Koroner arter hastalığına eşlik eden apikal hipertrofik kardiyomiyopati: bir olgu sunumu

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Introduction
Apical hypertrophic cardiomyopathy (ApHCMP) is
a rare form of hypertrophic cardiomyopathy, which is
diagnosed by giant T wave negativity on electrocardiogram (ECG) and “spade-like“ configuration of the left
ventricular (LV) cavity at end diastole on ventriculography (1,2). ApHCMP is accompanied by symptoms
and ECG changes indicative of myocardial ischemia
(3,4). There are very limited data about ApHCMP coexisting with coronary artery disease (CAD) (5-7). We
present an interesting case of CAD who was later found
to have ApHCMP and a decrease in giant T wave negativity after coronary artery bypass grafting (CABG).
Case Report
A 52-year-old man who had previously documented
CAD was referred to our department with a typical
chest pain. He was a heavy smoker with hypercholesterolemia. He had a history of percutaneous coronary
intervention (PCI) to the right coronary artery at another medical center 7 years ago. Physical examination was normal. His ECG showed sinus rhythm, LV
hypertrophy (SV1+RV5 46 mm), and giant negative
T waves (>10 mm) in leads V2-6, I and avL (Figure
1). On transthoracic echocardiographic examination left ventricular diameters were within normal limits and left atrial diameter was increased (41 mm).
Interventricular septum and posterior wall thickness
were 12 and 11 mm, respectively. However, apical
segments of left ventricle could not be visualized
because of poor image quality. Coronary angiography revealed 70% stenosis in the mid-portion of the
left anterior descending artery (LAD), 80% stenosis
in the proximal segment of the left circumflex coronary artery (Figure 2) and 98% stenosis in the proximal segment of the right coronary artery (RCA). Left
ventriculography demonstrated a “spade-like” configuration on the right anterior oblique view (Figure
2). Surgical treatment was suggested and CABG (left
* Department of Cardiology, Çukurova University School of Medicine
**Department of Emergency Medicine, Çukurova University School of
Medicine
Reprint request: Dr. Abdi Bozkurt, Department of Cardiology, Çukurova
University School of Medicine, 01330, Adana, Turkey
E-mail: abozkurt@cu.edu.tr
Date submitted: April 29, 2008 • Date accepted: June 09, 200956 • March 2010 • Gulhane Med J Bozkurt et al.
internal thoracic artery to the LAD and saphenous
vein grafts to the obtuse margin branch and to the
RCA) was performed 4 weeks later. Subsequent ECGs
showed decreases in both R and S waves (SV1+RV5 27
mm) and negative T waves (3-6 mm). Negative T waves also returned to positive in leads V2-3 (Figure 3).
Discussion
Although ApHCMP is not associated with sudden
cardiac death and has a benign prognosis in terms of
cardivascular mortality, one third of the patients experience serious cardivascular complications, such as
myocardial infarction, congestive heart failure and arrhythmias (7). There are only a few case reports about
ApHCMP coexisting with CAD (5,6). Furthermore,
most of the ApHCMP patients with myocardial infarction have normal coronary arteries (7). On the
other hand, ApHCMP may be confused with myocardial ischemia or acute coronary syndrome (3,4). In
our case, the T wave negativity primarily suggested
Figure 1. Electrocardiogram shows left ventricular hypertrophy and giant negative T waves (>10 mm) in leads V2-6, I and avL
Figure 2. Coronary angiogram shows 70% stenosis in the mid-portion of the left anterior descending artery and 80% stenosis in the proximal
segment of the left circumflex coronary artery (left). A “spade-like” configuration of left ventricle at the right anterior oblique view (right)Volume 52 • Issue 1 Apical hypertrophic cardiomyopathy • 57
progression of CAD as the patient had a known history of CAD and PCI. Moreover, a significant stenosis
of LAD was supporting this observation. However,
left venticulography showed an ApHCMP coexisting
with CAD. Our patient was treated with CABG. To
our knowledge, this is the third case of CABG performed for CAD coexisting with ApHCMP. Two similar
cases have been previously reported (5,6).
Typical giant T wave negativity may decrease in
some patients with ApHCMP. Horita et al. have reported two cases of ApHCMP, in whom giant T waves
resolved during 10 years (8). The reason of this change was the development of dilated cardiomyopathy
in one patient and CAD in the other. Eriksson et al.
have also showed that the development of myocardial infarction usually causes loss of giant T wave
negativity (7). Our case had no myocardial infarcion
or dilated cardiomyopathy, and decrease in T wave
negativity and amplitudes of R and S waves were
observed after CABG. The possible reasons of these
changes might be results of CABG, such as decreasing
myocardial ischemia due to CAD and/or anatomical
changes in chest wall.
In conclusion, despite its low incidence, giant negative T waves on ECG may be considered as ApHCMP
even in the presence of documented coronary artery
disease, and T wave negativity may decrease after
revascularization.