I read the interesting report by Y-Hassan et al, published online ahead of print, on September 3, 2015, in the American Journal of Cardiology , about a 64-year-old woman who suffered midventricular Takotsubo syndrome (TTS) with subsequent full recovery, after the defeat of the Chilean national football (soccer) team by the Brazilian national team during the FIFA 2014 World Championship. The inception of her illness was 75 minutes after the onset of cardiac arrest of her husband who had an acute myocardial infarction (AMI), 2 hours after the completion of the game, and died from anoxic encephalopathy 3 days later. The investigators refer to a similar patient with “a midapical TS in a 56-year-old man,” which was “triggered by an acute emotional stress event after the defeat of his favorite soccer team during the Euro 2012 cup,” thinking that their “case is the second one,” I am aware of another case published 4 years ago of an 82-year-old Italian woman who suffered TTS, immediately after watching a football game in which Italy lost to Slovakia in the 2010 World Cup series, which frustrated and angered the patient, who blamed for the loss the Italian national team coach, Marcello Lippi. The investigators reported that case as “Lippi-induced” cardiomyopathy, implicitly referring to the homonym (or homophone) “λυπη,” which sounds in Greek like “Lippi,” but it means unhappiness, grief, or sorrow, rather than anger. Of interest is that, as the investigators remarked, happiness can also trigger TTS, as exemplified by a number of recent reports, suggesting that the intense exhilaration from winning a game of one’s favorite team may lead to TTS.

Another thought that the present report induces is whether even the AMI triggered in the patient’s husband shortly after the stressful football game could have been facilitated by an initial TTS, which subsequently destabilized/disrupted/ruptured a vulnerable atherosclerotic plaque in the patient’s left anterior descending coronary artery, causing thrombosis and AMI. The disrupted systolic motion of the left ventricular myocardium, with normokinetic/hyperkinetic myocardial territories abutting akinetic dyskinetic (ballooning) myocardial regions, could have led to a rupture of a coronary plaque in the left anterior descending coronary artery and coronary thrombotic occlusion resulting in AMI and cardiac arrest. Thus, I explicitly propose that in some cases of “classic” AMI, the underlying triggering mechanism could be TTS; this is parallel to a recent speculation that acute spontaneous coronary artery dissection may occasionally be due to TTS.