Rheumatic Fever and its Cardiac Manifestations in Children: An Update
1981; King Faisal Specialist Hospital and Research Centre; Volume: 1; Issue: 2 Linguagem: Inglês
10.5144/0256-4947.1981.131
ISSN0975-4466
Autores Tópico(s)Cardiovascular Effects of Exercise
ResumoCurrent Concepts in MedicineRheumatic Fever and its Cardiac Manifestations in Children: An Update Mohamed K. MardiniMD Mohamed K. Mardini Pediatric Cardiologist, Department of Pediatrics, King Faisal Specialist Hospital and Research Centre Search for more papers by this author Published Online::1 Oct 1981https://doi.org/10.5144/0256-4947.1981.131SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutINTRODUCTIONRheumatic fever with its cardiac involvement remains a significant public health problem especially in developing countries and the Middle East. Rheumatic heart disease is considered one of the few, eminently fatal, acquired heart diseases that can be prevented.At the King Faisal Specialist Hospital and Research Centre, 30 percent of 296 pediatric patients who underwent cardiac catheterization had advanced forms of rheumatic heart disease. Forty-three percent of 58 patients of all ages who underwent surgery for open commissurotomy were 20 years of age or younger with a mean age of 15 years. This is a strikingly high incidence when compared with 1.3 percent of 1000 commissurotomies reported in 1956 in the United States.1In this article, a review of the subject, with a short discussion of our experience with this disabling disease, is presented giving special emphasis to treatment and long-term prophylaxis.PREVALENCE, MORBIDITY, AND MORTALITYRheumatic fever, with its cardiac manifestations, is a world-wide health problem. The prevalence rates of rheumatic heart disease in South America, Africa, Asia, and the Middle East are about 22 to 33 per 1000 in urban slum school children. In 1974, the incidence of rheumatic heart disease in Japan was approximately 0.1 per 1000 in school children, dropping from 1.3 per 1000 in 1962.2 In Sweden, the incidence dropped from 0.25 per 1000 in 1930 to 0.025 per 1000 in 1964.3 In India, between 1.5 and 39 per 1000 suffered rheumatic heart disease in 1976; this was attributed to low, socioeconomic overcrowding and poor sanitary conditions.In 1940, rheumatic heart disease was the leading cause of death in United States school children between the ages of 5 and 19 years. In 1971, the World Health Organization reported that the crude mortality rate of rheumatic heart disease varied from 1.6 in Switzerland, 8.0 in the United States, to 27.5 in Egypt, per 100,000 of the general population.2 The higher figures might be applicable to the populations in most Middle Eastern countries.EPIDEMIOLOGYFor the past 30 years, during any winter in the United States, cultures from 20 to 30 percent of school children with severe sore throat would grow beta hemolytic streptococcus. However, of those children with positive group A streptococcus (GrAS), only one to three percent contracting the disease would develop heart involvement.3,5 Thus, 8 to 32 percent of United States school children could be carriers and have positive throat cultures for hemolytic strep group A.2 In the general population, and during epidemics of strep infection, only three percent of individuals with group A streptococcal pharyngitis would contract rheumatic fever. However, in an endemic situation, the incidence is less than one percent.6 The majority of all patients with rheumatic fever developed the disease approximately 30 days of the date of streptococcal throat infection onset. If streptococcal infection could be recognized in the early stage, rheumatic fever would be virtually eliminated. Unfortunately, this is very difficult because about half of the patients who develop rheumatic fever have histories of asymptomatic throat infection.HLA antigen was studied in 20 patients with rheumatic valvular disease, but there was no significant difference in those patients as compared to controls.7 Further studies are needed to see if a correlation exists between the HLA inheritance and the occurrence of rheumatic heart disease.7PATHOGENESISThe pathogenesis of rheumatic fever is not well understood; however, the association between rheumatic fever and GrAS has been well recognized for the past 100 years.8 Rheumatic heart disease is one of the manifestations of rheumatic fever which cannot develop without being preceded by GrAS pharyngitis. Several hypotheses have been proposed to relate group A streptococcus to rheumatic fever. It has been speculated that the L-forms strep, which lack a cell wall and are not