Rheumatic Heart Disease

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Introduction   

Rheumatic heart disease (RHD) is a systemic immune condition that arises as a complication of rheumatic fever, which often follows a beta-hemolytic streptococcal throat infection [1][11]. It is a major cause of acquired heart disease in children and adults worldwide, with a high prevalence in developing countries [2].  

Rheumatic heart disease is a chronic valvular condition caused by rheumatic fever, which develops after an untreated Streptococcus pyogenes infection. Estimates are that over 40 million people worldwide are living with rheumatic heart disease, resulting in over 300,000 deaths per year [2][5]. RHD often affects individuals under the age of 25, causing over 288,000 deaths per year in low- and middle-income countries [2]. Comprehensive national programs are essential for addressing and managing RHD in endemic areas. 

RHD often results from repeated or untreated episodes of acute rheumatic fever, leading to long-term damage to the heart muscle or valves, the most common being the mitral and aortic valves [2]. Early antibiotic treatment in children can often prevent the disease’s progression, but established cases require surgical intervention [5]. RHD involves inflammation and scarring of the heart valves due to an autoimmune reaction to streptococcal pharyngitis. This condition can cause valvular insufficiency or stenosis, myocarditis, and lead to severe complications such as pulmonary venous hypertension and congestive heart failure [4].  

Diagnosis may involve chest radiographs showing left atrial enlargement or signs of pulmonary venous hypertension. Preventing RHD focuses on treating streptococcal infections with appropriate antibiotics to prevent rheumatic fever. For those already affected, long-term antibiotic prophylaxis with benzathine penicillin G can prevent recurrent infections and further heart valve damage [3][5]. In endemic regions, prevention and control strategies include improving living standards, expanding access to healthcare, ensuring a consistent supply of antibiotics for primary and secondary prevention, and integrating these efforts into national health systems with adequate monitoring and surveillance [5]. 

With near eradication in high-income countries, RHD remains endemic in disadvantaged communities worldwide [6]. In Australia, RHD impacts Aboriginal and Torres Strait Islander people, who experience some of the highest acute rheumatic fever (ARF) and RHD incidence rates across the globe [7]. The End RHD in Australia: Study of Epidemiology (ERASE) project determined that the Indigenous age-standardized RHD prevalence was 60 times higher than non-Indigenous prevalence, with females experiencing double the disease burden of males [7].  

The REMEDY study, a prospective cohort study conducted in low- and middle-income countries across Africa and Asia, revealed different progression rates to death or complications compared to those seen in high-income countries such as Australia. Previous Australian research, utilizing register data from the Northern Territory, indicated that within ten years of an RHD diagnosis, 18.6% of patients developed heart failure, 62.7% required surgical or percutaneous intervention, and 10.3% died [6].  

Understanding the likelihood and factors that contribute to the progression of Rheumatic Heart Disease (RHD) is essential for assessing both current and emerging control policies. Variations in RHD progression across different age groups or regions may require customized approaches. 

Case Study: Rheumatic Heart Disease (RHD) 

John, a 17-year-old male from a rural area, presents to the clinic with complaints of shortness of breath, chest pain, and swelling in his legs. He reports a history of frequent sore throats during childhood, which were often untreated due to limited access to healthcare. Six months ago, he experienced a severe sore throat and fever, followed by swollen, painful joints and a rash on his chest. A local clinic diagnosed him with acute rheumatic fever and administered antibiotics. However, his symptoms have persisted and worsened, leading to his current visit. 

Medical History 

• Frequent episodes of sore throat during childhood, often untreated. 

• Six months ago: Diagnosed with acute rheumatic fever following a severe sore throat, fever, joint pain, and rash. 

Differential Diagnosis 

• Endocarditis 

• Functional mitral regurgitation associated with viral myocarditis 

• Mitral valves prolapse due to degenerative myxomatous disease 

Etiology 

Rheumatic heart disease in John is a consequence of untreated and repeated attacks of rheumatic fever. This has resulted in stiffening and misshaping of the valve cusps, the merging of the commissures, and the contraction and merging of the chordae tendineae. Over time, these changes have resulted in valvular stenosis and/or regurgitation, affecting the mitral valve. 

