Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heart-muscle disease where the muscle of the right ventricle (the heart’s lower right chamber) is gradually replaced by scar and fat. This weakens the right ventricle and makes its electrical signaling unstable. As a result, people can have abnormal heart rhythms (ventricular arrhythmias), fainting, heart failure, or—rarely—sudden cardiac death. ARVC is usually inherited and often starts to show up in the teen or young-adult years, but it can appear later. NCBI+1 Doctors now use the umbrella term arrhythmogenic cardiomyopathy (ACM), which includes right-dominant disease (classic ARVC), left-dominant disease, and mixed or biventricular forms. The disease can begin “electrical” (arrhythmias with little structural change) and later become structural with visible scarring on imaging. This is why follow-up over time is important. AHA Journals+1 Scar and fat disrupt how electrical signals travel through the right ventricle. Signals detour around scar, creating electrical “circuits” that can trigger fast rhythms (ventricular tachycardia). Exercise and adrenaline can make this worse by increasing wall stress on already fragile cell-to-cell connections. Heart Rhythm Journal+1

ARVC is a genetic heart-muscle disease where parts of the right ventricle are slowly replaced by scar and fat. This changes the heart’s electricity and structure, so fast dangerous rhythms (ventricular tachycardia) can occur, fainting can happen, and—rarely—sudden death. The disease can affect only the right ventricle, but sometimes it involves the left ventricle too (doctors now call the wider family “arrhythmogenic cardiomyopathy,” or ACM). Diagnosis uses a “criteria” system that adds up findings from ECG, signal-averaged ECG, Holter/monitoring, cardiac MRI, echocardiography, genetics, and family history. The older “2010 Task Force Criteria” and newer “Padua criteria” guide these decisions. Management focuses on: (1) stopping dangerous rhythms and preventing sudden death, (2) restricting high-intensity/competitive exercise, (3) using medicines to reduce arrhythmias, (4) catheter ablation for recurrent VT, and (5) implantable cardioverter-defibrillator (ICD) when risk is high. There is no proven “cure” pill yet; care is about protection and rhythm control. Oxford Academic+4AHA Journals+4AHA Journals+4

Why ARVC happens

Most cases start with variants (mutations) in “desmosome” genes. Desmosomes are tiny protein “rivets” that tie heart cells together while the heart squeezes. When desmosomes are weak, intense mechanical stress (like heavy endurance exercise) can make micro-injury in the right ventricle wall. Over time, normal muscle is replaced by scar and fat, especially in the RV “triangle of dysplasia.” This scarring breaks the smooth spread of electricity, causing premature beats, runs of VT, or dangerous fibrillation. The mix of genes, stress, and time explains why symptoms can start in teen years or young adults, why athletes are at higher risk, and why the disease can progress slowly from “electrical only” to “structural plus electrical.” ScienceDirect+2PMC+2

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Another names

Common alternate names.
You may see ARVC called arrhythmogenic right ventricular dysplasia (ARVD), arrhythmogenic cardiomyopathy – right-dominant type, or simply ARVC/D. Older papers often use ARVD; newer guidelines prefer ARVC or ACM. NCBI+1

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Types

Right-dominant (classic ARVC).
The right ventricle is the main site of scarring and dilation. People often have ventricular tachycardia with a left bundle branch block (LBBB) pattern on ECG because the abnormal rhythm starts in the right ventricle. NCBI

Left-dominant arrhythmogenic cardiomyopathy.
Some patients have similar “arrhythmogenic” scarring mainly in the left ventricle. This can look like myocarditis or dilated cardiomyopathy at first. It is still part of the same disease family, but the left side is more affected. AHA Journals

Biventricular (mixed) arrhythmogenic cardiomyopathy.
Both ventricles are involved. Symptoms and imaging come from changes on both sides, and arrhythmias may originate from either ventricle. AHA Journals

Disease phases (how it evolves).
Doctors describe a “concealed” phase (arrhythmias with little structural change), an “overt” phase (visible right-ventricle changes), and a “heart-failure” phase (weaker pump function). People can move between phases over years. NCBI

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Causes

ARVC is mostly genetic. Each “cause” below either directly causes ARVC (gene variants) or promotes/worsens it (modifiers).

