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The scale of myocardial involvement in varicella myocarditis
International Elsevier
Journal of Cardiology,
257
20 (1988) 257-262
IJC 00709
The scale of myocardial involvement in varicella myocarditis A. Lorber
t, Z. Zonk
2, E. Maisuls *, L. Dembo and T.C. Iancu 2
*, A. Palant
’
I Heart Institute and ’ Department of Paediatrics, Carmel Hospital and Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel (Received
5 January
1988; revision
accepted
4 February
1988)
Lorber A, Zonk Z, Maisuls E, Dembo L, Palant A, Iancu TC. The scale of myocardial involvement in varicella myocarditis. Int J Cardiol 1988;20:257-262. Two patients with varicella myocarditis are described. An arrhythmia associated with complete recovery occurred in the first patient whereas intractable congestive heart failure complicated by hemiplegia resulted in a fatal outcome in the other case. We stress the extent of myocardial involvement produced by the herpes zoster virus in the setting of varicella. Key words: Varicella; plegia
Myocarditis;
Arrhythmia;
Congestive heart failure;
Hemi-
Introduction Varicella, a highly contagious disease, usually runs a benign course, but, in the neonatal period and in immunocompromised patients, rare serious complications are encountered [l-3]. Cardiac involvement by the herpes zoster virus has been infrequently documented and very limited information is available regarding subclinical myocardial insult in the course of varicella [4]. It can only be assumed that the latter form is much more common than the cases that are diagnosed when the overt signs and symptoms of cardiac decompensation are more obvious [5,6].
Correspondence to: A. Lorber, Centre. Haifa 31096, Israel.
0167-5273/88/$03.50
M.D., Dept. of Cardiology,
0 1988 Elsevier Science Publishers
Paediatric
B.V. (Biomedical
Cardiology,
Division)
Rambam
Medical
258
Case Reports We describe our experience in the management of two children who presented with myocardial involvement 10 to 14 days following the onset of a typical skin rash of varicella. The diagnosis was reinforced by rising viral titers for herpes zoster.
Case 1 A previously healthy B-month-old boy, who was noted to have a tachycardia on a check-up 10 days after the onset of a typical skin rash of varicella, was referred to hospital for further assessment. He was asymptomatic from the cardiological point of view, and on examination, the typical skin lesions of varicella were seen. There were no signs of cardiac failure, but his heart rate was 240 beats per minute. An electrocardiographic tracing revealed a short lived supraventricular tachycardia which converted spontaneously to sinus tachycardia of 170 beats per minute. This was still disproportionate to the child’s normal body temperature and well-being. The tachycardia returned to normal within two days of hospitalisation. Evaluation of the chest radiograph was normal and echocardiography revealed good left ventricular function but left ventricular end diastolic dimensions were at the upper normal range for age. He was discharged without treatment. On subsequent examination in the out-patient clinic, he was asymptomatic and found to have no cardiac decompensation and no evidence of conduction or rhythm disturbances (Fig. 1).
a
b
C
Fig. 1. Electrocardiography rhythm strips of the first patient (at 25 mm/set). b: sinus tachycardia of 170 tachycardia of 240 beats per minute; c: normal sinus rhythm recorded in the outpatient clinic during follow-up
a: Supraventricular beats per minute; evaluation.
259
Case 2 A three-year-old girl was hospitalised 14 days after the onset of the typical skin rash of varicella because of increasing breathlessness and fatigue with a marked reduction of her appetite in the last three days prior to her admission. On examination, she had the typical crusts of healing varicella on her skin. There was no dyspnea nor tachypnea, but the liver was markedly enlarged. Her pulse was regular at 140 beats per minute, the apex was displaced to the left anterior axillary line in the sixth intercostal space. A 2/6 systolic murmur was heard at the apex, radiating to the left axilla, compatible with some degree of mitral regurgitation. Chest X-ray revealed cardiomegaly (cardiothoracic ratio of 64%) and pulmonary venous congestion (Fig. 2). Electrocardiography showed left ventricular hypertrophy, left atria1 enlargement, flattening of T waves in all inferolateral leads and marked alternation of electrical voltages (Fig. 3). Echocardiography revealed a markedly dilated left ventricle with left ventricular end-diastolic dimensions of 4.8 cm and end-systolic dimensions of 4.4 cm, resulting
Fig. 2. Chest
X-ray
of the second
patient, showing cardiomegaly, pulmonary venous congestion.
cardiothoracic
ratio
of 64%, and
260
Fig. 3. Standard electrocardiography of the second patient suggestive of left ventricular hypertrophy and left atria1 enlargement, flattening of T waves in inferolateral leads and marked electrical voltage alternans.
r
.-^
*
I
Fig. 4. M-mode echocardiography obtained from the left parasternal position, revealing a short axis view of a markedly dilated left ventricle and minimal posterior pericardial effusion (e). Left ventricular systolic dimensions = 4.4 cm, left ventricular diastolic dimensions = 4.8 cm. left ventricular ejection fraction of 18% and fraction of shortening of 8%.
