Pathogenesis of Rheumatic Heart Disease

Rheumatic heart disease (RHD) is a chronic condition resulting from acute rheumatic fever (ARF), an inflammatory disease triggered by Group A Streptococcus infection. It primarily affects the heart valves, leading to progressive damage and complications.

Etiology and Pathogenesis

RHD develops due to an autoimmune response following untreated or inadequately treated streptococcal throat infections. The molecular mimicry between streptococcal antigens and cardiac tissue proteins leads to immune-mediated damage.

Key Pathogenic Mechanisms

• Streptococcal Infection: Initiates an immune response against bacterial antigens.
• Molecular Mimicry: Cross-reactivity between streptococcal M protein and cardiac myosin.
• Inflammatory Cascade: Activation of cytokines and immune cells causing tissue damage.
• Fibrosis and Valve Damage: Chronic inflammation leads to scarring and stenosis of heart valves.

Clinical Progression and Course

RHD manifests with valvular dysfunction, predominantly affecting the mitral and aortic valves. The disease progresses through acute, chronic, and advanced stages.

Stages of Disease Progression

1. Acute Phase: Characterized by pancarditis, fever, and joint involvement.
2. Chronic Phase: Persistent valvular damage leading to stenosis or regurgitation.
3. Advanced Disease: Heart failure, atrial fibrillation, and increased risk of thromboembolism.

Diagnosis and Management

Early diagnosis is crucial to prevent complications. Echocardiography, serological tests, and clinical criteria aid in diagnosis.

Management Strategies

• Antibiotic Therapy: Penicillin prophylaxis to prevent recurrent infections.
• Anti-inflammatory Treatment: Corticosteroids and NSAIDs for acute inflammation.
• Surgical Intervention: Valve repair or replacement in severe cases.

Prevention and Public Health Measures

Preventive strategies include early treatment of streptococcal infections, improved healthcare access, and vaccination research.