1. PKP2 gene variants (plakophilin-2). The most common genetic cause; it weakens the desmosomes that glue heart cells together. Cells detach under stress, leading to scarring. NCBI

2. DSP gene variants (desmoplakin). Often linked to left-dominant or biventricular disease and skin/hair findings in some families. NCBI

3. DSG2 gene variants (desmoglein-2). A desmosomal protein; changes increase cell detachment and scarring. NCBI

4. DSC2 gene variants (desmocollin-2). Another desmosomal gene linked to classic ARVC patterns. NCBI

5. JUP gene variants (plakoglobin). Rare, can be part of syndromes with hair/skin signs (Naxos disease). NCBI

6. TMEM43 gene variants. A founder variant (p.S358L) is tied to aggressive disease in some populations. NCBI

7. FLNC gene variants (filamin C). Cytoskeletal protein; variants can cause arrhythmogenic or dilated phenotypes with high arrhythmia risk. ScienceDirect

8. DES gene variants (desmin). Intermediate filament defects may lead to arrhythmogenic scarring and conduction problems. NCBI

9. PLN gene variants (phospholamban). Calcium-handling protein; certain variants show arrhythmogenic and dilated features. NCBI

10. RBM20 gene variants. Splicing regulator; can produce arrhythmogenic cardiomyopathy phenotypes with malignant arrhythmias. ScienceDirect

11. Multiple-gene (digenic) inheritance. Some patients carry >1 relevant variant, often with earlier or more severe disease. NCBI

12. Family history of ARVC or sudden death. A strong clue because ARVC is usually inherited in an autosomal-dominant pattern with variable expression. NCBI

13. Endurance/high-intensity exercise (modifier). Heavy exercise can increase penetrance, drive earlier onset, and raise arrhythmic risk in gene carriers. PMC+1

14. Male sex (modifier). Men have higher arrhythmic risk and earlier expression, likely due to hormonal and activity differences. Heart Rhythm Journal

15. Inflammation/myocarditis-like episodes (trigger). Inflammatory “hot phases” can worsen scar and provoke arrhythmias. AHA Journals

16. Mechanical wall stress (modifier). Any factor that raises right-ventricle wall stress (e.g., frequent high-intensity training) may accelerate disease. PMC

17. Autonomic/sympathetic surges (trigger). Adrenaline during exertion or strong emotions can trigger ventricular tachycardia. Heart Rhythm Journal

18. Aging (modifier). Some carriers stay silent for years; changes accumulate and appear later. NCBI

19. Incomplete penetrance/variable expressivity. Not every carrier develops ARVC, but they remain at risk and need screening. NCBI

20. Unknown/idiopathic cases. A minority have clinical ARVC with no variant found using current tests; research is ongoing. NCBI

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Symptoms

1. Palpitations. A feeling that the heart is racing, pounding, or skipping beats—often the first sign. NCBI

2. Light-headedness or near-fainting. Abnormal rhythms reduce blood flow to the brain and cause dizziness. NCBI

3. Fainting (syncope). A sudden blackout can occur with fast ventricular rhythms, especially during exercise. Heart Rhythm Journal

4. Chest discomfort. Some feel tightness or pain, sometimes during “hot phases” that mimic myocarditis. AHA Journals

5. Shortness of breath on exertion. As the right ventricle weakens, pumping to the lungs is less effective. NCBI

6. Reduced exercise tolerance. People tire early or can’t keep prior training levels. PMC

7. Awareness of skipped beats at rest. Extrasystoles (PVCs) are common and may increase with stress or caffeine. NCBI

8. Episodes of very fast heartbeat (VT). Sustained VT may cause severe symptoms or require emergency care. Heart Rhythm Journal

9. Night-time palpitations. Arrhythmias can appear at rest or sleep due to autonomic swings. Heart Rhythm Journal

10. Swelling of legs/ankles. A sign of right-sided heart failure when disease is advanced. NCBI

11. Abdominal bloating or liver fullness. Fluid retention from right-sided failure can cause these. NCBI

12. Worsening symptoms during heavy training. Exercise can unmask or intensify arrhythmias in gene carriers. PMC

13. Family red flags. Close relatives with ARVC, ICDs, or sudden death under age 40 suggest risk. NCBI

14. Skin or hair features in special syndromes. Rare forms (e.g., Naxos) include woolly hair and palm keratoderma. NCBI

15. No symptoms. Some carriers feel fine; screening still matters because first events can be serious. NCBI

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Diagnostic tests

(Grouped so you know why each is used. Your doctor chooses based on your story, family history, and guideline criteria.)