261
in left ventricular ejection fraction of 18% and fraction of shortening of 8% with minimal posterior pericardial effusion (Fig. 4). The aortic root measured 1.4 cm and the left atrium 2.5 cm. No thrombi or vegetations could be seen. The evidence was compatible with a diagnosis of severe dilated cardiomyopathy due to varicella perimyocarditis. She was treated with diuretics and digitalis with some clinical improvement and, on repeated echocardiography, the pericardial fluid disappeared. She was discharged and was seen regularly in the out-patient clinic on a weekly basis, and seemed to do a little better. Six weeks after her discharge from hospital, she was admitted with left hemiplegia and clinical evidence of deteriorating heart failure. Computerised axial tomography was normal but, in spite of maximal medical and respiratory support, she died as a result of intractable heart failure.
Discussion Varicella is a frequent and highly contagious disease in the paediatric age group, with a course that is usually benign. Significant complications are rare and most frequently occur in immunocompromised patients and neonates [l-3]. Autopsy evidence of myocardial involvement has been described in patients dying of unrecognised myocarditis and from other complications of varicella [7-91. Manifestations of heart disease due to varicella are rare. They are recognised when there are rhythm disturbances and electrocardiographic abnormalities of rhythm, conduction or repolarisation [5,10-131 and when signs and symptoms of congestive heart failure become evident [14-161. The cases presented here illustrate the extremes in the presentation of varicella myocarditis. The first patient presented with supraventricular tachycardia which reverted spontaneously to sinus tachycardia without evidence of cardiac decompensation. Recovery was complete without any cardiac sequels. In contrast, the second patient developed progressive heart failure with poor myocardial function and low cardiac output. Her course was further complicated by an acute left hemiplegia, considered to be as a result of an embolus. She died in spite of maximal medical and ventilatory support. Potentially lethal arrhythmias have been described in varicella carditis, including various forms of ventricular tachycardia and fibrillation [lo]. Various degrees of atrioventricular heart block could be markers of infective myocarditis [7,12,17-201. The damage to the conduction system is usually reversible, but could result in permanent atrioventricular heart block with pacemaker dependency [7]. Although overt clinical evidence of varicella myocarditis is rare, increased awareness could identify manifestations, such as irregularities of the pulse or mild and transient reduction in functional capacity. Since the reduction in functional capacity is associated with markedly reduced left ventricular function, mild to moderate ventricular dysfunction could be clinically difficult to establish. The wide range of severity and variety of cardiac involvement in varicella leads us to the assumption that subclinical forms of myocarditis are probable during epidemics of varicella, similarly to those described and associated with other infections [21]. Another aspect worthwhile noting is that, in our second case, the
262
onset of hemiplegia was cardiac in origin, as opposed to direct or post-inflammatory involvement of the central nervous system by the herpes zoster virus.