susceptible to penicillin, could perhaps remain within the cell then, later, revert to a pathogen in the development of acute rheumatic fever.9 Another hypothesis has been based on the observation that the serum level of the antistreptolysin S, which inhibits the activity of toxic streptolysin S substance, is decreased during the acute attacks of rheumatic fever.10-12 It has been assumed, therefore, that heart damage seen in rheumatic patients has been a result of streptolysin S accumulation. The hypothesis of the hypersensitivity reaction to streptococcal antigens, such as streptolysin O, that is toxic to the myocardium, is another. The antibody, antistreptolysin O, shows a significant increase in about three-quarters of patients with acute rheumatic attack. Autoimmune mechanism is the most recent, attractive, and acceptable hypothesis in the pathogenesis of acute rheumatic heart disease. It can be divided into three categories.The streptococcus, or its toxic products, could injure the myocardial cells; the injured cells, in turn, may act as a foreign antigen. Its antibody could then attack the myocardial fibers causing the rheumatic cardiac involvement.A limited number, 11 of 70, of such M-protein serotypes as C51, 27, M11, and M6 are present in the GrAS wall and share a common antigen with myocardial sarcolemma and smooth muscle of the blood vessels.13–16 Therefore, GrAS pharyngitis could produce cross-reactive antibodies against the myocardium as well as the smooth muscle of the blood vessels.17–19Goldstein demonstrated antibody cross-reactivity against GrAS and structural glycoprotein of the human and oxen heart valves. The presence of these antibodies in the serum of rheumatic heart patients has been documented.20G. E. Burch, et al. reported the coxsackie B-4 virus to be the cause and the GrAS to be the conditioning agent of acute rheumatic fever development.21,22 Other group B viruses also play a role in the development of acquired heart disease in children.23 The recurrence rates of rheumatic heart disease after GrAS pharyngitis is about 50 percent in C51 and 20 percent in serotype 17.24 Risk of further cardiac involvement increases with the number of attacks, which could be due to the subclinical cardiac involvement during the first attack. Cardiac involvement may become obvious with the recurrence of the disease.25EXPERIENCEAt the King Faisal Specialist Hospital and Research Centre (KFSH), most of the patients admitted with acute rheumatic fever had moderate to severe forms of rheumatic heart involvement. This could be due to the late referral to specialist, severe form of the disease, or the frequent and recurrent attacks within a short period of time. The frequent recurrence could be attributed to the prevalence of a very virulent GrAS in the country, the socioeconomic status of this group of people, or to the social custom of gathering more frequently than is seen in the Western world. Perhaps the most likely reason is the inappropriate treatment and inadequate use of penicillin prophylaxis, if it is used at all.ResearchA collaborative research project is in progress involving this Hospital, the University of Tennessee, Riyadh University, and Children's Hospital in Riyadh. Scientists at the University of Tennessee have succeeded in purifying M protein and making possible vaccine development for acute rheumatic fever prevention and thus, possible eradication of new cases of rheumatic heart disease.13'26Two hundred ninety-six congenital and acquired heart disease patients underwent cardiac catheterization from August 1976 through December 1979 at KFSH. Seventy-eight of those had rheumatic valve disease, 32 percent, which is similar to the incidence reported in India.4As a guideline for rheumatic fever diagnosis, we used the Jones criteria that was modified by the American Heart Association in 1955.27 Thirty percent of the rheumatic heart patients who underwent cardiac catheterization at this Hospital were children less than 16 years of age. Most had histories of two to six attacks of the disease within six months to three years before admission; some had apparent, continuous rheumatic activities over a period of months. Only 40 percent of these patients had positive histories of sore throat prior to attack. Other symptoms seen included fever, migratory joint pain and swelling, chest pain usually followed by dyspnea, and congestive heart failure. Generally, these patients do not seek medical help until the heart disease becomes incapacitating. When they do seek help, often during the second or third attack, they fail to comply with treatment