Jagminas Rokas, Šerpytis Rokas, Šerpytis Pranas, Glaveckaitė Sigita
Faculty of Medicine, Vilnius University, LT-03225 Vilnius, Lithuania.
Clinic of Cardiac and Vascular Diseases, Institute of Clinical Medicine, Faculty of Medicine, Vilnius University, LT-03225 Vilnius, Lithuania.
Medicina (Kaunas). 2024 Dec 28;61(1):32. doi: 10.3390/medicina61010032.
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.
左心室肌小梁增多(LVHT)曾是一种罕见的表型特征。随着诊断成像技术的进步,越来越多的人被诊断出患有LVHT。科学数据表明,在体力活动水平非常高的人群中,这种心肌病存在过度诊断的可能性。我们描述了一名无病史的年轻运动员的病例,他在马拉松比赛中出现晕厥。初步评估显示肌钙蛋白I升高;经胸超声心动图显示心室肌小梁增多,随后心脏磁共振成像(CMR)显示左心室肌小梁增多(LVHT)。在随后的倾斜试验评估中,血管迷走性晕厥被确定为晕厥的可能病因。建议患者停止运动并避免使用咖啡因等兴奋剂。在29个月的随访中,CMR显示非致密化与致密化心肌比例恢复正常,左心室功能改善,未再报告晕厥发作。这是一名业余耐力运动员左心室尖部生理性肌小梁增多的例子,在停止训练后非致密化与致密化心肌层比例恢复正常。生理性肌小梁增多是运动诱导的心脏重塑的良性组成部分,必须与心肌致密化不全心肌病和其他导致晕厥的病理情况相鉴别。该病例强调了在运动员中区分生理性肌小梁增多与病理性LVHT的重要性,突出了运动诱导的心脏重塑可通过停止训练恢复正常。