CARDIOLOGY CASE:
MYOCARDITIS PRESENTING AS SUDDEN CARDIAC ARREST Avaneesh Jakkoju, MD, Robert O. Drutel, MD, Jameel Ahmed, MD, Pedro R. Cox-Alomar, MD, Paul A. LeLorier, MD, and D. Luke Glancy, MD
A 17-year-old woman with no significant past medical history was transferred from another hospital for further management after a cardiac arrest. For several weeks the patient had been taking an over-the-counter weight- loss supplement called Xenadrine, which contains turmeric extract, alpha lipoic acid, safflower seed oil extract, coconut oil extract, black pepper extract and a few other undisclosed ingredients listed as naturally sourced energy, and another supplement that reportedly contains Yohimbine. For 4 days prior to presentation the patient complained of pleuritic non-exertional chest pain. The day of her admission, she had similar chest pain while playing competitive soccer, and after arriving at home she went to her room to rest. Shortly thereafter her mother heard her collapse and found her daughter unresponsive, pale, and without a pulse. The mother started chest compressions and summonedemergency medical service, which found the patient in ventricular fibrillation. Epinephrine, amiodarone, and 2 transthoracic electrical shocks restored sinus rhythm. At the outside hospital she was intubated and because of frequent short runs of non-sustained ventricular tachycardia she received another bolus of amiodarone. She was hemodynamically stable and did not require vasopressors. Her white blood cell count was 22140/mm³ (reference 3900 – 12700); D-Dimer level was 12.06 μg/ml (reference 0-499); Troponin I was 6.241 ng/ml (reference 0.00-0.026); brain natriuretic peptide was 121 pg/ ml (reference 0-99); and C-reactive protein was 35.3 mg/L (reference 0.0-8.2). Toxicology and pregnancy screens were negative. Computed tomography of her head showed no acute abnormalities. An electrocardiogram was recorded (Figure 1), and she was transferred to our hospital where she underwent further testing.
ng/ml (reference 0.00-0.026) at the outside facility and continued to trend downward, as did her white blood cell count, during her current hospital stay. Three days following her arrest a repeat echocardiogram showed normal left ventricular systolic function with an EF of > 55%. Her short-term memory rapidly improved. An exercise stress test did not reveal signs of ischemia or elicit any arrhythmia. The patient was fitted with a wearable defibrillator (LifeVest) and discharged home on metoprolol succinate and lisinopril. Two months after the arrest, no arrhythmia has been detected by the wearable defibrillator. Follow-up MRI with gadolinium continues to show late enhancement. In the United States approximately 360,000 cases of out-of-hospital cardiac arrest occur each year,¹ and the incidence of death from sudden cardiac arrest (SCA) in persons less than 35 years of age has been estimated from 1.0 to 6.4 per 100,000 patient years.² Coronary artery disease (CAD) is the most common cause for SCA constituting about 80% cases, followed by non-ischemic cardiomyopathy accounting for another 10% to 15%. The most common cause in patients less than 35 years old, however, is hypertrophic cardiomyopathy. Other causes which are seen predominantly in youngpatients include longQT syndrome, short QT syndrome, channelopathies, and congenital heart disease.³ Previous studies have reported anywhere from 2% to 42% of cases of SCA due to myocarditis.⁴⁵
Signal averaged electrocardiogram was unremarkable. Coronary arteriography was normal. Endomyocardial biopsy revealed normal endocardium with minimal focal myocardial fibrosis and subendocardial thickening. Electron microscopy of the endomyocardial biopsy showed normal myocytes, mitochondria, glycogen, and a normal amount of interstitial tissue without any abnormal fibrillary connective tissue or amyloid deposits. The patient had a left ventricular ejection fraction (EF) of 40% and no structural abnormality on transthoracic echocardiogram. Electrophysiological testing foundnoabnormal atrioventricular connection or inducible arrhythmia. There was delayed enhancement from base to apex in the posterior-inferior wall of the left ventricle on cardiac magnetic resonance imaging (MRI) (Figure 2).
Figure 2. Cardiac MRI with gadolinium showing delayed enhancement of the posterior-inferior wall of the left ventricle. Cardiac MRI can be a crucial tool in the diagnosis of myocarditis. It shows myocardial edema on T2 weighted images, capillary leak on early gadolinium enhancement, and myocardial necrosis or fibrosis by late gadoliniumenhancement.⁸
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8 J LA MED SOC | VOL 171 | NO. 1
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