regimen and penicillin prophylaxis as well as with general instructions. We have noted this from the histories of rheumatic heart patients initially treated outside KFSH. They tend to drop the long-term use of prophylaxis three to six months after the first attack.Most of the patients followed at this Hospital comply well with the full course of treatment, to long-term IM injections of penicillin, or other prophylactic measures. We feel that this is directly related to the time taken to instruct, properly, the patient and the family about the gravity of the disease, the improved prognosis following strict adherence to the established treatment regimen, as well as the interest showed to him by the entire Hospital staff.The majority of our pediatric patients are chronically ill and emaciated with significantly advanced rheumatic heart damage. Such a patient is generally admitted with severe, and sometimes intractable, congestive heart failure, respiratory difficulties, chronic liver disease, and failure to thrive. X-rays show an enlarged heart with cardio-thoracic ratio exceeding 65 percent. This sometimes indicates a situation in which the enlarged left atrium compresses the right, main-stem bronchus producing partial right, middle-lobe collapse, demonstrated by 30 of 78 pediatric patients. Figure 1. In addition, the left, main-stem bronchus was displaced posteriorly and upwardly by the tremendous increase in the size of the left atrial cavity. On M-mode echocardiogram, the left atrial diameter was twice, or more, the diameter of the aorta. We also used cross-sectional and M-mode echocardiography for evaluating the severity of the rheumatic mitral and aortic valve disease and evaluating left ventricular performance of critically ill patients with acute rheumatic carditis compared to normal subjects.28–30 Serologic tests differentiating between rheumatic and non-rheumatic mitral valve disease that has been described by S. T. Shulman and his group are not applicable in this Hospital.31 However, antistreptolysin titer (ASO), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) tests in acute and follow-up states of the disease have been helpful measures.Figure 1. A. Chest x-ray of a nine-year-old child with a history of rheumatic heart disease with frequent recurrent attacks since four years of age. Note the marked cardiomegaly with huge left atrium causing shelfing of the left main-stem bronchus and elevation with partial compression of the right main-stem bronchus with partial atelectasis of the right middle lobe. B. Following surgery for mitral valve replacement, the chest x-ray showed significant decrease in the total heart size especially in the left atrial size. Note the normal right main-stem bronchus.Download FigureFigure 2. A. Left ventricular (LV) cineangiogram of the same patient in systole (LVS). B. The patient in diastole (LVd). These demonstrate the significant degree of the left atrial (LA) enlargement with severe degree of mitral regurgitation.Note that the aortic route is faintly delineated.Download FigureAt KFSH, there was a total of 281 patients with rheumatic heart disease who underwent cardiac catheterization from February 1976 through December 1979. Table 1. Of those, 78 were pediatric patients (range 6 to 16 years; mean age 12 years) and 203 adults. In the pediatric patients, the mitral regurgitation lesion alone (33 percent) or in association with aortic regurgitation (14 percent) were the most frequent lesions. The incidence of mitral stenosis alone or in association with other valve lesions in our pediatric age group was 15 percent. This is an extremely high figure compared with a two to three percent incidence seen in the United States and Norway.32 The incidence of aortic regurgitation lesions is ten percent, that is less than the incidence of mitral stenosis. In adults, the incidence of mitral stenosis lesion is 26 percent constituting the most prevalent rheumatic heart lesion. The second most frequently occurring lesion in our adult patients is the mitral regurgitation lesion with 19 percent incidence. In the 282 adult and pediatric patients, mitral stenosis alone or in association with other valve lesions (32 percent) is the most frequently occurring rheumatic valve lesion. This is followed by isolated mitral regurgitation (23 percent) and isolated aortic regurgitation (15 percent).Table 1. Cardiac catheterization from February 1976 through December 1978 at King Faisal Specialist Hospital of 281 patients with rheumatic valve diseases. Total number of pediatric cardiac catheterizations during the same period was 296. (Incidence of