child to include the entire family, and not just for a year but for years to come. If obesity is induced simply, beyond the breast and into the bottle, then it can be prevented simply, as an exercise in early nutritional program¬ ming. If obesity is learned at the level of the family, the group, or the culture, then both prevention and therapy are more complicated. The pediatrician may then have to serve not just as physician for the child, but as physician and advisor to the family as a whole. STANLEY M. GARN, PHD Center for Human Growth and Development and Nutrition Unit School of Public Health University of Michigan 1111 E Catherine St Ann Arbor, MI 48109 or
Prolonged In
References 1. Garn SM, Clark DC, Ullman BM: Does obesity have a genetic basis in man? Ecol Food Nutr 4:57-60, 1975. 2. Eid EE: Follow-up study of physical growth of children who had excessive weight gain in first
six months of life. Br Med J 2:74-76, 1970. 3. Fisch RO, Bilek MK, Ulstrom R: Obesity and leanness at birth and their relationship to body habitus in later childhood. Pediatrics 56:521-527, 1975. 4. Abraham S, Lowenstein FW, Johnson CL: Preliminary Findings of the First Health and Nutrition Examination Survey, United States, 1971-1972: Dietary Intake and Biochemical Findings, publication (HRA) 74-1219. US Dept of Health, Education, and Welfare, 1974. 5. Hirsch J: Cell number and size as a determinant of subsequent obesity, in Winick M (ed): Symposium on Childhood Obesity. New York, Interscience Publishers Inc, 1975, pp 15-21. 6. Stunkard A, d'Aquili E, Fox S, et al: Influence of social class on obesity and thinness in children. JAMA 221:579-584, 1972.
SM, Clark DC, Guire KE: Growth, body and development of obese and lean children, in Winick M (ed): Symposium on Childhood Obesity. New York, Interscience Publishers Inc, 1975, pp 23-46. 8. Garn SM, Clark DC: Family-line origins of obesity, in Barness L (ed): Report of the Second Wyeth Nutrition Symposium. New York, Wyeth Laboratories, 1976. 9. Withers RFJ: Problems in the genetics of human obesity. Eur Rev 56:81-90, 1964. 10. Garn SM, Clark DC: Trends in fatness and the origins of obesity. Pediatrics, to be published. 11. Mason E: Obesity in pet dogs. Vet Rec 86:612-616, 1970. 12. Garn SM, Clark DC: Nutrition, growth, development and maturation: Findings from the Ten-State Nutrition Survey of 1968-1970. Pediatrics 56:306-319, 1975. 7. Garn
composition
PR Index in Rheumatic Fever
1920 Parkinson et al,1 and in 1924 Cohn and Swift,2 observed an association of acute rheumatic fever and prolongation of the PR interval of the electrocardiogram. Ziegler3 has noted that the PR interval is prolonged in 2% of normal children. Because the PR interval varies with age and heart rate, Mirowski et al4 devised the PR index to provide a standard by which the duration of the PR interval of a subject may be judged. A value greater than 1.0 is considered evidence of delay in atrioventricular (AV) conduction. In 1965, the revised Jones criteria5 listed prolongation of the PR interval as one of the minor criteria used in establishing the diagnosis of rheumatic fever. Other conduction abnormalities may be observed. These include second-degree heart block, complete heart block, AV dissociation, and junctional rhythm. Clarke and Keith6 detected AV conduction abnormalities in 84% of 508 patients with acute rheumatic fever.
