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Correspondence |
I read with interest the case of apical hypertrophic cardiomyopathy (HCM) reported by Ghersin et al [1]. The authors ably demonstrated the capabilities of multidetector CT in the evaluation of apical HCM, with the additional bonus of CT coronary angiography. As the early reports of this entity referred predominantly to Japanese males, it was initially thought to be confined to Japan. However, in 1982, we were among the first to report apical HCM outside Japan [2], yet it continues to constitute only about 2% of cases of HCM, whereas in Japan the apical variant is much more common.
I agree with the authors that the clinical course is far from benign in Western countries, particularly at long-term follow-up [3]. We have shown morphological, electrocardiographical and serious arrhythmic manifestations during 5 years to 20 years of follow-up. Sustained ventricular tachycardia and ventricular fibrillation necessitating the implantation of an internal defibrillator was described. Apical aneurysm formation was seen in a patient with normal coronary arteries at extended follow-up. This may create diagnostic difficulties relating to its aetiology [4]. It is interesting to speculate whether myocardial bridging described in this case will be detected more often in apical HCM utilizing the CT technique. This could have possible aetiological implications for the formation of aneurysms.
Finally, the angiographic characteristic spade-like configuration on angiography is observed at end-diastole and not in systole as described in the present report. In fact, in this entity, the vigorous contraction in systole results in obliteration of the apical segment. After all, it is always a good thing to "call a spade a spade".
Yours etc.,
Bet-el 26 Haifa, 34564 Israel. E-mail: edabinader{at}hotmail.com
Received for publication January 14, 2007. Accepted for publication July 3, 2007.
References
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