Hostname: page-component-7b9c58cd5d-9k27k Total loading time: 0 Render date: 2025-03-14T01:51:50.071Z Has data issue: false hasContentIssue false
  • English
  • Français

Advanced atrioventricular conduction block in acute rheumatic fever

Published online by Cambridge University Press:  24 May 2005

Eli Zalzstein ,
Rachel Maor ,
Nili Zucker  and
Amos Katz
Eli Zalzstein
Affiliation:
Pediatric Cardiology Unit, Department of Cardiology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Rachel Maor
Affiliation:
Pediatric Cardiology Unit, Department of Cardiology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Nili Zucker
Affiliation:
Pediatric Cardiology Unit, Department of Cardiology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Amos Katz
Affiliation:
Pediatric Cardiology Unit, Department of Cardiology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Rights & Permissions [Opens in a new window]

Abstract

We carried out a retrospective case control analysis to evaluate the outcome, and the need for treatment, of problems with atrioventricular conduction occurring during an acute attack of rheumatic fever, assessing the occurrence of second and third atrioventricular block versus first degree block.

We reviewed and analysed the clinical, electrocardiographic and echocardiographic records of all children diagnosed in a single institute as having acute rheumatic fever during a period of seven consecutive years.

During the period from October, 1994, through October, 2001, 65 children meeting the modified Jones criterions for acute rheumatic fever were hospitalized in the Soroka University Medical Center, Israel. First-degree atrioventricular block was identified in 72.3% of the children, and resolved with no specific treatment other than non-steroidal anti-inflammatory medications. Second-degree atrioventricular block of Mobitz type I, was observed in one child (1.5%), which progressed from first-degree block, and subsequently resolved. Complete atrioventricuar block was found in 3 children (4.6%), one progressing from Mobitz type I second-degree block, and two being seen as the first presentation. Of the three children with complete atrioventricular block, one patient was not treated, the second was treated with aspirin, and the final one with combined aspirin and steroids. The disturbances of conduction resolved in all three.

We conclude that advanced atrioventricular block is rare during acute rheumatic fever. If occurring, block appears to be temporary, and resolves with conventional anti-inflammatory treatment. Specific treatment, such as insertion of a temporary pacemaker, should be considered only when syncope or clinical symptoms persist.

Keywords

Rheumatic fevercarditisatrioventricular dissociation
Type
Original Article
Information
Cardiology in the Young , Volume 13 , Issue 6 , December 2003 , pp. 506 - 508
Copyright
© 2003 Cambridge University Press

Although the incidence of rheumatic fever has been declining steadily in the continental United States of America,1–3 outbreaks have been reported,4, 5 while in other parts of the world, it has always been a disease of significance. The Jones criterions6 are used to make an objective diagnosis. Carditis, a major sign, includes valvitis, pericarditis, and myocarditis. First-degree atrioventricular block is a well-known minor sign. Occasionally, although rarely, advanced conduction delay, such as second-degree or complete atrioventricular block, or even Stokes-Adams attacks, are important early signs of acute rheumatic fever, and may precede other signs. So as to evaluate the frequency of these arrhythmic findings, we have reviewed our experience with children admitted to our unit with acute rheumatic fever, focussing on the occurrence of advanced disturbances of conduction, and reviewing their treatment and outcome.

Patients and methods

We reviewed retrospectively the inpatient medical records of 65 children in whom the diagnosis of acute rheumatic fever was made according to the Jones criterions. All had been hospitalized in a seven-year period from October, 1994, through October, 2001, at the Soroka University Medical Center. We reviewed clinical data, past and family history, electrocardiographic recordings at admission and during the entire period of hospitalization, chest X-rays, and echocardiographic examinations. Special attention was given to patients with atrioventricular block of high degree.