On page 473 of this issue of the Journal, Sanyal et al report on a prospective study of 118 children with rheumatic fever, 44 normal children, and 25 febrile children to determine the frequency of occurrence of prolon¬ gation of the PR index. They subdi¬ vided the children into groups on the basis of presence of arthritis, chorea, or carditis. They observed that as a group, children with rheumatic fever had a greater frequency of prolonga¬ tion of AV conduction than found in normal children or in children with a febrile illness, as has been observed by others.'" Sanyal et al observed a significantly greater frequency of a prolonged PR index in patients with carditis than without. In contrast, Clarke and Keith6 and Feinstein et al7 concluded that there was no difference in the frequency of prolongation of the PR index in their rheumatic patients with or without carditis. Feinstein and DiMassa8 observed that the PR index was prolonged in 33% (average of
their two carditis groups) of patients with carditis and 28% of those with "no valvulitis." Mirowski et al4 report that the frequency of first-degree heart block was 40% in patients with rheumatic carditis and 33% in patients with polyarthritis. The frequency of a prolonged PR index observed by Feinstein and DiMassa,8 Mirowski et al," Clarke and Keith,6 and Sanyal et al in patients with carditis was 33%, 40%, 72%, and 53%, respectively. The occurrence of prolongation of AV conduction in patients without carditis observed by these same authors was 28%, 33% 73%, and 18%, respectively. One notes the relatively wide variation in frequency of prolonged PR index by these authors. Only in the study of Sanyal et al was a significant difference in the frequency of occurrence a prolonged PR index observed between patients with and without rheumatic carditis. In these four studies the occurrence of prolongation of the PR index varied widely in the carditis and noncarditis
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 06/08/2015
explanation for the varia¬ tion in the findings of these authors is unclear. Markowitz and Kuttner" have sum¬ marized some of the data on the changing pattern of rheumatic fever. In 1960, Bland1" commented on the decline in the severity of rheumatic carditis as observed over the previous four decades, and on the eightfold reduction in mortality. Wegman11 has tabulated the death rates from rheu¬ matic heart disease and rheumatic fever from many countries and noted the marked variation in death rates. Significant differences in prevalence rates of rheumatic heart disease among schoolchildren within the United States have been reported.'' Wilson et al'- reported that the recur¬ rence rates of rheumatic fever de¬ clined over a 20-year period from 1936 to 1956 among 782 patients. This same report concluded that the recurrence rates were greater for persons living in poorer environmental circum¬ groups. The
stances.
The study of Sanyal et al was under¬ taken in India. One may only specu¬ late as to what factors are involved in accounting for the greater frequency of prolongation of the PR index
observed by them in patients with carditis than in patients without carditis. Perhaps there are geograph¬ ical differences in the incidence of a prolonged PR index associated with acute rheumatic fever. Sanyal et al13 have emphasized the high incidence of carditis in particular countries in contrast to others. The frequency of carditis observed as a manifestation of rheumatic fever may range from 33% to 83%. Usually, a prospective study is more precise in identifying certain manifestations that are looked for on a systematic basis rather than by incidental observation. It is also probable that a greater accuracy was achieved in making measurements of the PR interval during recent studies, and that more frequent ECGs were obtained during the acute phase of rheumatic fever. Cristal et al14 observed AV dissocia¬ tion in 14 of 70 young adults with acute rheumatic fever. Dissociation occurred in 11 of the 14 patients during a first attack of rheumatic fever. Carditis, as established by Jones criteria, was diagnosed in only four of the 14 patients. The authors concluded that although the arrhyth¬ mia suggested a myocardial effect of
the rheumatic process, it did not corre¬ late with "carditis." Since patients with prolongation of the PR interval without carditis have recovered completely, and because of the apparent nearly equal frequency of occurrence in patients with and without carditis, it has been suggested previously that a prolonged PR index is not a specific manifestation of carditis. The investigation of Sanyal et al does not attempt to establish a cause-effect relationship. Regardless of the explanation of the differences among these studies, pro¬ longation of the PR index in a patient with symptoms and signs of rheu¬ matic fever should greatly increase one's suspicion of the diagnosis. The study of Sanyal et al may suggest a closer association of prolonged PR index and carditis. I believe additional prospective studies in several coun¬ tries may be necessary to clarify this
relationship.