Physical Examination 

• Auscultation: Apical pan-systolic murmur indicative of mitral regurgitation 

• Signs of congestive heart failure: Lower extremity edema, shortness of breath, orthopnea 

• Chest X-ray: Cardiomegaly and signs of pulmonary venous hypertension 

• Echocardiogram: Revealed thickening and restricted motion of the mitral valve leaflet, severe mitral regurgitation, and left atrial enlargement 

Pathophysiology 

Rheumatic heart disease is a chronic and progressive condition resulting from damage to the heart valves due to an abnormal immune response to Streptococcus pyogenes infection [1]. Acute rheumatic fever led to inflammation in the heart muscle and the formation of Aschoff nodules and MacCallum plaques, resulting in long-term fibrosis and scarring of the mitral valve [3]. 

Evaluation 

• Recent history of streptococcal infection confirmed by throat culture 

• Blood tests: Elevated inflammatory markers indicating ongoing inflammation 

• Echocardiogram: Detailed evaluation of the heart’s chambers and valves, confirming severe mitral regurgitation and left atrial enlargement 

• Electrocardiogram (ECG): Detecting arrhythmias and potential heart muscle damage 

Medical Management 

John’s management plan involves both medical and surgical interventions: 

• Antibiotic Prophylaxis: Most patients should use benzathine penicillin G long-term to prevent recurrent streptococcal infections and subsequent heart valve damage [8]. The intramuscular injection of long-acting penicillin G benzathine every 28 days, more effective compared to other regimens (Grade 2C) [8]. However, if a patient experiences an acute rheumatic fever (ARF) episode despite adhering to the 28-day regimen, a 21-day administration schedule may be more suitable [8]. 

• Medications: ACE inhibitors, diuretics, and beta-blockers to manage symptoms of heart failure and control blood pressure [3]. 

• Surgical intervention: Due to the severity of the mitral valve damage and the patient’s symptomatic heart failure, the medical team will perform valve repair or replacement surgery. 

Prognosis 

John’s prognosis depends on the success of the surgical intervention and adherence to long-term antibiotic prophylaxis. With appropriate treatment, he can expect significant improvement in symptoms and prevention of further complications. However, regular follow-up is essential to monitor his heart function and manage any emerging complications. 

Complications 

• Heart failure due to severe mitral regurgitation 

• Risk of bacterial endocarditis on damaged heart valves 

• Potential for arrhythmias and atrial fibrillation 

• Pulmonary hypertension due to chronic valve disease 

• Increased risk of stroke or blood clots due to arrhythmias 

Preventive Strategies 

• Early antibiotic treatment for streptococcal infections to prevent rheumatic fever 

• Ongoing prophylactic antibiotic treatment to prevent recurrent episodes of rheumatic fever 

• National programs to improve living standards, access to healthcare, and consistent antibiotic supply in endemic regions 

Case Study Summary 

John’s case highlights the critical importance of early diagnosis and treatment of streptococcal infections to prevent rheumatic fever and subsequent rheumatic heart disease. Comprehensive management, including both medical and surgical interventions, is essential to improve outcomes for patients with RHD. 

• How might John’s frequent untreated sore throats during childhood have contributed to his current diagnosis of rheumatic heart disease? 

• What are the key differences between endocarditis and rheumatic heart disease, and why is it important to differentiate between them in John’s case? 

• Considering John’s diagnosis and current symptoms, what are the potential risks and benefits of the planned surgical intervention for his mitral valve damage? 

Etiology 

Rheumatic heart disease is a long-term consequence of rheumatic fever, which can occur from either a single or repeated attacks [3]. This condition causes the stiffening and deformity of valve cusps, resulting in the fusion of the commissures as well as the shortening and fusion of the chordae tendineae [3]. Over two to three decades, these changes result in valvular stenosis and/or regurgitation [3]. Chronic rheumatic heart disease affects the mitral valve in 50% to 60% of cases [3]. In 20% of cases, both the aortic and mitral valves have combined lesions. Recurrent infections often affect the tricuspid valve in about 10% of cases, alongside mitral or aortic disease [3]. The pulmonary valve does not often experience impact [3].  

Rheumatic fever affects children and adolescents in low- and middle-income countries, and in regions with widespread poverty and limited healthcare access [2]. Those living in overcrowded and impoverished conditions are at the highest risk [2]. In areas where rheumatic fever and rheumatic heart disease are widespread, rheumatic heart disease stands as the most prevalent cardiac condition in pregnant women [2][9]. This condition contributes to high rates of maternal and perinatal complications and deaths [2][9]. Pregnant women with rheumatic heart disease face increased risks of adverse outcomes, including heart arrhythmias and heart failure, due to the additional pressure on the heart valves from increased blood volume [2][9]. Many women remain unaware of their rheumatic heart disease until pregnancy. 