Results

In all, we admitted 65 patients, of whom 37 (57%) were boys and 28 girls (43%). The mean age at admission was 10.7 ± 3.7 years, with a range from 4 to 17 years. Of the patients, 51% were of Arab-Bedouin origin, and 49% were Jewish. In 11 patients (16.9%), there was a family history of rheumatic fever in one or more of the family members, involving brothers or sisters in most instances. In 63 (97%) of the patients, a history of throat infection was positive, but in only 37 patients (57%) was this associated with fever. Titres of antistreptolysin O were positive in 51 patients (78%), but in only 11 patients (17%) was a throat culture positive for Streptococus hemolytic A. With regard to the major criterions as established by Jones, carditis was present in 28 patients (43%), migratory arthritis in 27 patients (42%), chorea in 5 patients (8%), subcutaneous nodules in 2 patients (3%), and a rash in 2 patients (3%). We also found minor criterions, with a past history of rheumatic fever in 11 patients (17%), arthralgia in 11 patients (17%), fever in 11 patients (17%), leukocytosis in 13 patients (20%), an elevated sedimentation rate in 14 patients (22%), and positive C reactive protein in 13 patients (20%).

Echocardiography was performed in all patients, with mitral regurgitation of varying degree found in 53 patients (82%). Aortic regurgitation was seen in 29 patients (45%), and combined aortic and mitral regurgitation in 18 patients (28%). None had evidence of impaired myocardial function or pericardial effusion.

Electrocardiographic recordings were available for 62 patients (95%). We found evidence of disturbances of conduction in 51 (79%) of the patients. Thus, first-degree atrioventricular block was found in 47 children (72%), all of whom presented with both arthritis and carditis. Second-degree atrioventricular block of Mobitz type I was diagnosed in one patient (1.5%), a seven year-old presenting with migratory arthritis and moderate mitral insufficiency detected by echocardiography. At admission, his electrocardiogram showed first-degree atrioventricular block with a PR interval of 0.23 s. He was treated with aspirin at a dose of 100 mg/kg. The second-degree block developed on the second day, without any hemodynamic effect, and resolved on the third day, the tracings reverting to normal atrioventricular conduction.

Complete atrioventricular block was diagnosed in three patients (4.7%). Their clinical summary is shown in Table 1. One patient was treated with aspirin, the second patient with both aspirin and a steroid agent, while the third was not treated with any anti-inflammatory agent. The atrioventricular block in this case was noted retrospectively, and reverted spontaneously to sinus rhythm. All patients were hemodynamically stable, and asymptomatic.

Table 1. Clinical summary of the patients manifesting advanced heart block.

Discussion

Prolongation of the PR interval is a common finding in acute rheumatic fever, and is a minor manifestation for diagnosis in the revised Jones criterions. Clark and Keith7 found prolonged PR intervals in almost nine-tenths of 508 children with acute rheumatic fever, with arrhythmias discovered in one-eighth of those with abnormal electrocardiograms. Of these, three had complete heart block, and one of these required artificial pacing for a Stokes-Adams attack.

In our study, we discovered three patients who had developed complete atrioventricular dissociations. Of these, one did not receive any anti-inflammatory treatment, while the other two received conventional anti-inflammatory treatment. Only one patient was treated with steroids. None of these patients were given atropine or beta-adrenergic agents, but valvitis had been present in two. There were no long-term sequels in any of our patients, with the advanced block lasting from two to four days. The complete block in our third patient had been asymptomatic, and was detected only at discharge.

Atrioventricular block of first degree is not a specific sign for carditis, and may present in many febrile conditions. Blocks of second or third degree are associated with various inflammatory conditions, but usually with involvement of the conduction system. Diphtheria and myocarditis, for example, are well known to produce advanced atrioventricular block.8, 9 Acute rheumatic fever has also been known to cause complete atrioventricular block,10–12 and has been reported with many other arrythmias.13–16 The exact mechanism by which the rheumatic process causes conduction disturbances is unknown. Immunologic relations between the group A streptococcus and the glycoproteins of cardiac valves, nonetheless, have been well established.17 Such a relationship, however, has yet to be associated with the conduction system. Furthermore, the atrioventricular node has a very low content of glycoprotein compared with the peripheral conduction system.18 Cristal et al.19 showed, in their study of 70 patients with acute rheumatic fever, that although atrioventricular block of advanced degree is a manifestation of cardiac involvement, it was not noted consistently to be associated with valvitis. While valvitis usually results in damage to the leaflets, with irreversible structural changes in the heart, advanced atrioventricular block appears to represent involvement of the conduction pathways in a reversible fashion. This can explain the appearance of complete heart block in our third patient, who demonstrated no valvar involvement.

