From the Guidelines
Acute rheumatic fever causes heart block due to inflammation of the heart tissues, specifically the conduction system, which can lead to various degrees of heart block, from first-degree to complete heart block, as a result of the autoimmune response triggered by group A streptococcal infection. When this infection occurs, it can trigger an autoimmune response, where antibodies mistakenly attack heart tissues, particularly the conduction system. This inflammatory process, called carditis, can affect the atrioventricular node and surrounding tissues, disrupting the normal electrical signals that coordinate heartbeats. The inflammation causes edema and cellular infiltration in the conduction pathways, physically impeding electrical impulse transmission from the atria to the ventricles. This interference results in various degrees of heart block, from first-degree (prolonged PR interval) to complete heart block in severe cases.
According to the most recent and highest quality study, 1, the management of heart block in acute myocarditis, which can be caused by acute rheumatic fever, involves temporary pacemaker insertion in patients with symptomatic heart block. The study also recommends pacing in patients with symptomatic sinus node dysfunction or AV block following myocarditis.
Key points to consider:
- Heart block is a complication of acute rheumatic fever, which can occur during the acute phase or as a long-term complication of rheumatic heart disease.
- The inflammation caused by the autoimmune response can lead to edema and cellular infiltration in the conduction pathways, resulting in heart block.
- The degree of heart block can vary, from first-degree to complete heart block, and may be temporary or permanent.
- Management of heart block in acute myocarditis involves temporary pacemaker insertion and pacing in patients with symptomatic sinus node dysfunction or AV block.
- The prognosis of patients with heart block due to acute rheumatic fever depends on the severity of the carditis and the presence of other complications, such as rheumatic heart disease.
In terms of morbidity, mortality, and quality of life, it is essential to prioritize the management of heart block in acute rheumatic fever to prevent long-term complications and improve patient outcomes. As stated in 1, rheumatic heart disease can lead to significant morbidity and mortality, with an estimated 233,000-468,164 individuals dying from the disease each year. Therefore, prompt and effective management of heart block is crucial to reduce the risk of long-term complications and improve patient outcomes.
From the Research
Acute Rheumatic Fever and Heart Block
- Acute rheumatic fever (ARF) is an autoimmune response to pharyngitis caused by infection with group A Streptococcus 2.
- The condition can lead to rheumatic heart disease (RHD), which is a notable cause of morbidity and mortality in resource-poor settings around the world 2.
- Cardiac involvement during ARF can result in RHD, which can cause heart failure and premature mortality 3.
- In rare cases, ARF can present with advanced atrioventricular (AV) conduction block, including complete heart block (CHB) 4.
Mechanism of Heart Block in ARF
- The exact mechanism of heart block in ARF is not fully understood, but it is thought to be related to the inflammatory response and autoimmune reaction triggered by the group A streptococcal infection 2, 3.
- The inflammation can affect the heart valves and the conduction system, leading to AV conduction abnormalities and potentially heart block 4.
- In some cases, the heart block may be reversible with treatment, such as corticosteroids 4.
Clinical Presentation and Diagnosis
- ARF typically presents as a febrile illness with clinical manifestations that could include arthritis, carditis, skin lesions, or abnormal movements 5.
- The cardiac manifestations of ARF are most concerning, as children may present in acute heart failure and may go on to develop valvular insufficiency or stenosis 5.
- The diagnosis of ARF is entirely clinical, without any laboratory gold standard, and relies on the Jones Criteria 6, 2.