Myocardial Apical Hypertrophy and Takotsubo Cardiomyopathy

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.