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This well-illustrated article considers the role of plain film examination of the adult patient with valvular heart disease caused by rheumatic heart disease. As stressed in Dr. Elliott's article in this symposium, the importance of interpreting anatomic information within the physiologic framework provided by assessing the pulmonary vasculature cannot be overemphasized.
BACKGROUND: Rheumatic heart disease is still a major health problem in developing countries such as India and, for the health planners to allocate funds, the actual prevalence of the disease should be known. This study aimed to assess the prevalence of rheumatic heart disease in rural school children in India. METHODS AND RESULTS: A total of 229,829 children between 6 and 18 years of age were screened as part of a school health program. All children with a valvar heart disease detected by the screening doctor were referred to a tertiary care center for evaluation by a cardiologist. The presence of cardiac lesions was confirmed by color Doppler examination. All children with known congenital heart disease were excluded from this study. A total of 374 children were found to have heart disease. Of these, 157 children were found to have rheumatic heart disease, confirmed by echocardiogram. Thus, the current prevalence of rheumatic heart disease is 0.68 per 1000 children. CONCLUSIONS: In the largest school survey conducted to date in India, we report the prevalence of rheumatic heart disease to be 0.68 per 1000 children. Our study suggests that there may have been a dramatic decline in the prevalence of rheumatic heart disease in India.
Three cases of chronic rheumatic heart disease with involvement of all four valves are presented. The involvement of tricuspid and pulmonary valves was suspected clinically and was confirmed by two-dimensional echo, Doppler, hemodynamic and angiographic findings. These findings were also verified surgically and histopathologically in 2 cases. One of the cases died after cardiac catheterization; the other 2 cases were treated surgically with success.
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Rheumatic fever and rheumatic heart disease can be prevented by simple methods of primary health care. Well-organized prevention programmes can be cost-effective. Lasting benefit depends on the maintenance of both local interest and financial support from governments.
OBJECTIVE: To describe the epidemiological and clinical features of acute rheumatic fever and rheumatic heart disease in the Top End of the Northern Territory. METHODS: A retrospective review (in some instances as far back as the 1960s) of all cases of known or suspected acute rheumatic fever or rheumatic heart diseases, with prospective validation of clinical status where necessary. Cases were ascertained from hospital and community medical clinic records and medical staff; and from records and health staff of 10 rural communities. RESULTS: Three hundred and eighty-six revised Jones criteria-confirmed episodes of acute rheumatic fever were documented in 249 individuals (99% Aboriginal). The annual incidence of confirmed acute rheumatic fever between 1989 and 1993 was 254 per 100,000 Aboriginal people aged 5 to 14 years. A more accurate estimate of 651 per 100,000 came from 10 rural communities with more complete information. As of 1995, there were 286 people living with established rheumatic heart disease (95% Aboriginal). The point prevalence of rheumatic heart disease among Aboriginal people was 9.6 per 1000, with a rate of 24 per 1000 in one large rural community. Sydenham's chorea was common, and associated with later rheumatic heart disease in 49% of cases. There was a preponderance of females with acute rheumatic fever, rheumatic heart disease and chorea. CONCLUSIONS: In Aboriginal people in rural northern Australia the incidence of acute rheumatic fever is higher than that reported anywhere in the world, and the prevalence of rheumatic heart disease is among the highest in the world. While continuing attention must be paid to alleviating the causes of these diseases of poverty, immediate action is needed to improve diagnosis of acute rheumatic fever, adherence to secondary benzathine penicillin prophylaxis regimens, and follow-up of rheumatic heart disease cases.