Despite its eradication in numerous regions globally, rheumatic heart disease continues to be widespread in sub-Saharan Africa, the Middle East, Central and South Asia, and the South Pacific. It remains a health concern among immigrants, older adults in high-income countries, and Indigenous populations [2]. 

Epidemiology 

Rheumatic heart disease (RHD) stands as the most significant form of acquired heart disease affecting children and young adults in developing nations. In regions where the disease is prevalent, RHD contributes to 15-20% of all heart failure cases [3]. The regions with the highest incidence rates are Oceania, Central Sub-Saharan Africa, and South Asia. In these areas, there are 444 cases per 100,000 population, compared to only 3.4 cases per 100,000 in nonendemic regions. Rheumatic heart disease (RHD) impacts populations in impoverished areas with poor healthcare access and substantial exposure to group A streptococcus [2].  

A systematic review and meta-analysis have shown that silent Rheumatic Heart Disease (RHD) occurs at a significantly higher rate (21.1 per 1,000 individuals) compared to symptomatic RHD (2.7 per 1,000 individuals), with the former being seven to eight times more prevalent [1][9]. The incidence of RHD escalates with age, from 4.7 per 1,000 five-year-olds to 21.0 per 1,000 sixteen-year-olds [9][10]. These findings indicate that the actual RHD burden might be twice as high as the estimates reported in the Global Burden of Disease study [9]. Cytokine production drives these lesions’ growth and progression, initiated by monocytes in the acute phase and continued by T cells in the chronic phase [9][10]. 

Pathophysiology 

Rheumatic heart disease (RHD) is a chronic and progressive condition resulting from damage to the heart valves, leading to heart dysfunction [1]. This disease is a complication of acute rheumatic fever (ARF), an autoimmune disorder triggered by group A streptococcal throat infections [1]. An abnormal immune response to a Streptococcus pyogenes infection, classified as group A streptococcus, damages the heart valves in rheumatic heart disease (RHD) [1].  

Acute rheumatic fever develops about three weeks after group A streptococcal pharyngitis, affecting joints, skin, brain, and heart [1][11]. Recurrent episodes of rheumatic fever can lead to progressive fibrosis of the heart valves resulting in rheumatic valvular heart disease, which, if untreated, may cause heart failure or death [1][11]. The exact pathophysiology of RHD remains unclear, but it involves rheumatic carditis characterized by Aschoff nodules and MacCallum plaques, which result from inflammation in the heart muscle occur in nodules in hearts affected by rheumatic fever [1][12]. 

RHD follows ARF in 30-45% of cases, involving all three heart layers due to cytokines and other inflammatory molecules released against the streptococci, as well as immune cell attacks on cardiac tissues. CD4+ T cells and macrophages play prominent roles in this attack, with molecules like VCAM-1 aiding their attachment to the valves [13]. Genetic susceptibility is necessary for RHD to develop [14].  

The basic mechanism, known as T-cell molecular mimicry, involves antigens on group A streptococci stimulating CD4+ T cells, which then cross-react with similar peptides in heart tissue [13][14]. This antigen-T cell reaction leads to the destruction of heart valve endocardium tissue [13][14]. Cytokines such as TNF-α, IL-1, and IL-2 overproduce in ARF, triggering acute and long-term inflammatory responses that continue even after the infective agent dies [13][14]. 

The characteristic RHD lesion, the Aschoff nodule, consists of granuloma cells and contains various immune cells. Cytokine production drives the growth and progression of these lesions, initiated by monocytes in the acute phase and followed by T cells in the chronic phase [13][14]. The pathogenesis begins with a pharyngeal infection by Streptococcus pyogenes, followed by antigen presentation to immune T and B cells [1][13][14]. Skin infections with the same bacteria strain do not result in ARF [18]. Activation of CD4+ cells leads to the production of specific antibodies (IgM and IgG) by B lymphocytes, which react with similar structured proteins or peptides in heart tissue, causing inflammation [13][14]. This immune activation also affects joints, causing swelling and pain, and can result in chorea and skin rashes or nodules [1][13][14]. 

The molecules mimicking each other may include a spiral protein in M protein and N-acetyl-beta-D-glucosamine antigens in S. pyogenes, and myosin in cardiac muscle [18][19]. Antibodies formed against these antigens cross-react with human heart valve tissue. The overexpression of VCAM-1 molecules causes CD4+ cells to adhere to and infiltrate the valve endothelium, activating a cellular immune response and inflaming the valve tissue with new blood vessel growth [20].  