rheumatic heart disease was 30 percent of the total pediatric catheterized patients.)Table 1. Cardiac catheterization from February 1976 through December 1978 at King Faisal Specialist Hospital of 281 patients with rheumatic valve diseases. Total number of pediatric cardiac catheterizations during the same period was 296. (Incidence of rheumatic heart disease was 30 percent of the total pediatric catheterized patients.)Sixty-one of the 78 catheterized pediatric patients with rheumatic valve disease underwent open-heart surgery during the period between May 1978 (when the Baylor Open-Heart Surgery Program began at this Hospital) and January 1980. Table 2.Table 2. King Faisal Specialist Hospital open heart surgery for valve anuloplasty, commissurotomy, and replacement on 61 of 78 pediatric patients with rheumatic valve disease, May 1978 through January 1980Table 2. King Faisal Specialist Hospital open heart surgery for valve anuloplasty, commissurotomy, and replacement on 61 of 78 pediatric patients with rheumatic valve disease, May 1978 through January 1980Forty-nine of the 61 surgical patients (80 percent) had single valve surgery whereas 12 (20 percent) required multiple valve surgery. Thirty-seven patients (60 percent) required prosthetic single valve replacement with or without the need for repair of the other valves. Three patients (5 percent) required aortic and mitral valve replacement with prosthetic valves.The high number of patients that required valve replacement is discouraging, in a potentially preventable disease, considering the short- and long-term complications of all the artificial valves that are available on the market. The high incidence of mitral valve stenosis, 13 of 61 (21 percent), in our pediatric patients with rheumatic valve disease requiring commissurotomies, is striking. At this Hospital 58 patients of all ages underwent surgery for open-heart commissurotomy from May 1978 through January 1980. Twenty-five of 58 patients were 20 years of age or less with a mean age of 15 years. This is an incidence of 43 percent which is significantly high when compared with only 1.3 percent of 1000 commissurotomies reported in 1956 in the United States in patients of less than 20 years of age.1 This figure, however, is even less than the 34 percent of 373 commissurotomies reported in Southern India.33 Tight mitral stenosis has never been a common lesion in children in the Western world. The occurrence of mitral stenosis in the younger age group seen in the Eastern and tropical countries would pose the question as to whether there are two different diseases with different etiologies, or is it related to a more virulent M-protein serotype seen here?One of the youngest patients who underwent commissurotomy at this Hospital was diagnosed at the age of eight years and had the procedure done at age nine years. Double mitral and aortic valve replacement surgery was performed on two young children, one nine and another ten years of age. A seven-year-old patient underwent mitral valve repair and then, within a few days, replacement as a result of severe, postoperative hemolysis.PATHOLOGYRheumatic heart disease may present in unusual ways. It may involve the conduction pathway causing complete A-V block, as was seen in one of our 78 pediatric patients, Wolff-Parkinson-White syndrome during acute rheumatic carditis, sinus node suppression, and trifascicular block. Other possibilities include constrictive pericarditis and endomyocardial fibrosis.35–39A seven-year-old boy presented to us with pericardial tamponade; open pericardial drainage revealed old blood. This patient required long-term intensive care measures because of severe congestive heart failure and poor myocardial function in association with mitral and aortic valve disease. Another of our pediatric patients presented with rheumatic carditis and pneumonitis which responded only to corticosteroid treatment.The pathologic, myocardial, and valvular changes in rheumatic fever have been well described as having cell degeneration, transformation into variety of cells, regeneration, and subsequently, fibrosis.40 The description and incidence of Aschoff cells and bodies have also been widely reviewed.40–42PREVENTIONRheumatic heart disease is considered to be one of the few acquired chronic heart diseases with morbidity and mortality that can be prevented. Proper and early diagnosis and treatment of GrAS throat infection can, to some extent, prevent rheumatic fever and carditis. Unfortunately, 40 to 50 percent of rheumatic patients may have had subclinical or asymptomatic throat infections which make