We read with great interest the recent article in CHEST (September 2007) on tako-tsubo cardiomyopathy (TTC) by Kurowski et al1and would like to congratulate the authors for their elegant study. In 35 patients with TTC, they reported the occurrence of emotional stress events in 15 patients (42.8%) including a case of near-drowning syndrome (NDS). In our clinical series2 of 52 patients (51 women; mean [± SD] age, 63.58 ± 10.55 years), an emotional stress event was documented in 43.2%. We also registered a 57-year-old woman presenting with TTC after the occurrence of NDS.2A few hours after the event, ECG changes developed, and a typical echocardiographic pattern of apical ballooning with a mild increase in serum troponin level was seen. Left ventriculography confirmed the apical ballooning, and coronary angiography revealed normal coronary arteries. ECG changes and apical contraction abnormalities were completely reversed within 3 weeks. Drowning is an extremely stressful situation that leads, via the uncommon combinations of different pathophysiologic mechanisms, to sympathetic nerve activation (SNA).3 In patients with NDS, submersion in liquid causes hypoxemia due to fluid aspiration or reflexive laryngospasm. Once hypoxemia occurs, cerebral hypoxia, pulmonary reflexes, and concomitant panic and/or struggle induce SNA.3Hypoxemia related to NDS could have induced transient myocardial dysfunction mediated by an SNA. Although the pathogenesis of TTC remains unclear, a common pathophysiologic pathway seems to be an exaggerated sympathetic activation.4 Thus, SNA could be considered the “real” link between NDS and TTC.