This increased blood supply brings more T cells, extending the T-cell attack to more valve areas [20]. Granulomas (Aschoff bodies) form beneath the endocardial layer, and calcification linked to osteopontin levels in the blood occurs as part of this inflammation [18][19][20]. Elevated inflammation markers like CRP and oxidation products indicate RHD in patients. Researchers now focus on the endothelium covering heart valves as the target of immunologic damage, which explains why only throat infections with group A streptococci cause ARF, unlike skin infections with the same bacteria [1][21]. 

History & Physical 

A recent history of strep infection or rheumatic fever is crucial for diagnosing rheumatic heart disease. Symptoms of rheumatic fever emerge 1 to 6 weeks following a bout of strep throat, although sometimes the initial infection may be so mild it goes unrecognized or has resolved by the time the individual consults a healthcare provider.  

The most common symptoms of rheumatic fever include fever; swollen, tender, red, and very painful joints (often knees and ankles); lumps under the skin (nodules); a red, raised, lattice-like rash (often on the chest, back, and belly); shortness of breath and chest discomfort; uncontrolled movements of arms, legs, or facial muscles; and weakness [22]. Rheumatic heart disease symptoms depend on the extent of valve damage and may include shortness of breath (often with activity or when lying down), chest pain, and swelling. 

Rheumatic fever is the leading cause of acquired heart disease in children and young adults worldwide, occurring 2 to 3 weeks after a group A beta-hemolytic streptococcal pharyngeal infection [1]. Carditis (inflammation of the heart muscle) is the most serious manifestation of rheumatic fever, with symptoms and signs varying based on the affected heart areas, including the pericardium, myocardium, or heart valves [1][24]. A pericardial friction rub on auscultation suggests pericarditis, while signs of congestive heart failure indicate myocarditis, characterized by lower extremity edema, shortness of breath with exertion or rest, abdominal distension, or orthopnea [24]. Elevated inflammation markers like CRP and oxidation products indicate RHD in patients. Researchers now focus on the endothelium covering heart valves as the target of immunologic damage. This shift explains why only throat infections with group A streptococci cause ARF, unlike skin infections with the same bacteria [24]. 

Mitral regurgitation, identified as an apical pan-systolic murmur on auscultation, is the most common valvular lesion, whereas aortic regurgitation is less common [25]. In patients with a history of rheumatic heart disease, any change in the character of a murmur or the presence of a new murmur on auscultation suggests acute rheumatic heart fever [24][25]. Rheumatic heart disease affects the left-sided cardiac valves, with the tricuspid and pulmonary valve being less affected, though this is uncommon without mitral valve involvement [1][26].  

Evaluation  

Rheumatic heart disease (RHD) often follows a recent or concurrent strep infection, detectable via throat culture or blood test. During a routine physical exam, clinicians may detect a murmur or rub, indicative of blood leaking around a damaged valve or inflamed heart tissues rubbing against each other [25][26]. Diagnosing RHD involves a thorough health history, physical examination, and several tests. 

An echocardiogram (echo) is essential for evaluating the heart’s chambers and valve [27]. Using sound waves, it provides a detailed image of the heart, revealing valve damage, backflow of blood, fluid accumulation, and heart enlargement [27]. For more comprehensive imaging, clinicians might use a transesophageal echo (TEE), which involves sedating the patient and inserting a probe into the throat. An electrocardiogram (ECG) records the heart’s electrical activity, identifying arrhythmias and potential heart muscle damage. A chest X-ray assesses lung and heart size, while a cardiac MRI offers detailed heart images. Blood tests can also detect infection and inflammation.  

Rheumatic heart disease causes myocarditis, congestive heart failure, arrhythmias like atrial fibrillation, and valvular heart disease [28]. Myocarditis can lead to conduction disturbances, necessitating an electrocardiogram (EKG) to detect various forms of heart block [29]. A chest X-ray evaluates for cardiomegaly or pulmonary vascular congestion, signs of heart failure. A transthoracic echocardiogram is more accurate than auscultation in detecting RHD [30]. An echocardiogram diagnoses subclinical RHD without detecting a murmur.  

Mitral regurgitation is common in young people with RHD, while mitral stenosis is the most frequent cause across the globe [27]. Descriptions of the mitral valve in echocardiography often include terms like “dogleg,” “elbow,” or “hockey-stick” deformities, which indicate thickening and restricted motion of the anterior mitral valve leaflet [30].  