prevention of the initial attack much more difficult. However, once the patient has clinical manifestations of exudative pharyngitis, without evidence of viral upper respiratory infection such as hoarseness, conjunctivitis, and cough, he should have the throat cultured and begin oral penicillin therapy at the same time. This is especially important with the very sick, walk-in, or unreliable patient.34 If the results of the culture are positive for GrAS, oral penicillin treatment should continue for a total period of ten days or, preferably, a single IM injection of long-acting benzathine penicillin should be given. If the culture is negative, penicillin should be stopped. However, in a compliant, reliable patient, it is safer to delay treatment until diagnosis is confirmed. A few days' delay in starting treatment is not harmful in preventing the first attack of rheumatic fever.43If a dependable laboratory is unavailable, a single IM injection of benzathine penicillin should be given at the time of diagnosis, even without the throat culture. Erythromycin or lincomycin, in appropriate dosages, should be given to patients who are allergic to penicillin, if no strep resistance to the drugs has been reported in that area.34 Sulfonamides and tetracyclines should not be used for treatment of strep pharyngitis.44The incidence of anaphylactic shock to penicillin is about one per 50,000. Routine penicillin skin tests, performed on all new patients at this Hospital, may decrease this already low occurrence.Tonsillectomy occasionally may be helpful in patients with recurrent tonsillitis of GrAS origin, in spite of penicillin prophylaxis. Vaccination against GrAS, that may become available in the near future, would be another, effective means of prevention and probable eradication of rheumatic heart disease. Extensive and exciting work has been done in this field by E. H. Beachey and his associates.13,14,26It is essential for the patient with valve disease to maintain oral hygiene with adequate dental care. Bacteremia can easily originate in the mouth and cause subacute endocarditis. Antibiotic prophylaxis to prevent subacute endocarditis should be given for routine dental procedures, bronchoscopy, tonsillectomy, and adenoidectomy. It is also advisable for minor surgery of infected tissues, genitourinary tract and gastrointestinal manipulation, or major surgery. The dosages and schedule should be given according to the recommendations of the American Heart Association.*TREATMENTMedicalOnce a patient contracts rheumatic fever, he should be started on a long-term penicillin prophylaxis regimen in order to prevent recurrence of the disease and further damage to the myocardium and valves. Life-long prophylaxis is recommended because episodes of rheumatic fever have been noted in patients up to 36 years of age as well as recurrences up to 20 years following the initial mitral lesion.4 Also, mitral stenosis can occur after recurrent attacks of subclinical rheumatic heart disease, but none of the patients who received this prophylaxis developed mitral stenosis.45 In addition, following regular IM injections of benzathine penicillin, 70 percent of the patients with acute mitral regurgitation lost their murmurs from four days to eight and one-half years after first being heard.45Benzathine penicillin, given IM every 21 days, is a more acceptable schedule in the Middle Eastern countries than the monthly injection recommended in the West. It better maintains adequate blood levels and prevents reinfection in crowded, low socioeconomic surroundings.46 In unpublished data collected by the author while practicing in Lebanon, about 15 percent of patients receiving the monthly injections had recurrences of rheumatic fever. Only two of 78 (three percent) rheumatic patients seen at this Hospital who were receiving the injections every 21 days had recurrences.Although oral penicillin V prophylaxis (250 mg twice daily) can be as affective as injections, patients are often noncompliant so this is not the preferred therapy. Table 3 gives the recommended dosages for benzathine penicillin injections and penicillin alternatives.Table 3. Recommended dosages for penicillin injections and penicillin alternatives for rheumatic heart disease prophylaxis.Table 3. Recommended dosages for penicillin injections and penicillin alternatives for rheumatic heart disease prophylaxis.Compliance is a real problem and often the patient refuses or discontinues permanent prophylactic therapy. In this case, every effort should be made to keep him on the treatment plan for a minimum of five years from the time the