Acute Rheumatic Fever and Rheumatic Heart Disease

Introduction: Acute rheumatic fever (ARF) followed by partner rheumatic heart disease (RHD) is a serious problem in pediatric health problems around the world. It is surprising that New Zealand is one of the largest contributors and ARF has the largest number of cases in the world (Jaine, Baker, and Venugopal, 2008). This article describes the pathophysiology and epidemiology of ARF and RHD. It focuses on the impact of illness on children of Maori and Pacific Islands, in particular ARF is mostly exclusive among these ethnic groups (Atatoa-Carr, Bell, & Lennon, 2008; Sopoaga, Buckingham, & Paul, 2010).

Rheumatic heart disease is caused by myocardial injury caused by inflammation and scarring caused by heart valve and rheumatic fever. Rheumatic fever is usually caused by an abnormal reaction of the body against streptococcal infections starting from childhood sore throat or tonsillitis. People in low and middle income countries with cardiovascular disease and other non-communicable diseases have difficulty accessing effective and equitable medical services to meet their needs. As a result, many people in middle and low income countries are found in the process of illness, usually died of young people with cardiovascular disease and other non-communicable diseases, in the most productive year.

The term rheumatic heart disease refers to various kinds of acute and chronic heart diseases that can occur due to rheumatic fever, not to a single disease. Any part of the heart, including the pericardium and endocardium, can be damaged by inflammation caused by rheumatic fever. However, the most common form includes cardiac valves, particularly mitral valves. The coronary arteries open in the longitudinal direction. The coronary artery is surrounded by epicardial fat and extends from left to right in the center of the picture. Increased epicardial fat is associated with an increase in total fat. There are many fats here, suggesting a risk factor for atherosclerosis. The coronary arteries show only mild atherosclerosis, occasionally only yellowish brown lipid plaques, no decrease is seen.

Acute rheumatic fever is only a sequela of pharyngeal infections, but acute glomerulonephritis can follow infections of the pharynx or skin. There is no adequate explanation for the precise etiology of acute rheumatic fever following streptococcal pyoderma or the exact etiology of acute rheumatic fever, but abnormal or enhanced immune responses appear to be essential. Furthermore, the persistence of an organism may be due in part to the higher affinity of organisms adhering to host pharyngeal cells, which is associated with an increased likelihood of rheumatic fever. Acute glomerulonephritis is caused by the deposition of the antigen-antibody-complement complex on the glomerular basement membrane. The antigen may be derived from Streptococcus or it may be a host tissue type (cross-reactive epitope of endocardium, myocyte membrane, vascular smooth muscle) with antigenic determinants similar to streptococcal antigen. Acute rheumatic fever can cause permanent damage to the heart valve