In 2012, the World Heart Federation (WHF) established age-specific criteria for echocardiographic diagnosis of RHD [31]. These criteria establish the minimum standards for diagnosing RHD by echocardiography and guide clinical practice. However, the WHF has not updated the criteria since their initial release. The criteria remain a critical tool for identifying RHD in high-risk populations and continue to inform both research and clinical practices worldwide [31]. 

World Heart Federation (WHF) Established Age-Specific Criteria 

For individuals aged 20 years or younger, definite RHD includes: 

• Pathological mitral regurgitation and two morphological mitral valve features, 

• Mitral stenosis with a mean gradient ≥ 4 mmHg, 

• Pathological aortic regurgitation and two morphological aortic valve features, 

• Borderline disease of both the aortic and mitral valves. 

Borderline RHD includes: 

• Two morphological mitral valve features without pathological regurgitation or stenosis, 

• Pathological mitral regurgitation, 

• Pathological aortic regurgitation. 

Normal findings involve: 

• Mitral regurgitation not meeting all Doppler criteria, 

• Aortic regurgitation not meeting all Doppler criteria, 

• Isolated morphological features without stenosis or regurgitation, 

• Morphological features of the aortic valve without stenosis or regurgitation. 

For individuals older than 20, definite RHD includes: 

• Pathological mitral regurgitation and two mitral valve features, 

• Mitral stenosis with a mean gradient ≥ 4 mmHg, 

• Pathological aortic regurgitation and two aortic valve features (for those under 35), 

• Pathological aortic regurgitation and two mitral valve features. 

Morphological features of RHD for the mitral valve include: 

• Anterior mitral valve leaflet thickening ≥ 3 mm, 

• Chordal thickening, 

• Restricted leaflet motion, 

• Excessive leaflet tip motion during systole. 

For the aortic valve, features include: 

• Irregular or focal thickening, 

• Coaptation defect, 

• Restricted leaflet motion, 

• Prolapse. 

Pathologic mitral regurgitation must meet all Doppler criteria: 

• Seen on two views, 

• Jet length ≥ 2 cm on one view, 

• Peak velocity ≥ 3 m/s, 

• Pansystolic jet in one envelope. 

Pathologic aortic regurgitation must also meet all Doppler criteria: 

• Seen on two views, 

• Jet length ≥ 1 cm on one view, 

• Peak velocity ≥ 3 m/s, 

• Pandiastolic jet in one envelope. 

Revised Jones Criteria for Rheumatic Fever Diagnosis 

The Jones criteria for diagnosing rheumatic fever vary between low-risk and high-risk populations [15][16]. These criteria set the minimum standards for diagnosing RHD by echocardiography and guide clinical practice. However, the WHF has not updated the criteria since their initial release [15][16].  

These revisions aim to ensure that the criteria are applicable and sensitive to specific epidemiological contexts, thereby enhancing the ability to identify and treat rheumatic fever across diverse patient groups [15][16]. By differentiating between low-risk and high-risk populations, the criteria can better accommodate variations in the incidence and clinical manifestations of the disease. 

Major Criteria 

• Carditis (clinical or subclinical) 

• Arthritis 

• Minimal risk: Only polyarthritis 

• Considerable risk: Monoarthritis or polyarthritis 

• Chorea 

• Erythema marginatum 

• Subcutaneous nodules 

Minor Criteria 

• Arthralgia 

• Minimal risk: Polyarthralgia 

• Considerable risk: Monoarthralgia 

• Fever 

• Minimal risk: Hyperpyrexia (≥ 38.5°C) 

• Considerable risk: Hyperpyrexia (≥ 38.0°C) 

• Inflammatory markers 

• Minimal risk: ESR ≥ 60 mm/h and/or CRP ≥ 3.0 mg/dl 

• Considerable risk: ESR ≥ 30 mm/h and/or CRP ≥ 3.0 mg/dl 

• Prolonged PR interval (considering age-related differences; only if carditis is not a major criterion) 

Medical Management  

The primary goals of acute rheumatic fever therapy are to alleviate symptoms, prevent cardiac valve damage, and eradicate streptococcal infection [3][32]. For patients diagnosed with acute rheumatic fever, the goal is to suppress the inflammatory response to minimize its impact on the heart and joints. Long-term secondary antibiotic prophylaxis and continuous prevention of Streptococcus pyogenes (group A streptococcus) infections are essential to prevent future recurrences [3][32].  