murmur disappeared. For maximum benefit, the prophylaxis should be continued indefinitely but, at a minimum, it should not be discontinued before the patient reaches the age of 21 years.At this Hospital, the treatment of choice for acute rheumatic fever, with or without acute carditis but no cardiomegaly or with mild mitral regurgitation, has been salicylates, 60 to 120 mg/kg per day for a period of six weeks to three months, keeping the serum salicylate level at 20 to 30 mg%. In cases such as carditis with cardiomegaly, moderate to severe mitral or any degree of aortic valve involvement with or without congestive heart failure, prednisone two milligrams per kilogram per day, or 40 to 60 mg/m2 for 7 to 15 days, tapering off over a period of four to six weeks. We have encountered three patients who were prednisone-dependent, and all three required a combination of prednisone and aspirin. In this situation, when prednisone is tapered off and aspirin is started, aspirin should be given for six weeks to three months after the discontinuation of prednisone. The clinical response of the patient in association with improved serology test results, such as ESR, CRP, and ASO, are helpful means to assess the index of activities of the disease.Bed RestBed rest for acute rheumatic fever is still a controversial issue which is difficult to accomplish in early childhood. Our patients with polyarthritis, with or without carditis but neither cardiomegaly nor congestive heart failure, are allowed limited bedroom activities and bathroom privileges. As soon as they are free of joint symptoms, they are allowed routine, indoor activities. They are not allowed to resume full activities until they have been off treatment for two weeks without evidence of rebound.Patients with significant cardiomegaly, valve disease, and congestive heart failure should be on strict bed rest until the congestive heart failure is under control and the patient is out of the toxic state. This may take one to two weeks. Then, the patients are allowed bedroom activities and bathroom privileges for another one to two weeks. Finally, routine indoor activities are allowed for another two to three weeks and the patient may return to school two to three weeks after successful medical treatment without evidence of rebound.SurgicalSurgery is far from the optimum in providing definite relief for very advanced and disabling, end-stage carditis. Under certain conditions, surgery has a considerable short- and long-term rate of morbidity and mortality. To date, no ideal heart valve prosthesis is available. All surgical patients, with or without valve replacement, should continue on penicillin prophylaxis after surgery. These patients should also be instructed of the need for subacute endocarditis prophylaxis.Surgical indications for valve surgery have been a controversial but widely reviewed issue. 48–55SUMMARYThe high incidence of rheumatic fever and rheumatic heart disease continue to be a serious public health problem in developing countries. In Saudi Arabia, we observe the most severe form of the disease, with the complications that occur in the younger age group no longer seen in the Western world. This disease, therefore, could be called the juvenile “malignant” form.The majority of patients do not seek medical help until they have several recurrences and subsequently develop advanced stage heart involvement. This disease, with its high morbidity and mortality, is still preventable. Prevention can be achieved by emphasizing the importance of proper treatment of GrAS pharyngitis and early diagnosis and treatment of rheumatic fever. Patients and families should be properly instructed concerning the importance of long-term penicillin prophylaxis for prevention of the disease and development of its complications.Polyvalent GrAS vaccine, that is under intensive investigation, is another means of prevention and probable eradication of the disease which may become available in the near future.