A) Physical exam (bedside checks)

1. Vital signs and general look. Doctors check pulse, blood pressure, breathing rate, and signs of low oxygen or distress. This helps judge stability and whether urgent rhythm treatment is needed. AHA Journals

2. Jugular venous pressure (neck vein exam). A raised JVP hints at right-sided congestion from a weak right ventricle. AHA Journals

3. Heart and lung exam. Extra heart sounds, murmurs, crackles, or an enlarged, forceful RV impulse may suggest structural disease or failure. AHA Journals

4. Leg and abdominal swelling check. Edema or liver enlargement suggests advanced right-sided failure. AHA Journals

5. Exercise-related questioning and risk review. A targeted discussion of training volume, syncope during sport, and family history guides next tests and activity advice. American College of Cardiology

B) “Manual” bedside maneuvers (simple, no machines)

6. Orthostatic vitals. Checking blood pressure/heart rate from lying to standing can reveal instability after arrhythmia or medicines. AHA Journals

7. Carotid sinus massage (rarely, in clinic). Sometimes used to clarify supraventricular rhythms; not used during suspected VT, but part of rhythm assessment in selected cases. AHA Journals

8. Valsalva maneuver coaching. Helps distinguish some rhythm types and may reduce palpitations briefly; not a treatment for VT but useful in evaluation. AHA Journals

C) Laboratory / Pathological tests

9. High-sensitivity troponin during “hot phases.” A bump can appear during inflammatory episodes that mimic myocarditis, helping time imaging and rest from sport. AHA Journals

10. BNP/NT-proBNP for heart-failure load. Elevated levels suggest ventricular strain and guide follow-up. AHA Journals

11. Genetic testing with counseling. Tests for ARVC genes (e.g., PKP2, DSP, DSG2, DSC2, JUP, TMEM43; and others) confirm diagnosis in many and enable family screening. Pre- and post-test counseling is essential. NCBI+1

12. Endomyocardial biopsy (selected cases). Tissue sampling may show fibrofatty replacement or inflammation, but sensitivity is limited and the test carries a small risk; used when results will change management. Heart Rhythm Journal

D) Electro-diagnostic tests (electrical evaluation)

13. 12-lead ECG. Classic findings are T-wave inversion in V1–V3, epsilon waves, and ectopic beats. ECG is a major criterion in modern diagnostic systems. AHA Journals

14. Signal-averaged ECG. Detects “late potentials” that reflect slow conduction around scar; this supports the diagnosis in some patients. AHA Journals

15. 24–48-hour Holter (or patch monitor). Counts PVCs and catches runs of VT that you might not feel; longer monitoring improves yield. Heart Rhythm Journal

16. Exercise treadmill (with ECG). Helps trigger and document arrhythmias safely under supervision and assesses fitness and symptoms. American College of Cardiology

17. Electrophysiology (EP) study. In the lab, doctors map circuits and test if VT is inducible; this can guide ablation or risk decisions in selected people. Heart Rhythm Journal

E) Imaging tests (structure and scar)

18. Transthoracic echocardiogram (echo). Looks for right-ventricle dilation, reduced function, and regional wall-motion changes; also checks left ventricle. Heart Rhythm Journal

19. Cardiac MRI (CMR) with late gadolinium enhancement. The key imaging test. It shows scar/fatty replacement, detects subtle regional changes, and supports modern Padua/International diagnostic criteria. American College of Cardiology+1

20. Cardiac CT (selected). Used when MRI is not possible; shows structure and can help exclude other causes, but MRI is preferred for tissue characterization. Heart Rhythm Journal

