To the Editor:
I appreciated the article by Roy and colleagues1 in the Texas Heart Institute Journal. To the authors' knowledge, theirs were the first reported cases in which apical-variant hypertrophic cardiomyopathy was masked by apical ballooning from stress-induced cardiomyopathy. The authors added information about 5 reported cases of patients with hypertrophic cardiomyopathy (HCM) who had experienced an episode of takotsubo cardiomyopathy, all of whom had the obstructive HCM “with asymmetric septal hypertrophy, not apical-variant HCM.” What was actually observed is a recently detected phenomenon of apparent left ventricular (LV) apical hypertrophy,2,3 which occasionally is seen in the subacute and chronic phase of convalescence from takotsubo cardiomyopathy. It is caused by transient myocardial edema.4 Kato and colleagues3 observed apical hypertrophy of the LV at approximately 3 weeks after onset, when the wall motion had improved; the ventricular wall gradually became thinner, and the transient apical hypertrophy was attributed to hypertrophic signaling in the myocardium, which was stimulated by catecholamines.3 Myocardial edema with a hypertrophic LV apex has been reproducibly detected on cardiac magnetic resonance images4 and echocardiograms. Whether the LV hypertrophy1 represents apical HCM or takotsubo-induced myocardial edema can be resolved by observing subsequent electrocardiograms of these patients for chronically persisting giant negative T waves5 and R waves6 in the mid-precordial leads, and by comparing old and follow-up echocardiograms.
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