A 47-year-old man was referred from an outside facility with complaints of recurrent falls. He had been referred to a neurologist for evaluation of recurrent unexplained syncope. Each event was non-convulsive, random, and preceded by a sudden loss of balance that would progress to falling due to altered mental status. There was no apparent triggering factor, post-event confusion, or loss of either bowel or urinary continence. He had been evaluated twice at a local healthcare facility for these falls, but no cause was identified.He was referred to us on the third presentation after suffering multiple facial and thoracic injuries. He had no evident cardiopulmonary symptoms. Because he was adopted, he had no knowledge of any family history history of cardiac events. His past medical history included bipolar disorder, tobacco abuse, alcohol dependence, and atypical facial pain. His home medications were carbamazepine, lamotrigine, olanzepine, diazepam, and venlafaxine. The only recent change in his medications was a carbamazepine dose reduction because a provider at an outside facility had thought that this might be contributing to his symptoms. On review of his past medical records (more than 10 years prior), left ventricular hypertrophy had been mentioned, but it had not been followed-up in subsequent evaluations. Previous computerized tomography (CT) of the head and neck had been unremarkable.Clinically, the patient was alert, awake, and oriented. Blood pressure was 123/63 mmHg, pulse 83 beats/minute, temperature 99.6ºF, respirations 20 breaths/ minute, and oxygen saturation 95% on room air. He had no orthostatic hypotension. The physical examination was normal except for the multiple facial swellings and left-sided chest wall tenderness he had sustained from the falls. Apical hypertrophic cardiomyopathy (AHC) is a rare variant of hypertrophic cardiomyopathy. Since its description by Sakamoto in 1976 in Japanese patients, our understanding of this entity has evolved. Although cardiac magnetic resonance imaging has emerged as the gold standard for diagnosing AHC, clinical attention must be drawn to the unique electrocardiographic features that provide the initial clues to making the diagnosis. In this case, we present a 47-year-old man with AHC who presented with recurrent syncope, but anomalies on his electrocardiogram went unnoticed on two clinical encounters. He was subsequently admitted to our service and rapidly diagnosed after we observed the very classical findings in the plain twelve lead electrocardiogram done at the time of admission. In a clinical encounter involving a patient presenting with recurrent syncope, special attention must be focused on the electrocardiogram to decipher the unique diagnostic features it might show.