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• W3126184844 abstract "Introduction Abrupt onset of atrial arrhythmias in a young athlete should lead to consideration of excesses of stimulants, such as caffeine, herbal remedies, supplements, illicit drugs, hyperthyroidism, viral infections, anemia, and myocarditis. We have found palpitations to be reported in about 10% of our athletes but rarely have they affected athletic performance as much as they did in this case. Presentation A 20-year-old elite collegiate male endurance runner presented with a complaint of palpitations. The palpitations were described as feelings of “skipped beats” with hard runs that resolve with rest in about 1 min. He did not have any chest pain, syncope, neurologic symptoms, or shortness of breath. He was able to finish races but with slower times than normal. One month prior to the onset of palpations, he had a fever to 103.5°F, myalgias, headache, cough, and congestion and was diagnosed with positive influenza A subtype H3 via nasal swab. He had a medical history of reactive airway disease and no surgical history or family history of sudden cardiac death, arrhythmia, or cardiomyopathy. He was taking daily magnesium and iron and did not take any supplements nor caffeine. He was a division 1 NCAA distance runner with multiple awards and honors. On physical examination, he had normal first and second heart sounds and a physiologic third heart sound. He had occasional extra beats prior to a regular S1 S2 heart beats during the examination. Initial electrocardiogram (EKG) revealed normal sinus rhythm. Laboratories including thyroid function, electrolytes, erythrocyte sedimentation rate, C-reactive protein, and ferritin were within normal limits. EKG 3 wk later demonstrated atrial bigeminy (Fig.). A cardiac exercise test was then performed showing exceptional exercise capacity in the elite class (82 mL O2·kg−1·min−1), with atrial bigeminy present at rest and in recovery. A cardiac magnetic resonance imaging with and without contrast showed a normal ejection fraction, mildly dilated ventricles, and no evidence of fibrosis or cardiomyopathy. He had a total of three 8-d electrocardiogram (ECG) patch monitors beginning 3 wk after presentation. The first heart ECG patch showed atrial bigeminy, and the last revealed runs of atrial fibrillation and atrial flutter lasting up to 10 min with 1.1% total burden.Figure: EKG 3 wk after presentation demonstrating atrial bigeminy.After discussion of conservative versus interventional management, a course of 10 mg of oral prednisone daily for 14 d was prescribed to reduce any possible atrial myocardial inflammation. Five months after initial symptoms, his symptoms persisted with running. At this time, an electrophysiological study was obtained and discovered a single left pulmonary vein focus for the atrial fibrillation during repeated chemical stimulation. As a result of these findings, failed response to oral prednisone, and patient desire to return to running, an isolated single left pulmonary vein ablation was performed for the atrial fibrillation, and a cavo tricuspid isthmus ablation was performed for the atrial flutter and bigeminy. After resting 1 wk from the ablation, he gradually increased his running volume and intensity. At 1 month postablation, he had returned to his full training load with reduced palpitations and arrhythmias during ECG monitoring. At near 2 months postablation, he had decreased his times in several events and ran his first sub 4-min mile. Discussion Abrupt onset of atrial arrhythmias in a young athlete should lead to consideration of excessive alcohol ingestion, lack of sleep, and the possible acquired causes listed in the Table (1–4). Our athlete had a viral illness 2 months prior, which could be consistent with an atrial myocarditis; however, there were no increased inflammatory markers or imaging studies that further supported atrial myocarditis. Additionally, his laboratories, including thyroid function tests, were negative, and he denied any supplements, drugs, or caffeine intake. Table - Causes of abrupt onset of atrial arrhythmias in a young athlete. Cause of Arrhythmia Associated Symptoms Types Excess stimulants Headache, tremor, insomnia Caffeine, amphetamines Illicit drugs, herbal remedies and supplements Variable Anabolic steroids, erythropoietin, growth hormone, insulin-like growth factor, β-2 agonists, diuretics, cannabinoids, glucocorticoids, alcohol, β blockers, narcotics Hyperthyroidism Weight loss, heat intolerance, tremulousness, anxiety, insomnia, and diaphoresis Subclinical hyperthyroidism, thyroiditis, exogenous thyroxine Myocarditis/viral infection History of preceding infection Adenovirus, parvovirus B19, human herpes virus 6 and enterovirus Anemia Pallor Iron deficiency anemia, thalassemia The management of exercise-induced atrial bigeminy, and subsequently, atrial fibrillation and atrial flutter as in our patient are controversial in regard to return to play guidelines. The 2015 American Heart Association and American College of Cardiology Task Force 9 Scientific Statement on return to play for competitive athletes with arrhythmias and conduction defects states “athletes with atrial fibrillation should first undergo a workup that includes thyroid function and questions regarding drug use. There is Class I, Level C Evidence that if athletes have low-risk atrial fibrillation that is well tolerated and self-terminating, they may participate in all competitive sports without therapy” (5). Although our patient's arrhythmias were self-limiting, they were limiting his competitive abilities, and he was symptomatic with palpitations. There was a near 50% internal division between an international group of experienced sports cardiologists and electrophysiologic specialists recommending watching and waiting versus interventional procedures. An argument for conservative management was that if this was a temporary inflammatory condition from influenza-induced atrial myocarditis, the arrhythmias should self-resolve once the inflammation subsided. In addition to the risks associated with an interventional procedure, there is a risk for repeat procedures, as well as the result of a “stiff atria,” which could potentially limit future exercise performance. In a study of 182 endurance athletes performed by Calvo et al. (6), the adverse effects of interventional ablation included transient cerebrovascular ischemia (2.2%), transient inferior myocardial ischemia (1.6%), and cardiac tamponade (1.1%). A repeat ablation was performed in 67 (37%) of these 182 athletes. The “stiff atrial syndrome” may be seen in 1.4% to 8% of patients after radiofrequency ablation for atrial fibrillation. The pathophysiology is thought to be caused by ablation-induced formation of scar tissue in the left atria, which can become fibrotic and stiff, which can lead to diastolic dysfunction and pulmonary hypertension (7). This case highlights the lack of clinical guidelines for return to play in the management of paroxysmal atrial arrhythmias in elite athletes. As evident in this case, management is not well agreed upon for return to play. Treatment must take into consideration the etiology of the atrial arrhythmia, potential complications of persistent atrial arrhythmias, risks of invasive cardiac intervention, and the athlete's goals on future competition. Cardiac ablation may then be appropriate if conservative management has failed to resolve symptoms and return to play." @default.
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• W3126184844 date "2021-02-01" @default.
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• W3126184844 title "Palpitations in an Elite Running Athlete: When to Run Through the Beat? A Case Report" @default.
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