Unusual cause of exercise-induced ventricular fibrillation in a well-trained adult endurance athlete: a case report

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Abstract

Introduction
Sudden death has been defined as \an abrupt unexpected death of cardiovascular cause, in which the loss of consciousness occurs within 1 to 12 hours of onset of symptoms\" [1]. Although sudden deaths in athletes are dramatic and tragic occurrences, the total incidence of sudden death during sport is rather low. The annual incidence of sudden deaths in athletes under 35 years is 2.62 per 100,000 for male and 1.07 for female athletes [2], whereas the risk of sudden death in athletes over 60 years old can be 100-fold higher compared with young athletes [3]. The precise diseases responsible for sudden death differ considerably with regard to age. In young athletes, congenital malformations of the heart and/or vascular system cause the majority of deaths and can only be detected noninvasively by complex diagnostics [4,5]. In contrast, the underlying cause in older athletes who die suddenly is usually atherosclerosis of the coronary arteries [3]. Reports of congenital coronary anomalies as a cause of sudden death in older athletes are rare

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This case report presents a coronary anomaly as the most likely reason for an episode of exercise-induced ventricular fibrillation in a well-trained 48-year-old endurance athlete.

Case presentation
A 48-year-old, well-trained, long-distance runner collapsed at the finish of a half marathon. On the day of the incident, the air temperature was relatively high (25°C). Against his usual practice, the athlete tried to accelerate on the last hundred meters towards the finish line. Immediately after the collapse, cardiopulmonary resuscitation with defibrillation of ventricular fibrillation was successfully carried out.

There were no indications of cardiovascular and other serious diseases in the athlete's medical history. The athlete had never noticed any cardiac symptoms, in particular no anginal discomfort, dysrhythmia or episodes of cardiac syncope. Since youth, regular endurance training had been performed without any problems. Before the incident, his training load was 30 to 40 kilometres of running each week. The athlete's family history was also negative for cardiovascular diseases. He was taking no regular medication.

The patient was a 48-year-old man, stature 178 cm, body mass 83.6 kg, blood pressure (BP) 120/70 mmHg, heart rate 48/minute. Percussion and auscultation of the heart and lung showed no pathological findings. His troponin T level was slightly elevated in the emergency room (0.069 ng/ml), and significantly elevated 1 day after the myocardial infarction (0.392 ng/ml). It returned to normal levels within 5 days. An electrocardiogram (ECG) was performed and showed a normal axis and sinus rhythm, heart rate 65/minute, and no pathological findings. Echocardiography showed a normal configuration of the four chambers, with good left and right ventricular function. Laboratory findings showed elevated total cholesterol (217 mg/dl) and low-density lipoprotein (LDL)-cholesterol (161 mg/dl) levels, and reduced high-density lipoprotein (HDL)-cholesterol (47 mg/dl) levels. All other laboratory findings, in particular the electrolyte levels, were within normal ranges.

A coronary angiography was conducted because of the unknown etiology of the ventricular fibrillation. A coronary artery anomaly with a left-side origin of the right coronary artery (RCA) with minimal wall alterations was revealed. Multislice computed tomography of the coronary arteries confirmed these findings (Figures 1 and 2). Cardio-magnetic resonance imaging demonstrated a non-transmural late-enhancement of gadolinium in the basal ventricular posterior wall, on both right and left sides, with corresponding hypokinesia of the right ventricular wall and an ejection factor of 48%. Two days after the incident, an electrophysiology study showed inducible temporary polymorphic ventricular tachycardia and inducible ventricular fibrillation (Figure 3). The electrophysiology study was performed at the apex of the right ventricle (base-stimulation: 600 ms, extra-stimulations beginning with 250 ms). The myocardial scar could have been responsible for the induction of ventricular fibrillation. However, this finding was unspecific and did not completely clarify the etiology of the symptoms. No cardiac arrhythmia was detected in a 24-hour ECG.

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