Non-pharmacological treatments

1) Strict exercise restriction (no competitive/moderate–high intensity sports)
Purpose: Reduce mechanical stress that accelerates scar and lowers arrhythmia threshold.
Mechanism: Less wall stress → less micro-injury → fewer triggers and slower disease progression.
Details: Avoid endurance sports and vigorous intervals. Prefer low-intensity movement (leisure walking, gentle cycling). Train family and coaches about the diagnosis. Oxford Academic+2PMC+2

2) Personalized “safe activity” plan
Purpose: Keep you active safely, protect mental health, and maintain weight and mobility.
Mechanism: Structured low-intensity plan (e.g., 150 minutes/week of easy walking on flat terrain, supervised light stretching), with stop rules (palpitations, dizziness). European Society of Cardiology

3) Family screening and genetic counseling
Purpose: Find relatives at risk early and guide life choices.
Mechanism: Cascade testing for known family variants; periodic ECG/echo/CMR for relatives without a known variant but with possible risk. PubMed+1

4) Education on symptom triggers and red flags
Purpose: Earlier care when it matters.
Mechanism: Teach recognition of sustained palpitations, near-faint/faint, chest pain with rapid heart rate, new exercise intolerance; set clear emergency plans. Oxford Academic

5) Avoid dehydration, electrolyte loss, and stimulants
Purpose: Lower arrhythmia risk.
Mechanism: Maintain potassium and magnesium; avoid energy drinks/amphetamines; moderate caffeine and alcohol; avoid heat stress. Oxford Academic

6) Device strategy counseling (ICD readiness)
Purpose: Shared decisions about when to place an ICD, and what type (transvenous vs subcutaneous).
Mechanism: Discuss risk factors (sustained VT, syncope thought due to VT, severe RV/LV disease, extensive scar, family SCD). Oxford Academic

7) Rhythm monitoring plan
Purpose: Catch dangerous rhythms early.
Mechanism: Use Holter, event monitors, or loop recorders based on symptoms and risk; adjust meds and procedures accordingly. Oxford Academic

8) Vaccination and infection control
Purpose: Prevent fever/dehydration or myocarditis that can worsen arrhythmias.
Mechanism: Routine vaccines and early treatment of febrile illness reduce physiologic stressors. (Guideline-consistent general principle.) Oxford Academic

9) Pregnancy and life-planning consultation
Purpose: Plan safely for pregnancy, delivery, and postpartum when hormones and volume load change.
Mechanism: Pre-conception risk review, medicine review (avoid teratogens), delivery plan with cardiology/anesthesiology support. sochicar.cl

10) Psychological support
Purpose: Reduce anxiety/depression that follow lifestyle limits and ICD shocks.
Mechanism: Counseling, peer groups, and cognitive strategies improve quality of life and adherence. Oxford Academic

11) Medication safety checklist
Purpose: Avoid pro-arrhythmic/QT-prolonging drugs and harmful herbals.
Mechanism: Use a living list checked against cardiology guidance; pharmacists can co-review. Oxford Academic

12) Return-to-work/school planning
Purpose: Keep daily life stable with risk controls.
Mechanism: Tailor schedules, stress breaks, hydration reminders, and emergency action plans. Oxford Academic

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Drug treatments

Doses below are typical adult starting points—final choices must be individualized by a cardiologist.

1) Non-selective or cardio-selective beta-blockers (e.g., nadolol 20–40 mg once daily; metoprolol succinate 25–100 mg daily)
Class: Beta-blocker (Class II).
Purpose: First-line to blunt adrenaline-driven ventricular ectopy/VT.
Mechanism: Lowers sympathetic tone, reduces triggered activity.
Timing: Daily; titrate to symptom and heart-rate targets.
Side effects: Fatigue, low blood pressure, slow pulse; caution in asthma (non-selective types). Oxford Academic

2) Sotalol (80–160 mg twice daily)
Class: Class III + beta-blocker.
Purpose: Suppress recurrent VT/PVCs when beta-blocker alone is not enough.
Mechanism: Blocks potassium channels and beta-receptors, prolongs repolarization.
Timing: Scheduled dosing; check kidneys and QT interval.
Side effects: Torsades risk with prolonged QT, bradycardia, fatigue. Oxford Academic