References 1 Feldman S, Hughes WT, Daniel CB. Varicella in children with cancer. 77 cases. Pediatrics 1975;56:388-397. 2 Brunell PA. Fetal and neonatal varicella-zoster infections. Sem Perinatal 1983;7:47-56. 3 Kaplan L, Tully JB. “Viral” dissemination in patients with bronchogenic carcinoma: report of case with autopsy findings. Arch Path01 1953;56:312-322. 4 Thandroyen FT, Asmal AS, Armstrong TG. Varicella myocarditis producing congestive cardiomyopathy. Postgrad Med J 1981;57:199-201. 5 Kajalainen J, Viitasalo M, Kalq VR, Heikkila J. 24-hour electrocardiographic recordings in mild acute infectious myocarditis. Ann Clin Res 1984;16:34-39. 6 Kajalainen J, Heikkila J, Nieminen MS, et al. Etiology of mild acute infectious myocarditis. Relation to clinical features. Acta Med Stand 1983;213:65-73. 7 Hackel DB. Myocarditis in association with varicella. Am J Cardiol 1953;29:369-379. 8 Morales AR, Adelman S, Fine G. Varicella myccarditis. Arch Path01 1971;91:29-31. 9 Moore CM, Hem-y J, Benzing G, Kaplan S. Varicella myocarditis. Am J Dis Child 1969;118:899-902. 10 Fiddler GI, Campbell RWF, Pottage A, Godman MJ. Varicella myocarditis presenting with unusual ventricular arrhythmias. Br Heart J 1977;39:1150-1153. 11 Ettedgin JA, Ladusans E, Bamford M. Complete heart block as a complication of varicella. Int J Cardiol 1987;14:362-365. 12 Weinstein L, Shelokov A. Cardiovascular manifestations in acute poliomyelitis. N Engl J Med 1950;244:281-285. 13 Joos HA, Yu PNG. Electrocardiographic observations in poliomyelitis. Am J Dis Child 1950;80:22-23. 14 Moore CM, Henry J, Benzing III G, Kaplan S. Varicella myocarditis. Am J Dis Child 1969;118:899-902. 15 Levi GF, Prots C, Quadri A, Ratti S. Coxsackie virus heart disease and cardiomyopathy. Am Heart J 1977;93:419-421. 16 Noren CR, Tobin JD, Staley NA, Asinger RW. Association of varicella, myocarditis, and congestive cardiomyopathy. Pediat Cardiol 1982;3:53-57. 17 Arita M, Ueno Y, Masuyama Y. Complete heart block in mumps myocarditis. Br Heart J 1981;46:342-344. 18 Giles TD, Gohd RS. Respiratory syncytial virus and heart disease. A report of two cases. J Am Med Assoc 1976;236:1128-1130. 19 Smith WC. Coxsackie B myocarditis in adults. Am Heart J 1970;80:34-46. 20 Bromberg BI, Beekman RH, Heidelberg K. Heart block with viral myocarditis. J Pediatr 1986;108:709. 21 Lewes D, Rainford DJ, Lane WF. Symptomless myocarditis and myalgia in viral and mycoplasma pneumonia1 infections. Br Heart J 1974:36:924-932.
Journal of Cardiology,
257
20 (1988) 257-262
IJC 00709
The scale of myocardial involvement in varicella myocarditis A. Lorber
t, Z. Zonk
2, E. Maisuls *, L. Dembo and T.C. Iancu 2
*, A. Palant
’
I Heart Institute and ’ Department of Paediatrics, Carmel Hospital and Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel (Received
5 January
1988; revision
accepted
4 February
1988)
Lorber A, Zonk Z, Maisuls E, Dembo L, Palant A, Iancu TC. The scale of myocardial involvement in varicella myocarditis. Int J Cardiol 1988;20:257-262. Two patients with varicella myocarditis are described. An arrhythmia associated with complete recovery occurred in the first patient whereas intractable congestive heart failure complicated by hemiplegia resulted in a fatal outcome in the other case. We stress the extent of myocardial involvement produced by the herpes zoster virus in the setting of varicella. Key words: Varicella; plegia
Myocarditis;
Arrhythmia;
Congestive heart failure;
Hemi-
Introduction Varicella, a highly contagious disease, usually runs a benign course, but, in the neonatal period and in immunocompromised patients, rare serious complications are encountered [l-3]. Cardiac involvement by the herpes zoster virus has been infrequently documented and very limited information is available regarding subclinical myocardial insult in the course of varicella [4]. It can only be assumed that the latter form is much more common than the cases that are diagnosed when the overt signs and symptoms of cardiac decompensation are more obvious [5,6].
Correspondence to: A. Lorber, Centre. Haifa 31096, Israel.
0167-5273/88/$03.50
M.D., Dept. of Cardiology,
0 1988 Elsevier Science Publishers
Paediatric
B.V. (Biomedical
Cardiology,
Division)
Rambam
Medical
258
Case Reports We describe our experience in the management of two children who presented with myocardial involvement 10 to 14 days following the onset of a typical skin rash of varicella. The diagnosis was reinforced by rising viral titers for herpes zoster.
