The exact pathophysiology of TC is still a mystery. It usually presents as apical ballooning and basal hyperkinesis of the left ventricular myocardium as precipitated by emotional and physical stress, which is why it remains a special interest for neurocardiologists. Using radioactive metaiodobenzylguanidine (MIBG), a chemical structurally similar to norepinephrine, Akashi and colleagues3 in 2004 hypothesized that TC might be caused by neurogenic myocardial stunning due to autonomic imbalance. Initial MIBG myocardial scintigraphy depicted a unique pattern of ventricular asynergy with decreased uptake of MIBG during the acute phase of TC isolated in the apex, reflecting cardiac sympathetic denervation.3 This may explain why, despite high levels of catecholamines in the blood, the left ventricle would demonstrate apical hypokinesis with basal hyperkinesis.4 Three years later, Akashi and colleagues5 sought to prove this hypothesis clinically by analyzing domains of heart rate variability, parameters considered as measures of cardiac autonomic function. They found out that time domain heart rate variability parameters increased and coincided with decreased left ventricular wall motion during the acute phase of TC. These parameters significantly improved as left ventricular wall motion returned to normal, supporting their previous hypothesis.