Pediatr Cardiol 12:233-236, 1991

Pediatric Cardiology 9 Springer-Verlag New York Inc. 1991

Complete Heart Block from Mycoplasma

Pneumoniae

Infection

Brojendra N. Agarwala and David G. Ruschhaupt Division of Pediatric Cardiology, University of Chicago, Wyler Children's Hospital, Chicago, Illinois, U S A

SUMMARY. Complete heart block (CHB) in infants and children is usually congenital. Nonsurgical acquired CHB is rare. Occasionally, transient acquired CHB is seen in association with viral myocarditis. We describe here an unusual case of transient CHB in a 12-year-old boy with endomyocardial biopsy-proven myocarditis and evidence of Mycoplasma pneumoniae infection. KEY WORDS: Complete heart block - - Myocarditis - - M y c o p l a s m a

Infants and children with acute myocarditis may present with various electrocardiographic abnormalities, ranging from ST-T changes to tachyarrhythmia and complete heart block (CHB). Similarly, the clinical manifestations have a wide spectrum (e.g., chest pain to congestive heart failure and sudden death). CHB is usually congenital in infants and children [16]. Nonsurgical acquired CHB is rare. Occasionally, transient acquired CHB is seen in association with viral myocarditis [10, ll, 18, 19, 20]. We report here a 12-year-old patient with CHB and endomyocardial biopsy-proven myocarditis and serologic evidence of Mycoplasma pneumoniae infection. Case Report

History A 12-year-old black male was admitted to Wyler Children's Hospital Intensive Care Unit through the E m e r g e n c y R o o m where he presented with a history of s h o r t n e s s of breath, chest pain, fever, and vomiting. He was apparently in good health 7 days prior to admission when he complained of upper respiratory infection IURI). Two days prior to admission he was seen in a local hospital e m e r g e n c y room, he was diagnosed as having URI and sent h o m e on 650 mg a c e t a m i n o p h e n every 4 h as needed. At that time his heart rate was 100 beats/min. His past medical and family histories were noncontributory.

Address offprint reprints to: Dr. Brojendra N. Agarwala, Division of Pediatric Cardiology, The University of Chicago, Wyler Children's Hospital, 5841 S. Maryland A v e n u e , Hospital Box 132, Chicago, II 60637, USA.

pneumoniae

Physical e x a m i n a t i o n revealed a lethargic but oriented child with a heart rate of 32 b e a t s / m i n , a respiratory rate of 28/min, a blood p r e s s u r e of 100/40 m m H g (supine), and a temperature of 38~ (oral). A mild e r y t h e m a t o u s p h a r y n x was noted. The abdom e n was soft. A 1-cm tender liver edge was palpable at the midclavicular line below the right costal margin. Both lungs were clear to auscultation and percussion. Cardiovascular examination revealed a quiet p r e c o r d i u m with precordial maximal impulse at the sixth left intercostal space j u s t outside the midclavicle line without a n y palpable heave or thrill. Both the first and second heart s o u n d s were soft and no heart m u r m u r or rub were heard. In the e m e r g e n c y room, the electrocardiogram revealed C H B , an atrial rate of 90 b e a t s / m i n with a wide QRS ventricular escape r h y t h m at 30 b e a t s / m i n and R B B B pattern. Atropine at 0.4 mg i.v. increased the atrial rate (Fig. 1) from 90 to 160 with no effect on the ventricular rate. I n t r a v e n o u s isoproterenol drip (0.2 t~g/kg/min) increased the ventricular rate to 58 b e a t s / m i n and induced ventricular t a c h y c a r d i a that was well tolerated. The ventricular t a c h y c a r d i a was then controlled with lidocaine. A temporary t r a n s v e n o u s p a c e m a k e r catheter was inserted and he was paced at a rate of 80 b e a t s / m i n with significant clinical improvement. A d m i s s i o n e c h o c a r d i o g r a m revealed a mild pericardial effusion, dilated cardiac c h a m b e r with diminished left ventricular systolic function. T h e c h e s t x-ray s h o w e d a generalized cardiomegaly (Fig. 2). In the intensive care unit the patient received the following medications: L a s i x 20 mg b.i.d, daily, digoxin 0.125 mg daily, e r y t h r o m y c i n 250 m g Q6H for 10 d a y s , and prednisone 20 mg t.i.d, beginning the 1 lth d a y for 1 w e e k followed by 20 m g daily for 2 more weeks. H e a r t block d i s a p p e a r e d s p o n t a n e o u s l y in 48 h and his r h y t h m r e t u r n e d to sinus with 1 : l c o n d u c t i o n (Fig. 3). His cardiac function by e c h o c a r d i o g r a m and heart size on c h e s t x-ray have returned to normal. He u n d e r w e n t a myocardial biopsy (Fig. 4) during this acute p h a s e of the illness. The patient was discharged on medications 2 w e e k s from admission. Since discharge he has r e m a i n e d a s y m p t o m a t i c and maintained a sinus r h y t h m on Holter m o n i t o r on m a n y occasions.