Case 1 A previously healthy B-month-old boy, who was noted to have a tachycardia on a check-up 10 days after the onset of a typical skin rash of varicella, was referred to hospital for further assessment. He was asymptomatic from the cardiological point of view, and on examination, the typical skin lesions of varicella were seen. There were no signs of cardiac failure, but his heart rate was 240 beats per minute. An electrocardiographic tracing revealed a short lived supraventricular tachycardia which converted spontaneously to sinus tachycardia of 170 beats per minute. This was still disproportionate to the child’s normal body temperature and well-being. The tachycardia returned to normal within two days of hospitalisation. Evaluation of the chest radiograph was normal and echocardiography revealed good left ventricular function but left ventricular end diastolic dimensions were at the upper normal range for age. He was discharged without treatment. On subsequent examination in the out-patient clinic, he was asymptomatic and found to have no cardiac decompensation and no evidence of conduction or rhythm disturbances (Fig. 1).
a
b
C
Fig. 1. Electrocardiography rhythm strips of the first patient (at 25 mm/set). b: sinus tachycardia of 170 tachycardia of 240 beats per minute; c: normal sinus rhythm recorded in the outpatient clinic during follow-up
a: Supraventricular beats per minute; evaluation.
259
Case 2 A three-year-old girl was hospitalised 14 days after the onset of the typical skin rash of varicella because of increasing breathlessness and fatigue with a marked reduction of her appetite in the last three days prior to her admission. On examination, she had the typical crusts of healing varicella on her skin. There was no dyspnea nor tachypnea, but the liver was markedly enlarged. Her pulse was regular at 140 beats per minute, the apex was displaced to the left anterior axillary line in the sixth intercostal space. A 2/6 systolic murmur was heard at the apex, radiating to the left axilla, compatible with some degree of mitral regurgitation. Chest X-ray revealed cardiomegaly (cardiothoracic ratio of 64%) and pulmonary venous congestion (Fig. 2). Electrocardiography showed left ventricular hypertrophy, left atria1 enlargement, flattening of T waves in all inferolateral leads and marked alternation of electrical voltages (Fig. 3). Echocardiography revealed a markedly dilated left ventricle with left ventricular end-diastolic dimensions of 4.8 cm and end-systolic dimensions of 4.4 cm, resulting
Fig. 2. Chest
X-ray
of the second
patient, showing cardiomegaly, pulmonary venous congestion.
cardiothoracic
ratio
of 64%, and
260
Fig. 3. Standard electrocardiography of the second patient suggestive of left ventricular hypertrophy and left atria1 enlargement, flattening of T waves in inferolateral leads and marked electrical voltage alternans.
r
.-^
*
I
Fig. 4. M-mode echocardiography obtained from the left parasternal position, revealing a short axis view of a markedly dilated left ventricle and minimal posterior pericardial effusion (e). Left ventricular systolic dimensions = 4.4 cm, left ventricular diastolic dimensions = 4.8 cm. left ventricular ejection fraction of 18% and fraction of shortening of 8%.
261
in left ventricular ejection fraction of 18% and fraction of shortening of 8% with minimal posterior pericardial effusion (Fig. 4). The aortic root measured 1.4 cm and the left atrium 2.5 cm. No thrombi or vegetations could be seen. The evidence was compatible with a diagnosis of severe dilated cardiomyopathy due to varicella perimyocarditis. She was treated with diuretics and digitalis with some clinical improvement and, on repeated echocardiography, the pericardial fluid disappeared. She was discharged and was seen regularly in the out-patient clinic on a weekly basis, and seemed to do a little better. Six weeks after her discharge from hospital, she was admitted with left hemiplegia and clinical evidence of deteriorating heart failure. Computerised axial tomography was normal but, in spite of maximal medical and respiratory support, she died as a result of intractable heart failure.
