina visits even when vision seems stable. AAO Journal

3. Use an Amsler grid weekly and report new waves, kinks, or gray spots. AAO Journal

4. Heart-healthy diet emphasizing leafy greens and fish. National Eye Institute

5. Consider AREDS2 if you meet AMD criteria—ask your eye doctor first. National Eye Institute

6. Wear UV/HEV-blocking sunglasses outdoors. National Eye Institute

7. Control blood pressure, cholesterol, and diabetes with your primary-care team. Retina Specialists

8. Take medications exactly as prescribed; never stop blood thinners without medical advice. AAO Journal

9. Prioritize sleep and physical activity for vascular health. Retina Specialists

10. Organize rides and reminders so you never miss injection/PDT visits. Lippincott Journals

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When to see a doctor—right away

• Sudden wave or bend in straight lines, new blurry or gray spot, or drop in central vision

• New floaters, flashes, or a curtain-like shadow—possible hemorrhage

• After an injection: worsening pain, marked redness, pus, or vision drop—rule out infection/inflammation

• Any new bleeding or heavy distortion when you look at faces or text

These signs can mean active leakage or bleeding and need urgent retina evaluation. AAO Journal

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What to eat—and what to avoid

Eat more of:

1. Leafy greens (spinach, kale) for lutein/zeaxanthin. BrightFocus Foundation

2. Colorful vegetables (peppers, broccoli) and citrus/berries for vitamin C. BrightFocus Foundation

3. Fatty fish (salmon, sardines) 1–2×/week for omega-3s (dietary source preferred). National Eye Institute

4. Nuts and seeds (almonds, sunflower seeds) for vitamin E and healthy fats. BrightFocus Foundation

5. Whole grains and legumes for vascular health.

Limit/avoid:

1. Smoking (not a food—but the biggest harm). PMC
2. Ultra-processed, high-salt foods if you have hypertension. Retina Specialists
3. Sugary drinks and refined carbs—spikes strain vessels over time. National Eye Institute
4. Trans fats—swap to olive oil/avocado oil.
5. Beta-carotene supplements in current or former smokers; use AREDS2 instead. National Eye Institute

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Frequently asked questions

1. Is PCV the same as wet AMD?
   They are closely related. Many experts treat PCV as a subtype of wet AMD. It often needs similar injections but can respond especially well to PDT combined with anti-VEGF. AAO JournalPubMed

2. Can PCV be cured?
   We usually control it rather than “cure” it. With the right plan, many people keep useful, stable vision for years. PMC

3. How do doctors confirm PCV?
   OCT suggests it, but ICGA is the best test to show the polyp and the branching network when the diagnosis is unclear. NCBI

4. What treatment works best?
   Two strong paths:

• Aflibercept monotherapy (many eyes do well).

• Ranibizumab + PDT (often higher polyp closure and fewer injections). Your retina doctor chooses based on imaging and your eye’s response. PMCPubMed

5. Will I need many injections?
   At first, yes—monthly for several visits. If the eye dries and stays stable, intervals often extend to 8–12 (or more) weeks. PMC

6. Is PDT safe?
   When done correctly, yes—photosensitizer + targeted light. You avoid strong light for 48 hours afterward. Rarely, bleeding or pigment changes can occur. NCBI

7. What about faricimab (Vabysmo)?
   Early PCV data are promising for fewer visits and good anatomic results; larger PCV-specific trials are underway. IOVSClinicalTrials.gov

8. I heard Beovu (brolucizumab) lasts longer. Should I get it?
   It can dry the retina well, but it has a known risk of intraocular inflammation/retinal vasculitis. Many doctors use it selectively or prefer alternatives. ophthalmologyretina.org

9. Can vitamins fix PCV?
   No. AREDS2 vitamins may lower AMD progression risk in the right stage, but they don’t treat active PCV. Injections and/or PDT do. National Eye Institute

10. Will both eyes be affected?
    It’s possible. That’s why regular checks of the other eye matter. AAO Journal

11. What if I’m on blood thinners?
    Don’t stop them yourself. Your retina and medical teams will coordinate care around procedures. AAO Journal

12. Can I prevent PCV?
    You can’t guarantee prevention, but not smoking, eating for eye health, and keeping BP/lipids in range support macular health. PMCNational Eye Institute

13. Are gene or stem-cell treatments available now?
    They are experimental and mainly targeted to AMD. Ask about clinical trials if you’re interested. NatureOxford Academic

14. What happens if I skip visits because I see fine?
    Fluid can return before you notice. Skipping appointments risks permanent scarring and vision loss. AAO Journal

15. What should I do today if lines look wavy?
    Cover one eye and check each eye. If new distortion or a dark spot is present, call your retina clinic urgently. AAO Journal

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 22, 2025.