GEORGE BENZING III, MD Department of Pediatrics Division of Cardiology Children's Hospital University of Ohio Cincinnati, OH 45229
References 1. Parkinson J, Gross AH, Gunson EB: The heart and its rhythm in acute rheumatism. Q J Med 13:363-367, 1920. 2. Cohn AE, Swift HF: Electrocardiographic evidence of myocardial involvement in rheumatic fever. J Exp Med 39:1-5, 1924. 3. Ziegler RF: Electrocardiographic Studies in Normal Infants and Children. Springfield, Ill, Charles C Thomas Publisher, 1951, pp 35-45. 4. Mirowski M, Rosenstein BJ, Markowitz M: A comparison of atrio-ventricular conduction in normal children and in patients with rheumatic fever, glomerulonephritis, and acute febrile illness. Pediatrics 33:334-340, 1964. 5. Jones criteria (modified) for guidance in the diagnosis of rheumatic fever, Council on Rheu-
matic Fever and Congenital Heart Disease of the American Heart Association. Circulation 32:664\x=req-\ 668, 1965. 6. Clarke M, Keith JD: Atrioventricular conduction in acute rheumatic fever. Br Heart J 34:472-479, 1972. 7. Feinstein AR, Harrison FW, Spagnuolo M, et al: Rheumatic fever in children and adolescents. Ann Intern Med 60(suppl 5):87-123, 1964. 8. Feinstein AR, DiMassa R: Prognostic significance of valvular involvement in acute rheumatic fever. N Engl J Med 260:1001-1007, 1959. 9. Markowitz M, Kuttner AG: Rheumatic Fever. Philadelphia, WB Saunders Co, 1965, pp 1-8.
10. Bland EF: Declining severity of rheumatic fever. N Engl J Med 262:597-599, 1960. 11. Wegman ME: Some international aspects of rheumatic fever. Pediatrics 15:627-630, 1955. 12. Wilson MG, Lim WN, Birch AM: Decline of rheumatic fever: Recurrence rates of rheumatic fever among 782 children for 21 consecutive calendar years (1936-56). J Chronic Dis 7:183-190, 1958. 13. Sanyal SK, Thapar MK, Ahmed SH, et al: The initial attack of acute rheumatic fever during childhood in North India. Circulation
49:7-12, 1974.
14. Cristal N, Stern J, Gueron M: Atrioventricular dissociation in acute rheumatic fever. Br Heart J 33:12-15, 1971.
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 06/08/2015
Prolonged In
References 1. Garn SM, Clark DC, Ullman BM: Does obesity have a genetic basis in man? Ecol Food Nutr 4:57-60, 1975. 2. Eid EE: Follow-up study of physical growth of children who had excessive weight gain in first
six months of life. Br Med J 2:74-76, 1970. 3. Fisch RO, Bilek MK, Ulstrom R: Obesity and leanness at birth and their relationship to body habitus in later childhood. Pediatrics 56:521-527, 1975. 4. Abraham S, Lowenstein FW, Johnson CL: Preliminary Findings of the First Health and Nutrition Examination Survey, United States, 1971-1972: Dietary Intake and Biochemical Findings, publication (HRA) 74-1219. US Dept of Health, Education, and Welfare, 1974. 5. Hirsch J: Cell number and size as a determinant of subsequent obesity, in Winick M (ed): Symposium on Childhood Obesity. New York, Interscience Publishers Inc, 1975, pp 15-21. 6. Stunkard A, d'Aquili E, Fox S, et al: Influence of social class on obesity and thinness in children. JAMA 221:579-584, 1972.