We conclude, therefore, that although atrioventricular block of advanced degree occurring in a child can be a dramatic event during acute rheumatic fever, it appears to be a temporary event, resolving over a period of days with conventional treatment. Specific treatment, such as a temporary pacemaker, should be considered only when there is syncope due to the block, or there is a Adams-Stokes attack.

References

Land MA, Bisno AL. Acute rheumatic fever: a vanishing disease in suburbia. JAMA 1983; 249: 895–898.Google Scholar
Markowitiz M. The decline in rheumatic fever: Role of medical intervention. J Pediatr 1985; 106: 545–550.Google Scholar
Gordis L. The virtual disappearance of rheumatic fever in the United States: lessons the rise and fall of disease. Circulation 1985; 72: 1155–1162.Google Scholar
Ferrieri P. Acute rheumatic fever, the come back of disappearing disease. Am J Dis Child 1987; 141: 725–727.Google Scholar
Hosier DM, Craenen JM, Teske DW, Wheller JJ. Resurgence of acute rheumatic fever. Am J Dis Child 1987; 141: 730–733.Google Scholar
Guidelines for the diagnosis of rheumatic fever. Jones Criteria. 1992 update. Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association. JAMA 1992; 268: 2069–2074.
Clark M, Keith JD. Atrio ventricular conduction in acute rheumatic fever. Br Heart J 1972; 34: 472–479.Google Scholar
Phornphutkul C, Damrongsak D, Silpisornkosol S. Steroid therapy in cardiac conduction disturbances in children with diphtheria. Mod Med Asia 1978; 38: 43–44.Google Scholar
Uemura A, Morimoto S, Hiramitsu S, Hishida H. Endomyocardial biopsy finding in 50 patients with idiopathic atrioventricular block: presence of myocarditis. Jpn Heart J 2001; 42: 691–700.Google Scholar
Malik JA, Hassan C, Khan GO. Transient complete heart block complicating acute rheumatic fever. Indian Heart J 2002; 54: 91–92.Google Scholar
Thakur AK. Complete heart block as a first manifestation of acute rheumatic fever. Indian Heart J 1996; 48: 428–429.Google Scholar
Shah CK, Gupta R. Persistent complete heart block following acute rheumatic fever in a 12 year old girl. Jassoc Physician India 1993; 41: 389–390.Google Scholar
Lenox CC, Zuberbuhler JR, Park SC, Neches WH, Mathews RA, Zoltun R. Arrhythmias and Stoke-Adams attack in acute rheumatic fever. Pediatrics 1978; 61: 599–603.Google Scholar
Freed MS, Sacks P, Ellman MH. Ventricular tachycardia in acute rheumatic fever. Arch Intrn Med 1985; 145: 1904–1905.Google Scholar
Liberman L, Hordof AJ, Alfayyadh M, Salafia CM, Pass RH. Torsade de pointes in a child with acute rheumatic fever. J Pediatr 2001; 138: 280–282.Google Scholar
Singhi S, Shrivastava S. Sinus node dysfunction in acute rheumatic carditis: a case report. Indian Heart J 1979; 31: 305–308.Google Scholar
Goldstein I, Halpern B, Robert L. Immunological relationship between streptococcus A polysaccharide and the structural glycoproteins of heart valve. Nature 1967; 213: 44–49.Google Scholar
Gee DJ. A glycoprotein in cardiac conducting tissue. Br Heart J 1969; 31: 588–590.Google Scholar
Cristal N, Stern J, Gueron M. Atrioventricular dissociation in acute rheumatic fever. Br Heart J 1971; 33: 12–15.Google Scholar
Figure 0

Table 1.