Myopericarditis Associated with Parainfluenza Virus Type I Infection
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Case Reports Acta Cardiol Sin 2006;22:163-9 Myopericarditis Associated with Parainfluenza Virus Type I Infection Jien-Jiun Chen,1 Ming-Tzer Lin,1 Lung-Chun Lin,1 Chuen-Den Tseng1 and Fu-Tien Chiang1,2 Myopericarditis is not uncommon, but often under-diagnosed. In fulminant cases, it may lead rapidly to circulatory failure or malignant arrhythmia, causing mortality. In this report, we describe a 41-year-old man who had episodes of convulsion one week after an upper respiratory tract infection. His electrocardiograms (ECGs) recorded during attack showed ventricular tachycardia. He had pulmonary edema and shock in the hospitalization course. The serial ECGs showed widespread PR depression, ST elevation and T-wave inversion afterwards, typical of myopericarditis change. The patient recovered finally. A paired serology test showed fourfold elevation of Parainfluenza virus type I antibody titer, suggesting that the parainfluenza virus might be the causative agent. This case illustrates that the parainfluenza virus might have a causative role in acute myopericarditis in which the clinical course is fulminant. Key Words: Myopericarditis · Ventricular tachycardia · Parainfluenza virus INTRODUCTION ual status of health until 7 days prior to admission, when he started to have cough, rhinorrhea and mild fever. Myopericarditis is a disease with both pictures of my- While watching television at about 9 pm on the day be- ocarditis and pericarditis. The presentations are variable, fore admission, he suddenly had generalized convulsion from fatigue, dyspnea, chest pain, to sudden death.1 Patients and cyanosis, lasting for several minutes. He regained his may recover fully upon rapid diagnosis and best supportive consciousness spontaneously. There was no post-ictal care. The etiology is protean. Despite vigorous studies for confusion. At a regional hospital, he was found to have the offending mechanism or microorganism, it is not found hyponatremia (129 mmol/l) and hypokalemia (2.7 mmol/ occasionally. We encountered a patient with myopericarditis, l). A brain computed tomography (CT) scan was nega- whose disease presented as ventricular tachycardia (VT). We tive. Intravenous potassium chloride and saline were found Parainfluenza virus infection the possible etiology. administered. The patient had generalized convulsion and cyanosis again at 4 am the next day. He was found to have pulseless VT (Figure 1). He received cardiopul- CASE REPORT monary resuscitation immediately. Amiodarone was in- fused. Recovery of spontaneous circulation was achieved This was a 41-year-old man who had been in his us- 5 minutes later. He was transferred to our medical center on the same day. The patient was an alcoholic, and he had consumed Received: August 16, 2005 Accepted: July 7, 2006 0.5-1 pack of cigarettes per day for a couple of years. He 1Department of Internal Medicine, 2Division of Cardiology and De- denied illicit drugs use or having systemic diseases. He partment of Laboratory Medicine, National Taiwan University Hos- did not have syncope, presyncope, or seizure episodes pital, Taipei, Taiwan. Address correspondence and reprint requests to: Dr. Fu-Tien Chiang, before. The patient’s family members all had flu-like Division of Cardiology, Department of Internal Medicine, National symptoms at the same time. His close relatives did not Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei, Taiwan. Tel: 886-2-2356-5426; Fax: 886-2-2395-7219; E-mail: have heart disease or sudden death history. [email protected] On examination, the temperature was 37.6 °C, the 163 Acta Cardiol Sin 2006;22:163-9 Jien-Jiun Chen et al. Figure 1. While the patient had convulsions, the ECG monitor showed ventricular tachycardia. pulse was 102/min, and the respiration was 18/min. The blood pressure was 123/99 mmHg. The patient was in a confused state. The conjunctivae were pink. The neck was supple. The lung field was clear; the heart sound was re- gular, without murmur or friction rub. Other physical examinations were unremarkable. After admission, the patient’s consciousness became clear. The ECG showed sinus tachycardia, PR depression and flattened T-waves (Figure 2A). Generalized convul- sion recurred, with monitor leads showing polymorphic VT. After defibrillation, the heart rhythm became nor- mal. The patient’s electrolytes were managed meticu- lously. Lidocaine was infused, instead of amiodarone, because the later ECG showed prolongation of the QTc. The patient developed desaturation progressively be- ginning the afternoon of the 2nd hospital day. A chest radiograph (CXR) revealed pulmonary interstitial pat- tern, more dominant on the left side (Figure 3). He was intubated due to hypoxemic respiratory failure. His blo- od pressure dropped after intubation and dopamine was Figure 3. Chest X ray on the day of admission showed left-side dripped. Follow-up CXR disclosed frank pulmonary ed- interstitial pattern. Figure 2A. ECG after 1st VT episode showed sinus tachycardia, PR segments depression and flattened T-waves. Acta Cardiol Sin 2006;22:163-9 164 Myopericarditis Associated with Parainfluenza Virus ema. Meanwhile, his EKGs showed ST-T elevation (Figure tractility. 