BACKGROUND: The incidence of rheumatic heart disease is great in Brazil. We analyzed the distribution of human leukocyte (HLA) antigens in a Brazilian population sample with rheumatic fever or rheumatic heart disease, with the aim of better understanding the mechanisms involved. METHODS AND RESULTS: HLA class I (A, B, and C) and class II (DR and DQ) antigen distribution was studied in 40 patients with diagnosis of rheumatic fever or rheumatic heart disease and compared with a control group of 617 healthy individuals for class I typing, from which 118 were drawn for class II typing. A strong correlation between rheumatic fever and rheumatic heart disease and HLA-DRw53 (72.9% in the disease group versus 39% in the control group: p = 0.00061, relative risk, 4.2; etiologic fraction, 0.43) was found. We also found an increase in the frequency of HLA-DR7 (57.5% in the disease group versus 26.3% in control group: p = 0.00715; relative risk, 3.8; etiologic fraction, 0.56). HLA class I and HLA-DQ typing did not point to any association with these diseases. CONCLUSIONS: HLA-DR7 and HLA-DRw53 are markers for susceptibility to rheumatic fever and rheumatic heart disease in Brazil. These results could be explained by genetic differences resulting from racial or geographical diversity.
UNLABELLED: Acute rheumatic fever (ARF) is a non-suppurative inflammatory disease after group A, beta haemolytic streptococcal pharyngitis. Certain individuals can develop ARF. This finding implies variability in host predisposition to ARF. A variety of studies have linked specific genetic markers with ARF or rheumatic heart disease (RHD) as a sequelae of ARF. For this purpose, we aimed to search the role of polymorphisms in Toll-like receptor-2 and -4 (TLR2 and TLR4) gene in Turkish patients with RHD. This study included a total 84 patients with RHD, ages ranging between 18 and 65, 25 male and 59 female, fulfilling the revised classification criteria of Jones. One hundred forty healthy unrelated persons were selected as a control group. Genotype analysis: DNA was extracted from whole blood. TLR4 gene (Asp 299Gly and Thr399Ile) and TLR2 gene (Arg753Gln and Arg677Trp) polymorphisms were genotyped by the previously reported method. STATISTICAL ANALYSIS: binary logistic regression models were used. Results were expressed as odds ratios (OR) with corresponding 95% confidence intervals (95% CI). Significant level was predefined at 0.05. There was a significant difference for carrying Ile allele in the 399 position in the patients compared to healthy controls (OR = 5.26, 95% CI, 1.40-19.73, p = 0.014). In the TLR4 gene, Asp 299Gly polymorphism did not reach to a statistically significant value (OR = 3.02). We found no Arg753Gln polymorphism of the TLR2 gene in the patient group. There were three heterozygote samples in the healthy group. We did not detect Arg677Trp polymorphism of the TLR2 gene in both patient and control groups.
We compared the incidence of rheumatic heart disease in elementary schoolchildren from low and high socioeconomic groups; children from one of the schools were rescreened 10 years later. The results showed that the incidence of rheumatic heart disease was significantly higher in low socioeconomic group but it is gradually declining.
Acute rheumatic fever (ARF) and its chronic valvular sequelae are the delayed consequence of a pharyngeal infection with group A Streptococcus (GAS). Several GAS proteins have been shown to be superantigens, raising the possibility that the expansion or deletion of T cells expressing specific Vbeta regions might play a role in the pathogenesis of ARF or chronic rheumatic heart disease (RHD). We therefore analyzed by four-color flow cytometry, the Vbeta repertoire on CD3, CD4 and CD8 T cells from four ARF patients, 10 RHD patients and also nine healthy controls. A selective depletion of Vbeta2+ T cells was found only in the CD8 subset of chronic RHD patients. This is of interest since a number of GAS superantigens exert their effects on Vbeta2+ cells and because only CD8+ T cells from ARF and RHD patients undergo anergy in response to GAS superantigens. Our results suggests that an ongoing immune process is present in RHD patients and that CD8+ T cells may have an important immunoregulatory role in the pathogenesis of the disease.
BACKGROUND: Rheumatic valvular disease has been reported to be associated with HLA antigens. To determine whether genetic factors could be involved in the pathogenesis of rheumatic heart disease (RHD), we analyzed the distribution of HLA-A, HLA-B, and HLA-DR antigens in Turkish patients with chronic rheumatic heart disease. METHODS AND RESULTS: The association of class I and class II HLA antigens was examined in 107 ethnic Turkish patients with chronic RHD. The diagnosis was supported by echocardiography, cardiac catheterization, angioventriculography, and histological findings in patients who underwent valve replacement. Two hundred three control subjects, also of Turkish origin, were chosen. The phenotypes B16, DR3, and DR7 were encountered in a significantly higher frequency in patients with RHD compared with the control population (corrected p < 0.05, p < 0.00005, and p < 0.0005, respectively). There also was a decrease in the antigen frequency of DR5 in patients compared with controls (corrected p < 0.005). CONCLUSIONS: The results are consistent with the hypothesis that susceptibility to RHD is genetically linked, and this in turn may be associated mainly with HLA class II antigens and weakly with class I antigens, with DR3, DR7, and B16 influencing susceptibility and DR5 conferring protection.