Discussion Varicella is a frequent and highly contagious disease in the paediatric age group, with a course that is usually benign. Significant complications are rare and most frequently occur in immunocompromised patients and neonates [l-3]. Autopsy evidence of myocardial involvement has been described in patients dying of unrecognised myocarditis and from other complications of varicella [7-91. Manifestations of heart disease due to varicella are rare. They are recognised when there are rhythm disturbances and electrocardiographic abnormalities of rhythm, conduction or repolarisation [5,10-131 and when signs and symptoms of congestive heart failure become evident [14-161. The cases presented here illustrate the extremes in the presentation of varicella myocarditis. The first patient presented with supraventricular tachycardia which reverted spontaneously to sinus tachycardia without evidence of cardiac decompensation. Recovery was complete without any cardiac sequels. In contrast, the second patient developed progressive heart failure with poor myocardial function and low cardiac output. Her course was further complicated by an acute left hemiplegia, considered to be as a result of an embolus. She died in spite of maximal medical and ventilatory support. Potentially lethal arrhythmias have been described in varicella carditis, including various forms of ventricular tachycardia and fibrillation [lo]. Various degrees of atrioventricular heart block could be markers of infective myocarditis [7,12,17-201. The damage to the conduction system is usually reversible, but could result in permanent atrioventricular heart block with pacemaker dependency [7]. Although overt clinical evidence of varicella myocarditis is rare, increased awareness could identify manifestations, such as irregularities of the pulse or mild and transient reduction in functional capacity. Since the reduction in functional capacity is associated with markedly reduced left ventricular function, mild to moderate ventricular dysfunction could be clinically difficult to establish. The wide range of severity and variety of cardiac involvement in varicella leads us to the assumption that subclinical forms of myocarditis are probable during epidemics of varicella, similarly to those described and associated with other infections [21]. Another aspect worthwhile noting is that, in our second case, the
262
onset of hemiplegia was cardiac in origin, as opposed to direct or post-inflammatory involvement of the central nervous system by the herpes zoster virus.
References 1 Feldman S, Hughes WT, Daniel CB. Varicella in children with cancer. 77 cases. Pediatrics 1975;56:388-397. 2 Brunell PA. Fetal and neonatal varicella-zoster infections. Sem Perinatal 1983;7:47-56. 3 Kaplan L, Tully JB. “Viral” dissemination in patients with bronchogenic carcinoma: report of case with autopsy findings. Arch Path01 1953;56:312-322. 4 Thandroyen FT, Asmal AS, Armstrong TG. Varicella myocarditis producing congestive cardiomyopathy. Postgrad Med J 1981;57:199-201. 5 Kajalainen J, Viitasalo M, Kalq VR, Heikkila J. 24-hour electrocardiographic recordings in mild acute infectious myocarditis. Ann Clin Res 1984;16:34-39. 6 Kajalainen J, Heikkila J, Nieminen MS, et al. Etiology of mild acute infectious myocarditis. Relation to clinical features. Acta Med Stand 1983;213:65-73. 7 Hackel DB. Myocarditis in association with varicella. Am J Cardiol 1953;29:369-379. 8 Morales AR, Adelman S, Fine G. Varicella myccarditis. Arch Path01 1971;91:29-31. 9 Moore CM, Hem-y J, Benzing G, Kaplan S. Varicella myocarditis. Am J Dis Child 1969;118:899-902. 10 Fiddler GI, Campbell RWF, Pottage A, Godman MJ. Varicella myocarditis presenting with unusual ventricular arrhythmias. Br Heart J 1977;39:1150-1153. 11 Ettedgin JA, Ladusans E, Bamford M. Complete heart block as a complication of varicella. Int J Cardiol 1987;14:362-365. 12 Weinstein L, Shelokov A. Cardiovascular manifestations in acute poliomyelitis. N Engl J Med 1950;244:281-285. 13 Joos HA, Yu PNG. Electrocardiographic observations in poliomyelitis. Am J Dis Child 1950;80:22-23. 14 Moore CM, Henry J, Benzing III G, Kaplan S. Varicella myocarditis. Am J Dis Child 1969;118:899-902. 15 Levi GF, Prots C, Quadri A, Ratti S. Coxsackie virus heart disease and cardiomyopathy. Am Heart J 1977;93:419-421. 16 Noren CR, Tobin JD, Staley NA, Asinger RW. Association of varicella, myocarditis, and congestive cardiomyopathy. Pediat Cardiol 1982;3:53-57. 17 Arita M, Ueno Y, Masuyama Y. Complete heart block in mumps myocarditis. Br Heart J 1981;46:342-344. 18 Giles TD, Gohd RS. Respiratory syncytial virus and heart disease. A report of two cases. J Am Med Assoc 1976;236:1128-1130. 19 Smith WC. Coxsackie B myocarditis in adults. Am Heart J 1970;80:34-46. 20 Bromberg BI, Beekman RH, Heidelberg K. Heart block with viral myocarditis. J Pediatr 1986;108:709. 21 Lewes D, Rainford DJ, Lane WF. Symptomless myocarditis and myalgia in viral and mycoplasma pneumonia1 infections. Br Heart J 1974:36:924-932.