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Fig. 1. An electrocardiogram showing CHB with a ventricular rate of 30 beats/min. Note the blocked P waves are seen in lead V 1. Also, this electrocardiogram is showing evidence of left-axis deviation with RBBB.

Pediatric Cardiology Vol. 12, No. 4, 1991

enzymes were elevated. Creatine phosphokinase and lactate dehydrogenase were as high as 1036 and 592 U, respectively, and the sedimentation rate was 32 mm/h.

Fig. 2. Chest x-ray showing a generalized cardiomegaly with a transvenous pacemaker catheter tip in the right ventricle. Fig. 3. An electrocardiogram taken 48 h after the one shown in Fig. 1. It shows a normal sinus rhythm with left-axis deviation and LBBB. Fig. 4. Myocardial biopsy showing diffuse infiltration of lymphocytes and histocytes with myocyte necrosis. Interstitial edema is present with some early collagen deposit. Viral inclusions are not detected.

Laboratory Data Mycoplasma immuno gamma-M globulin (immuno fluorescent antibody) dilution titer was 10 in the acute stage and was increased to 20 in the convalescent stage. The IGG dilution titer was less than 8 (IFA test). The following viral acute and convalescent titers were negative: Coxsackie B (1-6), influenza A and B, parainfluenza (1-3), adenovirus, cytomegalovirus, rheovirus, respiratory syncitial virus (RSV), and mumps. The nasopharyngeal viral culture and bacterial culture for group A streptococcus were negative. Collagen profile including antinuclear antibodies, doublestrand DNA, and rheumatoid factors were negative. The cardiac

Discussion

In 1944, Eaton et al. [6] described a pathologic agent thought to cause atypical pneumonia. In 1962, Chanock et al. [4] identified this agent as mycoplasma, which is now known as Mycoplasma pneumoniae. It was isolated from patients with pneumonia and upper respiratory tract infections in school-age children. Rarely has this organism affected the cardiovascular system. Myocarditis from M. pneumoniae (Eaton agent) was reported in 1970 by Lewes and Rainford [14]. Gerz6n et al. [8] in 1972 identified M. pneumoniae as the cause of myocarditis in several patients. P6nk~i in 1979 [20] reported 560 patients with serologically proven M. pneumoniae infection, 25 (4.5%) had carditis, 19 perimyocarditis, and six pericarditis, none presented with CHB. Friedli et al. [7] in 1977 reported an 18-month-old infant presenting with a syncopal episode preceded by URI-like symptoms found to have CHB, presumably due to M. pneurnoniae

Agarwala and Ruschhaupt: Complete Heart Block

myocarditis. This heart block was permanent and required permanent pacing. No serologic diagnosis of the causative organism was made in this patient. As with M. pneumoniae infections generally, myocarditis occurs year-round, and associated pneumonia is not a constant feature. Clinically, it is a serious problem and is frequently complicated by arrhythmia (e.g., premature ventricular contractions, ventricular tachycardia, and fibrillation) [20]. Carditis associated with M. pneumonial infection may be caused by the following: 1. Direct invasion of the myocardium organism via either lymphatic [1, 15] or circulatory systems or from the lower respiratory tract per contamination. 2. Autoimmune mechanism as suggested by Brunner et al. [2, 3], who postulated that nonrespiratory manifestations of serologically confirmed M. pneumoniae infections (e.g., carditis, arthritis, and central nervous system infections) are caused by an immunological mechanism. They also pointed out that M. pneumoniae and streptococcus group A have a common antigenic property. 3. An increased tendency for intravascular coagulation has been noted in association with M. pneumoniae infections [5, 17]. Nonsurgically acquired CHB is unusual in childhood and may be the only manifestation of acute myocarditis. Extreme bradycardia causing poor peripheral circulation, congestive heart failure, or syncope are the emergency indications for a transvenous pacemaker to increase the cardiac output. Erythromycin should be given when mycoplasma is suspected as an etiology for myocarditis. In congestive heart failure, digitalis and diuretics should be given. The inflamed myocardium is very sensitive to digitalis. A lower threshold for digitalis toxicity in patients with myocarditis has been postulated. Therefore, it should be used in smaller doses with careful monitoring of the patient. Other arrhythmias (e.g., supraventricular and ventricular tachycardia) should be treated with appropriate antiarrhythmic drugs. The use of steroids is controversial. Kilborne et al. [12] have shown in animal experiments that when corticosteroids are given during the acute phase of the Coxsackie viral disease, both viral replication and myocardial necrosis are increased. Lerner et al. [13] have recommended that steroids be avoided at least during the first 10 days of the infection. If the active disease continues, the patient should receive a short course of steroids. Needle application of the pericardial effusion is