* The American Heart Association recommendations for dosages and schedule as applied at KFSH are available from the Hospital upon request.ARTICLE REFERENCES:1. Bailey CP, Bolton HE: "Criteria for and results of surgery for mitral stenosis" . NY State J Med 56:8251956. Google Scholar2. Shiokawa Y, Yamada T: "Epidemiology of rheumatic fever and rheumatic heart disease with surveillance of hemolytic streptococcus" . Jpn Cir J 41(2): 167–731977. Google Scholar3. Sievers J, Hall P: "Incidence of acute rheumatic fever" . Br Heart J 33(6):833–361971. Google Scholar4. Bhattacherjee TD, Kundu SC: "Profile of rheumatic heart diseases in India (editorial)" . J Indian Med Assoc 67(3): 78–801976. Google Scholar5. Gharagozloo RA, Daneshpajooh M, Ghavamian P: "Rheumatic fever and rheumatic heart disease among 56,800 inhabitants in southeast Teheran from 1972-1974" . Acta Trop (Basel) 33(3):215–221976. Google Scholar6. Ayoub EM: "How long should prophylaxis against rheumatic fever be continued?" Clin Pediat 9: 503–041970. Google Scholar7. Matsumori A, Hirose K, Walabayashi A, et al.: "HLA in hypertrophic cardiomyopathy and rheumatic heart disease" . Jpn Cir J 43:445–491979. Google Scholar8. Fleming PR: "Recognition of rheumatic heart disease" . Br. Heart J 39(10): 1045–501977. Google Scholar9. Joorabchi B: "Pathogenesis of rheumatic fever" . Clin Ped 8:4051969. Google Scholar10. Todd EW, et al.: "Anti-streptolysin S titers in rheumatic fever" . Lancet 2:12131939. Google Scholar11. Stollerman GH, Bernheimer AW: "Inhibition of streptolysin S by the serum of patients with rheumatic fever and acute streptococcal pharyngitis" . J Clin Invest 29:11471950. Google Scholar12. Hirschhorn K, et al.: "The action of streptolysin S on peripheral lymphocytes of normal subjects and patients with acute rheumatic fever" . Proc Natl Acad Sci USA 52:11511964. Google Scholar13. Beachey EH, Stollerman GH, Bisno AL: "A strep vaccine: how close?" Hosp Pract 14(11):49–571979. Google Scholar14. Beachey EH, Stollerman GH, Chiang EY, et al.: "Purification and properties of M protein extracted from group A Streptococci with pepsin: covalent structure of the amino terminal region of type 24 M antigen" . J Exp Med 145(6): 1469–831977. Google Scholar15. Kaplan MH, Dallenbach FD: "Immunologic studies of heart tissues, III. Occurrence of bound gamma-globulin in auricular appendage from rheumatic hearts; relationship to certain histopathologic features of rheumatic heart disease" . J Exp Med 113: 11961. Google Scholar16. Zabriskie JB, et al.: "An immunological relationship between streptococcal membranes and human heart tissue" . Fed Proc 23:3421964. Google Scholar17. Van de Rijn I, Zabriski JB, McCarey M: "Group A streptococcal antigens cross-reactive with myocardium. Purification of heart-reactive antibody and isolation and characterization of the streptococcal antigen" . J Exp Med 146(2): 579–991977. Google Scholar18. Hosein B, McCarty M, Fischetti VA: "Amino acid sequence and physico-chemical similarities between streptococcal M protein and mammalian tropomyosin" . Proc Natl Acad Sci USA 76(8):3765–681979. Google Scholar19. Kumagai N: "Rheumatic fever and streptococcal infection anti-streptococcal antibodies in rheumatic fever and rheumatic heart disease" . Jpn Cir J 39:167–681975. Google Scholar20. Goldstein I, et al.: "Immunological relationship between streptococcus polysaccharide and the structural glycoproteins of heart valve" . Nature (London) 213:441967. Google Scholar21. Burch GE, Giles TD, Colcolough HL: "Pathogenesis of "rheumatic" heart disease: critique and theory" . Amer Hear J 80:556–611970. Google Scholar22. Burch GE, Giles TD: "The role of viruses in the production of heart disease" . Am J Cardiol 29:231–401972. Google Scholar23. Pongpanich B, Na Ayuthya PS, Jayavasu J, et al.: "Coxsackie group B virus and acquired valvular heart disease in children" . J Med Assoc Thai 59(10): 452–561976. Google Scholar24. Kuttner AG, Krumweide E: "Observations of the effect of streptococcal upper respiratory infections on rheumatic children" . A three-year study. J Clin Invest 20:273–871941. Google Scholar25. Leonard R, Wenger NK: "Rheumatic fever without clinical evidence of carditis" . Amer J Dis Child 111:5331966. Google Scholar26. Beachey EH, Stollerman GH, Johnson RH, et al.: "Human immune response to immunization with a structurally defined polypeptide fragment of streptococcal M protein" . J Exp Med 150(4): 862–771979. Google Scholar27. Jones TD: The diagnosis of rheumatic fever. JAMA 126:4811944. Google Scholar28. Umeda T, Kuwako K, Machii K: "M-mode and cross-sectional echocardiographic evaluation of rheumatic mitral valve disease" . Jpn Cir J 43:297–3041979. Google Scholar29. Lewis BS, Geft IL, Milo S, et al.: "Echocardiography and valve replacement in the critically ill patient with acute rheumatic carditis" . Ann Thorac Surg 27(6): 529–351979. Google Scholar30. Conetta DA, Christie LG, Wise DE, et al.: "Echocardiography analysis of systolic and diastolic left ventricular wall motion in normal man" . Chest 76(1):76–821979. Google Scholar31. Shulman ST, Ayoub EM, Victorica BE, et al.: "Differences in antibody response to streptococcal antigens in children with rheumatic and non-rheumatic mitral valve disease" . Circulation 