Left ventricular hypertrabeculation (LVHT) used to be a rare phenotypic trait. With advances in diagnostic imaging techniques, LVHT is being recognised in an increasing number of people. The scientific data shows a possibility of over-diagnosing this cardiomyopathy in a population of people who have very high physical activity. We described the case of a young athlete with no medical history who presented with syncope during a marathon running race. Initial evaluation showed elevated troponin I, transthoracic echocardiography showed a trabeculated ventricle and subsequent cardiac magnetic resonance (CMR), revealed left ventricular hypertrabeculation (LVHT). During subsequent evaluation by tilt table testing, vasovagal syncope was identified as the likely aetiology of syncope. The patient was advised to cease sports and stimulants like caffeine use. At the 29-month follow-up, CMR showed normalisation of the non-compacted to compacted myocardial ratio and improvement in left ventricular function, with no further syncopal episodes reported. This is an example of physiologic hypertrabeculation of the LV apex in a recreational endurance athlete with normalisation of non-compacted to compacted myocardial layer ratio after detraining. Physiologic hypertrabeculation, a benign component of exercise-induced cardiac remodelling, must be differentiated from noncompaction cardiomyopathy and other pathologies causing syncope. This case underscores the importance of distinguishing physiologic hypertrabeculation from pathological LVHT in athletes, highlighting that exercise-induced cardiac remodelling can normalise with detraining.

Left ventricular hypertrabeculation (LVHT) used to be a rare phenotypic trait. With advances in diagnostic imaging techniques, LVHT is being recognised in an increasing number of people. The scientific data show the possibility of the overdiagnosis of this cardiomyopathy in a population of people who have very high levels of physical activity. We describe the case of a young athlete with no medical history, who presented with syncope during a marathon running race. Initial evaluation showed elevated troponin I; transthoracic echocardiography showed a trabeculated ventricle and subsequent cardiac magnetic resonance (CMR) revealed left ventricular hypertrabeculation (LVHT). During subsequent evaluation by tilt table testing, vasovagal syncope was identified as the likely aetiology of the syncope. The patient was advised to cease sports and stimulants like caffeine use. At the 29-month follow-up, CMR showed the normalisation of the non-compacted to compacted myocardial ratio and an improvement in left ventricular function, with no further syncopal episodes reported. This is an example of the physiological hypertrabeculation of the LV apex in a recreational endurance athlete, with the normalisation of the non-compacted to compacted myocardial layer ratio after detraining. Physiological hypertrabeculation, a benign component of exercise-induced cardiac remodelling, must be differentiated from non-compaction cardiomyopathy and other pathologies causing syncope. This case underscores the importance of distinguishing physiological hypertrabeculation from pathological LVHT in athletes, highlighting that exercise-induced cardiac remodelling can normalise with detraining.

Ectopic parathyroid adenoma is a rare pathology. We present a clinical case of a giant ectopic parathyroid adenoma (PA) in an unusual location, which brought significant diagnostical and therapeutical challenges. The tumour in the mediastinum was found incidentally on chest computed tomography (CT). A biopsy was conducted, and histological examination revealed a well-differentiated neuroendocrine tumour. The tumour was excised via right thoracotomy. The final histological examination revealed a parathyroid adenoma, which was unexpected for our team. After three years of observation, there is no evidence of tumour recurrence.