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only indicated for a hemodynamically significantsize pericardial effusion. The patient's cardiac involvement may be reversible to a different degree. The acute stage may progress to a chronic cardiomyopathy [9]. Therefore, a long-term careful follow-up is needed. We recommend endomyocardial biopsy when the cause of acute onset of CHB is in doubt, to confirm the definite diagnosis of acute myocarditis as evidence by myocardial necrosis, edema, cellular infiltration, culture, and viral inclusion bodies.

References 1. Andriushin JN (1969) Some materials to anatomical substantiation of spread of infection from tonsils and pharynx to heart. Arkh Anat 56:45-52 2. Brunner H, Horswood R, Chanock RM (1973) More sensitive methods for detection of antibody to mycoplasma pneumoniae. J lnfec Dis 127(Suppl):52-55 3. Brunner H, Prescott B, Greenberg H, James WD, Horswood R, Chanock RM (1977) Unexpectedly high frequency of antibody to Mycoplasma pneumoniae in human sera as measured by sensitive techniques. J Infect Dis 135:524-530 4. Chanock RM, Hayflick L, Barile MF (1962) Growth on artificial medium of an agent associated with atypical pneumonia and its identification as a PPLO. Proc Natl Acad Sci USA 48:41-49 5. De-Vos M, Van-Nimmen L, Baele G (1974) Disseminated intravascular coagulation during a fatal Mycoplasma pneumoniae infection. Acta Haematot 52:120-125 6. Eaton MD, Meiklejohn G, Van Herick W (1944) Studies on the etiology of primary atypical pneumonia. A filtrable agent transmissible to cotton rats, hamsters and chick embryos. J Exp Med 79:649-668 7. Friedli B, Renevey F, Rouge JC (1977) Complete heart block in a young child presumably due to Mycoplasma pneumoniae myocarditis. Acta Pediatr Scand 66:385-388 8. Gerz~n P, Granath A, Holmgren B, Zenerquist S (1972) Acute myocarditis. A follow-up study. Br Heart J 34:575583 9. Ghafour AS, Gutgesell HP (1979) Echocardiographic evaluation of left ventricular function in children with congestive cardiomyopathy. A m J Cardiol 44:1332-1338 10. Granath A, Kimby E, S6dermark T, Volpe U, Zetterquist S (1980) Stokes-Adams attacks requiring pacemaker treatment in three patients with acute non-specific myocarditis. Acta Med S t a n d 207:177-181

11. Johnson JL, Lee LP (1971) Complete atrioventricular heart block secondary to acute myocarditis requiring intracardiac pacing. J Pediatr 78:312-316 12. Kilborne ED, Wilson CB, Perrier D (1956) The induction of gross myocardial lesions via Coxsackie (pleurodynia) virus and cortisone. J Clin Invest 35:362-370 13. Lerner AM, Wilson FM (1973) Virus myocardiopathy. Prog Med Virol 15:63 14. Lewes D, Rainford DJ (1970) Echo virus and carditis. Lancet 1:520 15. Naftalin JM, Wellisch G, Kahana Z, Diengott D (1974) Mycoplasma pneumoniae septicemia. J A M A 228:565

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16. Nakamura FF, Nadas AS (1964) Complete heart block in infants and children. New Engl J Med 270:1261-1268 17. Nilsson IM, Rausing A, Denneberg T, Christenssen P (1971) Intravascular coagulation and acute renal failure in a child with mycoplasma infection. Acta Med Scand 189:359-365 18. Noren GR, Staley NA, Bandy CH, Kaplan EL (1977) Occurrence of myocarditis in sudden death in children. J Forensic Sci 22:188

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19. Onouchi Z, Haba S, Kiyosawa N, Shimazu S, Hamaoka K, Kusunoki T (1980) Stokes-Adams attacks due to acute nonspecific myocarditis in childhood. Jpn Heart J 21:307-315 20. P6nkfi A (1979) Carditis associated with Mycoplasma pneumoniae infection. Acta Med Scand 206:77-86 21. Thompson WM, Nolan TB (1966) Atrioventricular dissociation associated with Adams-Stokes syndrome, presumably due to mumps myocarditis. J Pediatr 68:601-607

Complete heart block from mycoplasma pneumoniae infection.

Complete heart block (CHB) in infants and children is usually congenital. Nonsurgical acquired CHB is rare. Occasionally, transient acquired CHB is se...
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