50:1244–511974. Google Scholar32. Chartikavanij K: Juvenile mitral stenosis. World Congress of Cardio (London) 1970 p 27. Google Scholar33. Cherian G, Vytlingam KI, Sukumar IP, et al.: "Mitral valvotomy in young patients" . Br Heart J 26:1571964. Google Scholar34. DiSciascio G, Taranta A: "Rheumatic fever in children" . Am Heart J 99(5): 635–581980. Google Scholar35. Kamiya T, Nishioka K, Nakano H, et al.: "A case of transient complete A-V block and WPW syndrome during acute rheumatic carditis" ., Jpn Cir J 41:1821977. Google Scholar36. Singhi S, Shrivastava S: "Sinus node suppression in acute rheumatic carditis. A case report" . Indian Heart J 31(5): 305–81979. Google Scholar37. Altieri PI, Johnson C, Crenshaw RP, et al.: "Rheumatic carditis causing acute trifascicular block" . Bol Asoc Med PR 63(12):323–261971. Google Scholar38. Aryanpur I, Raafat F, Zangeneh F: "Rheumatic valvulitis and constrictive pericarditis" . Report of case. Jpn Heart J 16(6): 749–551975. Google Scholar39. Bijlsma F: "Endomyocardial fibrosis and rheumatic heart disease in Mozambique" . Trans R Soc Trop Med Hyg 73(6):661–621979. Google Scholar40. McDonald HG, Calkins HE: "Degeneration of cardiac muscle followed by cell transformation, regeneration and fibrogenesis in rheumatic fever" . Exp Path Bd 15:185–951978. Google Scholar41. Roberts WC, Virmani R: "Aschoff bodies at necropsy in valvular heart disease. Evidence from an analysis of 543 patients over 14 years of age that rheumatic heart disease, at least anatomically, is a disease of the mitral valve" . Circulation 57(4):803–071978. Google Scholar42. Soloff LA: "Letter to the editor" . Circulation 56(3):499–5001977. Google Scholar43. Catanzaro FJ, Rammelkamp CH, Chamovitz R: "Prevention of rheumatic fever by treatment of streptococcal infections. II. Factors responsible for failures" . N Engl J. Med 259:511958. Google Scholar44. Brink WR, Rammelkamp CH, Denny FW, et al.: "Effect of penicillin and aureomycin on the natural course of streptococcal tonsillitis and pharyngitis" . Am J Med 10:3001951. Google Scholar45. Tompkins DG, Boxerbaum B, Liebman J: "Long-term prognosis of rheumatic fever patients receiving regular intramuscular benzathine penicillin" . Circulation 45(3): 543–511972. Google Scholar46. Padmavati S: "Rheumatic fever and rheumatic heart disease in developing countries" . Bull WHO 56(4): 543–501978. Google Scholar47. Keith JD: Rheumatic fever and rheumatic heart disease. In: Keith JD, Rowe RD, Vlad P, eds: Heart Disease in Infancy and Childhood. New York, Macmillan Publishing Co. Inc., 1978 pp 203–31. Google Scholar48. Smith HJ, Neutze JM, Roche AHG, et al.: "The natural history of rheumatic aortic regurgitation and the indications for surgery" . Br Heart J 38:147–541976. Google Scholar49. Weir EK, Matisonn RE, Smith AS, et al.: "Value replacement for rheumatic aortic incompetence in adolescents" . Thorax 33: 608–111978. Google Scholar50. Bonchek LI: "Indications for surgery of the mitral valve" . Am J Cardiol 46:155–581980. Google Scholar51. Fowler NO, Van Der Bel-Kahn JM: "Operations on the mitral valve: a time for weighing the issues" . Am J Cardiol 46:159–621980. Google Scholar52. Fowler NO, Van Der Bel-Khan JM: "Indications for surgical replacement of the mitral valve. With particular reference to common and uncommon causes of mitral regurgitation" . Am J Cardio 44:148–571979. Google Scholar53. Merin G, Simcha A, Gotsman , et al.: "Surgery of rheumatic tricuspid valve disease in children" . J Cardiovasc Surg 17:306–131976. Google Scholar54. Sheikhzadeh A, Tarbiat S. Paydar D, et al.: "Rheumatic tricuspid stenosis" . A clinical overview Acta Cardiol 33(6):431–421978. Google Scholar55. Manabe H, Oyama C, Kitamura S, et al.: "Valvotomy in young patients with rheumatic mitral stenosis" . Ann Thorac Swrg 23(3):245–481977. Google Scholar56. Chen SC, Laks H, Fagan L, et al.: "Valve replacement in children" . Circulation (Suppl 2) 56(3): 117–211977. Google Scholar57. Strauss AW: "Valve replacement in acute rheumatic heart disease. (Editorial.)" . / Pediatr 84(5): 786–871974. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 1, Issue 2October 1981 Metrics History Published online1 October 1981 KeywordsStreptococcus group AMitral valve insufficiencyAortic valve insufficiencyRheumatic heart diseaseRheumatic feverBenzathine penicillinACKNOWLEDGEMENTSThe author wishes to acknowledge information obtained from the Baylor Heart Team participating in the Open-Heart Surgery Program at King Faisal Specialist Hospital and Research Centre.InformationCopyright © 1981, Annals of Saudi MedicinePDF download
Referência(s)