The recommended regimen for secondary prophylaxis includes benzathine benzylpenicillin G intramuscular injections every four weeks [3][5][32]. For patients with penicillin hypersensitivity (non-severe) or immediate penicillin hypersensitivity: oral erythromycin 250 mg twice daily [3]. Therapy for rheumatic heart disease aims to prevent progression and optimize cardiac function. Using secondary antibiotic prophylaxis can reduce the long-term severity of the disease. 

Secondary antibiotic prophylaxis can reduce the long-term severity of RHD. Patients with RHD, including those on benzathine benzylpenicillin G prophylaxis, should receive amoxicillin prophylaxis before high-risk dental or surgical procedures [3]. These criteria establish the standards for diagnosing RHD using echocardiography and guide clinical practice. However, the WHF has not revised the criteria since their initial release [3].  

Rheumatic heart disease is a chronic condition with no cure, and the heart valve damage it causes is permanent. Severe rheumatic heart disease often requires surgical intervention to repair or replace damaged valves. Patients often need medications to manage symptoms of heart failure or heart rhythm abnormalities, and blood thinners to reduce the risk of blood clots. 

In low-income settings, surgical options are often unavailable or unaffordable, causing significant financial strain on families. 

Management of RHD encompasses both prevention and long-term care. The World Heart Federation states that secondary prophylaxis with penicillin injections every 3 to 4 weeks is the most cost-effective approach to preventing RHD progression by avoiding recurrent group A streptococcal infections and repeated episodes of acute rheumatic fever [32]. The optimal duration of secondary prevention remains unknown.  

For rheumatic mitral stenosis without regurgitation, arrhythmias, or left atrial thrombus, percutaneous mitral balloon valvuloplasty is the standard first-line therapy [1]. Severe valvular disease requires surgical intervention through valve replacement or repair. Manage patients who develop heart failure due to valve disease with medical therapy, including ACE inhibitors, diuretics, and beta-blockers, as tolerated [1][3]. Regular surveillance of patients diagnosed with rheumatic fever and RHD is crucial to enable early initiation of therapy. 

Prognosis 

Rheumatic heart disease (RHD) leads to at least 200,000 to 250,000 premature deaths per year and is the leading cause of cardiovascular mortality in children and young adults in countries with limited medical resources [2][5]. Without regular monitoring of valvular disease, patients may not seek medical attention until they experience severe heart failure, at which point surgery may no longer be an option.  

The primary outcome of interest was the time from the initial RHD diagnosis to a composite of death or any non-fatal cardiovascular complication, including surgical intervention, heart failure (HF), atrial fibrillation (AF), endocarditis, or stroke [6]. The four secondary outcomes of interest were the time to all-cause death, time to non-fatal cardiovascular complication composite, time to surgical intervention, and time to heart failure [6][33]. 

Complications 

Rheumatic heart disease can lead to serious conditions such as arrhythmia, atrial fibrillation, and heart failure, which increase the risk of stroke or blood clots [1]. Rheumatic heart disease remains latent or silent until cardiac complications develop in late adulthood. Common complications include infective endocarditis, embolic events, heart failure, pulmonary hypertension, and atrial fibrillation due to untreated severe valvular disease [1]. 

A ruptured heart valve is a medical emergency requiring surgical intervention to replace or repair the valve [22]. A narrowed or leaking heart valve can lead to heart failure. When rheumatic fever damages the heart valves, it can result in bacterial endocarditis, which is an infection of the heart’s inner lining [22]. Women with rheumatic heart disease should discuss potential complications of pregnancy and delivery with their healthcare provider before becoming pregnant [22].  

Conclusion

Rheumatic heart disease (RHD) remains a significant cause of morbidity and mortality globally, particularly in low- and middle-income countries where it often leads to severe complications such as heart failure and valvular disease [2]. The World Heart Federation (WHF) criteria established in 2012 for the echocardiographic diagnosis of RHD have become a critical tool in identifying and managing this condition [31]. These criteria have helped standardize the diagnosis and ensure early detection, thereby improving patient outcomes through medical and surgical interventions. 

Despite considerable progress in understanding and managing RHD, challenges persist in regions with limited healthcare access. Comprehensive national programs focusing on early antibiotic treatment, long-term prophylaxis, and improved healthcare infrastructure are essential in combating RHD. The case of John underscores the importance of early diagnosis and continuous management to prevent disease progression and severe complications. As research continues and diagnostic criteria evolve, tailored strategies for high-risk populations will be crucial in reducing the global burden of RHD. 

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