3) Amiodarone (e.g., loading 200 mg 2–3×/day then 100–200 mg/day maintenance)
Class: Broad Class III antiarrhythmic.
Purpose: Reduce VT burden when others fail or are not tolerated; often used with ICD.
Mechanism: Multichannel block; slows conduction and reduces re-entry.
Timing: Long half-life; careful loading and monitoring.
Side effects: Thyroid, liver, lung toxicity; photosensitivity; drug interactions—needs regular labs and exams. Oxford Academic

4) Flecainide (50–100 mg twice daily) in selected cases under specialist care
Class: Class Ic.
Purpose: Sometimes used adjunctively for PVC/VT suppression in carefully picked patients.
Mechanism: Sodium-channel block, slows conduction.
Timing: Close ECG and structural assessment required.
Side effects: Pro-arrhythmia in structural heart disease—specialist oversight essential. Oxford Academic

5) Mexiletine (150–200 mg two to three times daily) as add-on
Class: Class Ib.
Purpose: Reduce VT runs/PVCs as a helper drug when others insufficient.
Mechanism: Sodium-channel block, especially at fast rates.
Side effects: GI upset, tremor, dizziness; adjust in liver disease. Oxford Academic

6) ACE inhibitor/ARB (e.g., lisinopril 5–20 mg/day; losartan 25–100 mg/day) if LV/RV dysfunction
Class: Neurohormonal blocker.
Purpose: Standard heart-failure remodeling benefit when pump function is reduced.
Mechanism: RAAS blockade decreases wall stress and fibrosis signaling.
Side effects: Cough (ACEi), high potassium, kidney function changes. Oxford Academic

7) MRA (spironolactone 12.5–25 mg/day or eplerenone) if ventricular dysfunction
Class: Mineralocorticoid receptor antagonist.
Purpose: Add-on heart-failure therapy for remodeling and symptom control.
Mechanism: Anti-fibrotic/diuretic effects.
Side effects: High potassium, kidney issues; gynecomastia (spironolactone). Oxford Academic

8) Diuretics (e.g., furosemide) for congestion
Class: Loop diuretic.
Purpose: Control fluid overload when heart function is impaired.
Mechanism: Promotes salt/water excretion.
Side effects: Low potassium/magnesium, dehydration—replace electrolytes carefully. Oxford Academic

Notes: Drug choices are individualized. In ARVC/ACM, medicines reduce arrhythmias but do not replace exercise restriction or (when indicated) an ICD. Catheter ablation can reduce VT burden but recurrence is common due to disease progression. Oxford Academic

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Dietary molecular supplements

There is no supplement proven to cure or halt ARVC. These suggestions are supportive, mainly to optimize electrolytes and general heart health; always clear with your cardiologist.

1) Magnesium (e.g., magnesium glycinate providing 200–400 mg elemental/day)
Function/Mechanism: Supports cardiac ion balance and lowers risk of ectopy when low; deficiency can trigger arrhythmias.
Note: Avoid excess; adjust for kidney disease; target normal serum magnesium. Oxford Academic

2) Potassium (from diet; supplements only if prescribed)
Function/Mechanism: Normal potassium stabilizes cardiac repolarization; low levels increase ventricular ectopy.
Dosage: Food-first (bananas, spinach, legumes); supplement only under lab-guided care. Oxford Academic

3) Omega-3 (fish-oil) from food first (fatty fish 1–2×/week)
Function/Mechanism: General cardiovascular support; arrhythmia effect is inconsistent; not a treatment for VT.
Dosage: Prefer diet; capsules only if clinician advises. Oxford Academic

4) Vitamin D to replete deficiency (typical 800–2000 IU/day per labs)
Function/Mechanism: General health; deficiency is common; no direct ARVC evidence.
Note: Dose to lab targets; avoid high, unmonitored dosing. Oxford Academic

5) CoQ10 (100–200 mg/day) as optional adjunct
Function/Mechanism: Mitochondrial cofactor; evidence for ventricular arrhythmia prevention is limited; not disease-modifying in ARVC.
Note: Use only if clinician agrees; watch drug interactions (e.g., warfarin). Oxford Academic

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Immunity booster / regenerative / stem-cell drugs