2B). The echocardiography showed left ventricular (LV) The patient returned to his daily life after discharge. regional motion abnormality at inferior segments and A serology follow-up at outpatient clinic showed four- impaired LV contractility. There was no pericardial effu- fold increase in Parainfluenza virus type I antibody titer sion. He was diagnosed to have myopericarditis. The (Table 2), which may account for his myopericarditis. lung edema improved rapidly in 2 days, and he was ex- An ECG 6 weeks after this event showed normal T-wave tubated. His clinical course was complicated by rhabdomy- Table 1. Serial cardiac enzymes olysis. No more VT or convulsions were noted. The Hospital day CK CK-MB TnI cardiac troponin I data were highest on the admission U/l U/l Ng/mL day (2.64 ng/mL) and declined subsequently (Table 1). The creatine kinase (CK)-MB remained less than 5% of 1st 3140 073.4 2.640 2nd 5284 116.3 0.865 the CK value. ST-T elevation normalized a few days la- 4th 4662 102.4 0.054 ter. He was transferred to ordinary ward after stay in our 5th 114600 225.9 0.026 intensive care unit for 9 days. 6th 3981 061.1 ND The patient’s ECG evolved to T-wave inversion 13 8th 0486 018.3 ND days after this event (Figure 2C). He was subjectively 10th 0248 014.7 0 well. Follow-up echocardiography showed good LV con- ND = not done Figure 2B. ECG on the 2nd hospital day showed ST segment elevation and T-wave inversion. Figure 2C. ECG on the 12th hospital day evolved to big T-wave inversion. 165 Acta Cardiol Sin 2006;22:163-9 Jien-Jiun Chen et al. Table 2. Serology tests March 17th March 23rd April 11th Influenzae type A antibody 1:32+ 1:16+ 1:16+ Influenzae type B antibody 1:4+ 1:2+ 1:4+ Parainfluenzae type 1 antibody 1:2- 1:4+ 1:8+ Parainfluenzae type 2 antibody 1:2- 1:2+ 1:2- Parainfluenzae type 3 antibody 1:4+ 1:2+ 1:4+ Polio virus type 1 antibody 1:128+ ND ND Polio virus type 2 antibody 1:64+ ND ND Polio virus type 3 antibody 1:8+ ND ND Coxsackie virus antibody B1 1:2- 1:4+ 1:2+ Coxsackie virus antibody B2 1:2- 1:2+ 1:2- Coxsackie virus antibody B3 1:2- 1:2+ 1:2- Coxsackie virus antibody B4 1:2- 1:2- 1:2- Coxsackie virus antibody B5 1:2+/- 1:2- 1:2- Coxsackie virus antibody B6 1:2+/- 1:2- 1:2+ Enterovirus Type 70 antibody 1:2+ ND ND Mycoplasma pneumoniae IgG 1:2+ ND 1:2- Mycoplasma pneumoniae IgM Negative ND Negative ND = not done morphology and QT interval (Figure 2D). A thallium which might account for this myopericarditis episode. scan did not reveal perfusion defect under adequate stress. The patient presented his VT as generalized convul- The patient has not experienced symptoms of congestive sions. Besides seizure episodes, brain hypoperfusion re- heart failure or chest tightness till now. sulting from either tachycardia or bradycardia would oc- casionally induce motor activities or even generalized tonic-clonic convulsions.2 DISCUSSION The patient’s ECGs showed widespread PR depres- sion and then ST elevation. The differential diagnosis in- We have reported a patient with acute myopericar- cludes acute pericarditis, extensive antero-septal, lateral, ditis, presented as recurrent convulsion and polymorphic inferior myocardial infarction (MI), subarachnoid hem- VT. His clinical course was complicated by pulmonary orrhage (SAH), intracranial hemorrhage (ICH), tako- edema and cardiogenic shock. The serology data showed tsubo-like LV dysfunction, Osborn wave of hypother- fourfold increase in Parainfluenza type I antibody titer, mia, etc.3,4 The typical ECG changes of pericarditis, Figure 2D. ECG one and a month after this event became almost normal. Acta Cardiol Sin 2006;22:163-9 166 Myopericarditis Associated with Parainfluenza Virus though not necessarily present, are diffuse ST elevation family of paramyxoviridae.9 It mostly causes upper re- and PR depression.5 Both findings were present in our spiratory tract infection, but it occasionally invades the patient’s ECG. The ECG of pericarditis has four stages lower respiratory tract, causing bronchiolitis or pneumo- of evolutional change: diffuse ST elevation, normal, nia.9 It rarely causes viremia.9 The role of parainfluenza T-wave inversion, and normal again.5 It is difficult to virus in myocarditis/pericarditis is still controversial. A differentiate between MI and acute pericarditis from case series of parainfluenza virus myocarditis, based on ECG alone. The ECG of MI will often be convex ST serology diagnosis was reported.10 However, diagnosis elevation, and it is mostly confined to a territory.