SM, Clark DC, Guire KE: Growth, body and development of obese and lean children, in Winick M (ed): Symposium on Childhood Obesity. New York, Interscience Publishers Inc, 1975, pp 23-46. 8. Garn SM, Clark DC: Family-line origins of obesity, in Barness L (ed): Report of the Second Wyeth Nutrition Symposium. New York, Wyeth Laboratories, 1976. 9. Withers RFJ: Problems in the genetics of human obesity. Eur Rev 56:81-90, 1964. 10. Garn SM, Clark DC: Trends in fatness and the origins of obesity. Pediatrics, to be published. 11. Mason E: Obesity in pet dogs. Vet Rec 86:612-616, 1970. 12. Garn SM, Clark DC: Nutrition, growth, development and maturation: Findings from the Ten-State Nutrition Survey of 1968-1970. Pediatrics 56:306-319, 1975. 7. Garn
composition
PR Index in Rheumatic Fever
1920 Parkinson et al,1 and in 1924 Cohn and Swift,2 observed an association of acute rheumatic fever and prolongation of the PR interval of the electrocardiogram. Ziegler3 has noted that the PR interval is prolonged in 2% of normal children. Because the PR interval varies with age and heart rate, Mirowski et al4 devised the PR index to provide a standard by which the duration of the PR interval of a subject may be judged. A value greater than 1.0 is considered evidence of delay in atrioventricular (AV) conduction. In 1965, the revised Jones criteria5 listed prolongation of the PR interval as one of the minor criteria used in establishing the diagnosis of rheumatic fever. Other conduction abnormalities may be observed. These include second-degree heart block, complete heart block, AV dissociation, and junctional rhythm. Clarke and Keith6 detected AV conduction abnormalities in 84% of 508 patients with acute rheumatic fever.
On page 473 of this issue of the Journal, Sanyal et al report on a prospective study of 118 children with rheumatic fever, 44 normal children, and 25 febrile children to determine the frequency of occurrence of prolon¬ gation of the PR index. They subdi¬ vided the children into groups on the basis of presence of arthritis, chorea, or carditis. They observed that as a group, children with rheumatic fever had a greater frequency of prolonga¬ tion of AV conduction than found in normal children or in children with a febrile illness, as has been observed by others.'" Sanyal et al observed a significantly greater frequency of a prolonged PR index in patients with carditis than without. In contrast, Clarke and Keith6 and Feinstein et al7 concluded that there was no difference in the frequency of prolongation of the PR index in their rheumatic patients with or without carditis. Feinstein and DiMassa8 observed that the PR index was prolonged in 33% (average of
their two carditis groups) of patients with carditis and 28% of those with "no valvulitis." Mirowski et al4 report that the frequency of first-degree heart block was 40% in patients with rheumatic carditis and 33% in patients with polyarthritis. The frequency of a prolonged PR index observed by Feinstein and DiMassa,8 Mirowski et al," Clarke and Keith,6 and Sanyal et al in patients with carditis was 33%, 40%, 72%, and 53%, respectively. The occurrence of prolongation of AV conduction in patients without carditis observed by these same authors was 28%, 33% 73%, and 18%, respectively. One notes the relatively wide variation in frequency of prolonged PR index by these authors. Only in the study of Sanyal et al was a significant difference in the frequency of occurrence a prolonged PR index observed between patients with and without rheumatic carditis. In these four studies the occurrence of prolongation of the PR index varied widely in the carditis and noncarditis
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 06/08/2015
explanation for the varia¬ tion in the findings of these authors is unclear. Markowitz and Kuttner" have sum¬ marized some of the data on the changing pattern of rheumatic fever. In 1960, Bland1" commented on the decline in the severity of rheumatic carditis as observed over the previous four decades, and on the eightfold reduction in mortality. Wegman11 has tabulated the death rates from rheu¬ matic heart disease and rheumatic fever from many countries and noted the marked variation in death rates. Significant differences in prevalence rates of rheumatic heart disease among schoolchildren within the United States have been reported.'' Wilson et al'- reported that the recur¬ rence rates of rheumatic fever de¬ clined over a 20-year period from 1936 to 1956 among 782 patients. This same report concluded that the recurrence rates were greater for persons living in poorer environmental circum¬ groups. The
stances.
