A Case of Acute Myocarditis Caused by Pandemic (H1N1) 2009 Influenza Virus

Abstract

The new strain of swine-origin H1N1 influenza virus was initially described in April 2009, and the first cases of infection were reported in the Mexican state of Veracruz. As the disease spread rapidly to other countries, the World Health Organization declared the new strain of influenza virus as pandemic on June 11, 2009.1 Infection with this virus predominantly affects young patients in relatively good health, without documented underlying illnesses. Although the majority of them experience mild symptoms, severe complications associated with high mortality can occur. Acute myocarditis can cause substantial myocardial injury and lead to arrhythmia, atrioventricular block, cardiogenic shock and sudden cardiac death. The majority of myocarditis cases are of viral etiology and presentation can often mimic myocardial infarction, pulmonary embolism or acute heart failure. Although endomyocardial biopsy remains the gold standard, cardiac magnetic resonance imaging (CMRI) has recently been shown to be a powerful tool in the diagnosis of acute myocarditis. We present a rare case of acute myocarditis caused by H1N1 influenza virus in a young patient. An 18-year-old man of Greek origin was admitted with a 3-day history of fever, malaise, sore throat and dry cough, and a 5-hour history of central chest pain of sudden onset. The pain radiated to the left shoulder and was relieved when the patient leaned forward. The pain did not respond to sublingual glyceryl trinitrate. He was a smoker and had a history of spontaneous ventricular septal defect closure at the age of 3 years. On admission, his heart rate was 66 beats/min, oxygen saturation in room air was 98%, blood pressure was 115/75 mmHg, and axillary temperature was 37.1°C. Heart auscultation revealed normal heart sounds, a pericardial friction rub and no murmurs. Electrocardiography showed sinus rhythm, with incomplete right bundle branch block, ST segment elevation with biphasic T-waves in leads V3 and V4, and ST segment depression with biphasic T-waves in leads I, II and aVL. Chest radiography was normal. Echocardiography depicted normal left ventricular ejection fraction, with no regional wall motion abnormalities or pericardial effusion. White blood cell count was 12.5×109/L, C-reactive protein was 17.1 mg/L, and erythrocyte sedimentation rate was 17 mm/hr.