Difference Between Rheumatic Heart Disease and Infective Endocarditis

Key Difference – Rheumatic Heart Disease vs Infective Endocarditis
 

Rheumatic heart disease, which is a complication of rheumatic fever, is characterized by deforming valvular fibrotic disease, usually the mitral valve. On the other hand, infective endocarditis is a microbial infection of the heart valves or of the mural endocardium that leads to the formation of vegetations composing of thrombotic debris and organisms that are often associated with the destruction of underlying cardiac tissues. The key difference between the two diseases is, unlike infective endocarditis, which is purely due to infectious causes, rheumatic heart disease has an autoimmune component in its pathogenesis.    

CONTENTS

1. Overview and Key Difference
2. What is Rheumatic Heart Disease
3. What is Infective Endocarditis
4. Similarities Between Rheumatic Heart Disease and Infective Endocarditis
5. Side by Side Comparison – Rheumatic Heart Disease vs Infective Endocarditis in Tabular Form
6. Summary

What is Rheumatic Heart Disease?

Rheumatic fever is an inflammatory disease caused by the infection of group A streptococci which commonly affects children and young adults. There is a multisystem involvement with clinically significant changes taking place in the CNS, joints, and heart.

Initially, there is a pharyngeal infection by group A streptococci and the presence of their antigens triggers an autoimmune reaction that gives rise to the set of clinical features which we identify as rheumatic fever. The bacterium directly infects none of the affected organs.

Rheumatic heart disease, which is a complication of rheumatic fever, is characterized by deforming valvular fibrotic disease, usually the mitral valve.

Cardinal morphological changes happening in the mitral valve in rheumatic heart disease are,

• Thickening of leaflets
• Commissural fusion and shortening
• Thickening and fusion of tendinous cords

Clinical Features

• Changes in the heart sounds can be heard during the auscultation
• S1 is accentuated in the early disease
• P2 is also accentuated
• There is a decrease in the splitting of S2
• A diastolic murmur is usually heard over the cardiac apex

Investigations

• Antistreptolysin o titer
• ECG
• Echocardiogram
• Chest X-ray

Management

Proper treatment of rheumatic fever is extremely important in the prevention of the disease progressing into RHD.

• The residual streptococcal infection has to be treated with oral phenoxymethyl penicillin. This antibiotic should be given even when the culture results do not confirm the presence of group A streptococci.
• Any streptococcal infection that develops in the future should be treated.

To prevent cardiac manifestations, prophylactic treatments can be given. Patients who have had RHD should be given a dose of prophylactic antibiotics prior to dental procedures in order to prevent secondary infective endocarditis. In some patients surgical correction of the mitral stenosis is necessary.

What is Infective Endocarditis?

Infective endocarditis is a microbial infection of the heart valves or the mural endocardium. It leads to the formation of vegetations composed of thrombotic debris and organisms that are often associated with the destruction of underlying cardiac tissues. Bacteria are the commonest causative agents of infective endocarditis though it is possible to be due to the infections by other categories of organisms also. There are two main varieties of infective endocarditis as acute and subacute endocarditis. This classification is made based on the speed with which the clinical features develop.

Risk Factors

• Intravenous drug abuse
• Poor dental hygiene
• Intravascular cannulae
• Soft tissue infections
• Cardiac surgery and permanent pacemakers

Clinical Features consistent with both forms of Infective Endocarditis

• New valve lesion/ regurgitant murmur
• Embolic events of unknown origin
• Sepsis of unknown origin
• Hematuria, glomerulonephritis and renal infarctions
• Fever
• Peripheral abscesses of unknown origin

Modified Duke’s Criteria for the diagnosis of Infective Endocarditis

Major Criteria

• Blood culture/s positive for a characteristic organism or persistently positive for an unusual organism
• Echocardiographic evidence confirming the valvular lesions
• New valvular regurgitation

Minor Criteria

• Predisposing heart lesions or intravenous drug use
• Fever
• Microbiologic evidence including a single culture positive for an unusual organism
• Vascular lesions such as Janeway lesions and splinter haemorrhages

Investigations

• Blood cultures
• Echocardiogram

Management

Antibiotic treatment has to be commenced as soon as possible. Before the start of the empirical antibiotic therapy blood samples need be taken and be sent to cultures. Antibiotic therapy has to be continued for 4-6 weeks. The patient should respond to the antibiotics within the first 48 hours of their administration. The resolution of fever, decline in the level of serum markers of infection and relief of systemic symptoms will show the effectiveness of the therapy. Surgical intervention is necessary when the patient does not respond to the antibiotic therapy.

Subacute endocarditis is due to the infection of the previously damaged cardiac valves by low virulent bacteria such as Viridans streptococci. There is only a minimal destruction of the cardiac valves. The appearance of symptoms mentioned above can usually happen few weeks after the initial infection. Subacute endocarditis can be treated only with antibiotics.  

What is the Similarity Between Rheumatic Heart Disease and Infective Endocarditis?

• Both diseases are cardiac conditions with an infectious background.

What is the Difference Between Rheumatic Heart Disease and Infective Endocarditis?

Summary – Rheumatic Heart Disease vs Infective Endocarditis 

Rheumatic heart disease, which is a complication of rheumatic fever, is characterized by deforming valvular fibrotic disease, usually the mitral valve whereas infective endocarditis is a microbial infection of the heart valves or the mural endocardium and it leads to the formation of vegetations composed of thrombotic debris and organisms often associated with the destruction of underlying cardiac tissues. Autoimmune mechanisms contribute to the occurrence of RHD but not for the occurrence of infective endocarditis. This is the principle difference between the two disorders.

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Reference:

1.Kumar, Parveen J., and Michael L. Clark. Kumar & Clark clinical medicine. Edinburgh: W.B. Saunders, 2009.

Image Courtesy:

1.’Tonsillitis’By Michaelbladon (Public Domain) via Commons Wikimedia  
2.’Haemophilus parainfluenzae Endocarditis PHIL 851 lores’ By PHIL_Images (Public Domain) via Commons Wikimedia