Important: There are no immune-booster, regenerative, or stem-cell drugs proven to treat or reverse ARVC in people. Research is ongoing (preclinical/early translational) on pathways tied to desmosomal biology and fibrosis. Any “regenerative” claims for ARVC should be viewed as experimental and not standard care at this time. ScienceDirect+1

• 1) Stem-cell therapies: Not established for ARVC; not recommended outside trials. Mechanistic idea is to replace/repair scarred myocardium, but safety/effectiveness aren’t proven. Oxford Academic

• 2) Anti-fibrotic pipelines (research stage): Targeting fibrosis signaling is being studied in cardiomyopathies, but no approved ARVC-specific agent exists. Oxford Academic

• 3) Gene-targeted approaches (research stage): Because many cases are desmosomal, gene therapy/editing is a future possibility, but no clinical therapy is available yet. ScienceDirect

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Procedures / surgeries

1) Implantable cardioverter-defibrillator (ICD)
Procedure: A device is placed under the skin with a lead (or subcutaneously without transvenous leads) to detect and stop dangerous rhythms using pacing or shocks.
Why: It is the most effective protection against sudden death in high-risk ARVC/ACM. Indications include prior sustained VT/VF, syncope likely from VT, or high-risk substrate. Oxford Academic

2) Catheter ablation (endocardial ± epicardial)
Procedure: A thin catheter maps VT circuits; heat or cold energy scars the tiny spots causing VT.
Why: Reduces VT burden and shocks in patients with recurrent VT despite medicines; multiple procedures may be needed due to progressive scar. Oxford Academic

3) Left cardiac sympathetic denervation (selected refractory cases)
Procedure: Surgeons cut specific nerve pathways that ramp up adrenaline to the heart.
Why: Considered when VT storms persist despite medicines, ablation, and ICD therapies. Oxford Academic

4) Subcutaneous ICD (S-ICD)
Procedure: An ICD placed under the skin without leads inside veins/heart.
Why: Avoids transvenous lead complications in younger patients—but no pacing function; patient selection matters. Oxford Academic

5) Heart transplantation (rare)
Procedure: Replace the failing heart.
Why: End-stage biventricular failure or uncontrollable arrhythmias despite maximal therapy. Oxford Academic

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Prevention behaviors

1. No competitive or vigorous endurance exercise. Oxford Academic+1

2. Maintain electrolytes and hydration; avoid heat stress. Oxford Academic

3. Keep a personal “do-not-use” drug list (QT-prolongers/pro-arrhythmics). Oxford Academic

4. Regular follow-up (ECG, Holter, echo/CMR as advised). Oxford Academic

5. Family screening/genetics when ARVC/ACM is confirmed. PubMed

6. Plan pregnancy with cardiology if applicable. sochicar.cl

7. Avoid stimulants (illicit drugs, energy drinks, high-dose caffeine). Oxford Academic

8. Sick-day rules: treat fever early, drink fluids; seek care for palpitations with illness. Oxford Academic

9. ICD care plan if you have a device (magnet/shock education, airport/security advice). Oxford Academic

10. Mental health support to improve adherence and quality of life. Oxford Academic

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When to see a doctor

• Go to emergency now for sustained rapid pounding heartbeat, fainting/near-faint, chest pain with fast rhythm, or ICD shocks. These can be signs of dangerous VT needing urgent care. Oxford Academic

• Call your cardiologist soon for new palpitations, exercise intolerance, swelling, rising fatigue, or medication side effects (e.g., cough on ACEi, bradycardia on beta-blocker). Oxford Academic

• Routine visits: keep scheduled ECG/Holter/imaging and device checks to adjust therapy before problems escalate. Oxford Academic

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What to eat and what to avoid

• Eat: a heart-healthy pattern (vegetables, fruits, whole grains, beans, nuts, fish), with steady potassium and magnesium from foods; enough fluids; modest salt unless told otherwise. This supports stable electrolytes and overall cardiovascular health. Oxford Academic

• Avoid/limit: energy drinks, illicit stimulants, binge alcohol, and anything that dehydrates you (sauna/very hot weather without fluids). Avoid “unknown” supplements with stimulant herbs. Always check new supplements and prescriptions with your cardiologist first. Oxford Academic

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: September 23, 2025.