The study of Sanyal et al was under¬ taken in India. One may only specu¬ late as to what factors are involved in accounting for the greater frequency of prolongation of the PR index
observed by them in patients with carditis than in patients without carditis. Perhaps there are geograph¬ ical differences in the incidence of a prolonged PR index associated with acute rheumatic fever. Sanyal et al13 have emphasized the high incidence of carditis in particular countries in contrast to others. The frequency of carditis observed as a manifestation of rheumatic fever may range from 33% to 83%. Usually, a prospective study is more precise in identifying certain manifestations that are looked for on a systematic basis rather than by incidental observation. It is also probable that a greater accuracy was achieved in making measurements of the PR interval during recent studies, and that more frequent ECGs were obtained during the acute phase of rheumatic fever. Cristal et al14 observed AV dissocia¬ tion in 14 of 70 young adults with acute rheumatic fever. Dissociation occurred in 11 of the 14 patients during a first attack of rheumatic fever. Carditis, as established by Jones criteria, was diagnosed in only four of the 14 patients. The authors concluded that although the arrhyth¬ mia suggested a myocardial effect of
the rheumatic process, it did not corre¬ late with "carditis." Since patients with prolongation of the PR interval without carditis have recovered completely, and because of the apparent nearly equal frequency of occurrence in patients with and without carditis, it has been suggested previously that a prolonged PR index is not a specific manifestation of carditis. The investigation of Sanyal et al does not attempt to establish a cause-effect relationship. Regardless of the explanation of the differences among these studies, pro¬ longation of the PR index in a patient with symptoms and signs of rheu¬ matic fever should greatly increase one's suspicion of the diagnosis. The study of Sanyal et al may suggest a closer association of prolonged PR index and carditis. I believe additional prospective studies in several coun¬ tries may be necessary to clarify this
relationship.
GEORGE BENZING III, MD Department of Pediatrics Division of Cardiology Children's Hospital University of Ohio Cincinnati, OH 45229
References 1. Parkinson J, Gross AH, Gunson EB: The heart and its rhythm in acute rheumatism. Q J Med 13:363-367, 1920. 2. Cohn AE, Swift HF: Electrocardiographic evidence of myocardial involvement in rheumatic fever. J Exp Med 39:1-5, 1924. 3. Ziegler RF: Electrocardiographic Studies in Normal Infants and Children. Springfield, Ill, Charles C Thomas Publisher, 1951, pp 35-45. 4. Mirowski M, Rosenstein BJ, Markowitz M: A comparison of atrio-ventricular conduction in normal children and in patients with rheumatic fever, glomerulonephritis, and acute febrile illness. Pediatrics 33:334-340, 1964. 5. Jones criteria (modified) for guidance in the diagnosis of rheumatic fever, Council on Rheu-
matic Fever and Congenital Heart Disease of the American Heart Association. Circulation 32:664\x=req-\ 668, 1965. 6. Clarke M, Keith JD: Atrioventricular conduction in acute rheumatic fever. Br Heart J 34:472-479, 1972. 7. Feinstein AR, Harrison FW, Spagnuolo M, et al: Rheumatic fever in children and adolescents. Ann Intern Med 60(suppl 5):87-123, 1964. 8. Feinstein AR, DiMassa R: Prognostic significance of valvular involvement in acute rheumatic fever. N Engl J Med 260:1001-1007, 1959. 9. Markowitz M, Kuttner AG: Rheumatic Fever. Philadelphia, WB Saunders Co, 1965, pp 1-8.
10. Bland EF: Declining severity of rheumatic fever. N Engl J Med 262:597-599, 1960. 11. Wegman ME: Some international aspects of rheumatic fever. Pediatrics 15:627-630, 1955. 12. Wilson MG, Lim WN, Birch AM: Decline of rheumatic fever: Recurrence rates of rheumatic fever among 782 children for 21 consecutive calendar years (1936-56). J Chronic Dis 7:183-190, 1958. 13. Sanyal SK, Thapar MK, Ahmed SH, et al: The initial attack of acute rheumatic fever during childhood in North India. Circulation
49:7-12, 1974.
14. Cristal N, Stern J, Gueron M: Atrioventricular dissociation in acute rheumatic fever. Br Heart J 33:12-15, 1971.
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 06/08/2015