BACKGROUND: Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) occur at among the highest rates in the world in Aboriginal Australians of the Northern Territory. AIMS: To follow-up a previously-described cohort of Aboriginal children with RHD, in order to understand better the outcome of ARF and RHD in this population, and to identify areas where the impact of these diseases might be lessened METHODS AND RESULTS: Of a cohort of 33 children seen between 1980 and 1984, 27 survived until July, 1984. Twenty-five of the survivors were followed up for a mean of 10.6 years to a mean age of 24.1 years. The two deaths during follow-up were both due to RHD. Six people underwent valve replacement surgery; all were clinically healthy when last seen. Complications included two thromboembolic events and two episodes of endocarditis. Deterioration of RHD severity was associated with ARF recurrences (relative risk 3.6; 95% CI 1.7-7.6), and resolution of RHD was associated with having only mild valve lesions initially (risk difference 0.58; 95% CI 0.30 to 0.86). During follow-up, valve lesions tended either to resolve or to become more complex and severe, with a higher proportion of aortic valve lesions and multiple valve lesions. Of seven children with suspected past ARF, excluded from the original cohort because of normal cardiac findings at the time, three developed RHD, including one who died due to RHD and two with moderate or severe valve lesions. CONCLUSIONS: In Aboriginal Australians, poor outcomes of RHD are common, and are associated with ARF recurrences and early onset of more severe valve lesions. A coordinated ARF and RHD control programme is needed in this region, using a centralised register of patients, and concentrating on strategies to improve adherence to secondary prophylaxis regimens, better clinical care (including newer surgical techniques) and education of patients, families, and health staff.
AIMS: To investigate the involvement of enterovirus infection in chronic, rheumatic heart disease. METHODS AND RESULTS: Formalin-fixed, paraffin-embedded, surgical samples of valve tissue were examined for the presence of enteroviral RNA and virus capsid protein VP1 by in situ hybridization and immunostaining. Of 53 cases, 33 were patients with chronic rheumatic heart disease and 20 had Marfan's syndrome or degenerative valve disease. Enterovirus RNA was detected in 8 (24.2%) of 33 patients with chronic rheumatic heart disease by in situ hybridization using strand-specific oligonucleotide probes, complementary to conserved sequences in enterovirus genomic (positive strand) RNA. The replication template (negative strand) RNA also was found in seven of these eight cases. The viral capsid protein VP1 was detected in 16 (48.5%) of 33 patients with chronic rheumatic heart disease by immunohistochemistry and correlated with viral RNA detection. Virus was localized generally to valvular tissue. Neither viral RNA nor capsid protein VP1 were found in valvular tissue from any of the 20 comparison cases. CONCLUSIONS: This is the first demonstration of detection and localization of both enterovirus RNA and capsid protein in chronic rheumatic heart disease. The presence of negative strand RNA and VP1 indicates enteroviral RNA replication and protein synthesis and suggests an aetiological role of enterovirus in the pathogenesis of chronic rheumatic heart disease.
The features of rheumatic heart disease in 31 Nigerian children aged 5-11 years are presented. The majority of these children sought medical attention when they were in advanced cardiac failure. In approximately 23% of the children a past history of acute rheumatic fever was obtained. It is suggested that in developing countries, skin ulcers may be as important a focus of beta-haemolytic streptococcal infection as the throat is in developed countries in the aetiology of acute rheumatic fever. Rheumatic heart disease in developing countries present two main problems, namely, diagnosis and management including prophylaxis. The differential diagnosis of rheumatic heart disease in some tropical countries and the factors which affect the management of the disease are discussed.