Tako-Tsubo kardiyomiyopatisini taklit eden bir akut miyokard infarktüsü olgusu: kardiyak manyetik rezonans görüntülemenin rolü

PDF Dosyası: 

arastirmax_1397_pp_216-218.pdf

Introduction
The incidence of Tako-Tsubo cardiomyopathy
(TTC) is approximately 1% to 2% of the patients presenting with a acute coronary syndrome (ACS) (1).
TTC is an unique reversible cardiomyopathy which
is frequently precipitated by a stressful event and has
a clinical presentation that is indistinguishable from
a myocardial infarction (MI). Up to now there has
been no consensus on the diagnostic criteria for it.
Clinical presentation of most patients including ECG
and symptoms are equal with ACS. Cardiac magnetic
resonance imaging (CMRI) may provide insight into
potential pathophysiological mechanisms in TTC by
assessment of myocardial viability. There are limited
reports of CMR findings in patients with TTC (2).
Herein we report a 49-year-old woman presenting
with acute anterior MI in whom apical ballooning
was found and differential diagnosis was achieved by
CMRI.
Case Report
A 49-year-old woman with acute anterior MI was referred to our department for further evaluation after
initiation of the first line therapy with fibrinolytics.
After fibrinolytic infusion, she had been intubated
due to ventricular tachycardia (VT) and cardiac arrest.
She had been extubated 12 hours later and transferred
to our hospital. On hospital admission 12-lead surface
ECG demonstrated 2 mm ST segment elevation in leads V3-V6 accompanied with precordial poor R wave
progession and diffuse simetric T wave inversions. Her
previous cardiac history was unrevealing. Except for
a 2/6 grade apical systolic murmur, her cardiac examination was normal and lung fields were clear. Her
blood presurre was measured as 110/60 mmHg with
an aneroid sphygmomanometer and her pulse rate
was 92 bpm. On bedside echocardiographic examination, severe hypokinesis of the anterior wall sparing
basal segment with an ejection fraction of 40% and thrombus formation on the apex were detected. On
admission creatinine kinase (CK) was 425 U/L with
an MB fraction of 122 U/L. Her initial examination
revealed a left sided central facial paralysis and motor
aphasia with National Institute of Health Stroke Scale
score of 3 points was found on neurological examination. Cerebral magnetic resonance images revealed
an acute cerebral ischemia in the right frontal cortex.
As the patient was right handed, she had crossed aphasia. Subsequent diagnostic coronary angiography
revealed tortuous and normal coronary artery anatomy. Left ventriculogram showed hyperdynamic
basal contraction but hypokinesis of the midsegment
and akinesis of the apical segments compatible with
classic TTC (Figure 1). In CMRI late gadolinium enhancement demonstrated full thickness late myocardial enhancement in the apical area which was in
consistent with infarcted myocardium with microvascular obstruction foci (black arrows) and thrombus
(white arrow) in the left ventricular cavity (Figure 2).
In-hospital course of the patient was uneventful and
she was discharged from the hospital 5 days later with
medical therapy including warfarin.
Discussion
TTC (apical ballooning syndrome, stress induced cardiomyopathy, ampulla cardiomyopathy and broken
heart syndrome) was first described by Sato and coworkers in 1990 (1,3,4). TTC generally occurs in postmenopausal women and is indistinguishable from a MI.
Chest pain and dyspnea are usually initial symptoms
resembling acute MI, but syncope or cardiac arrest are
also encountered (1,3). Approximately two thirds of
the patients with TTC have an emotional or physical
stressful event (1). Concordantly our patient, who was
a prison guard, experienced sudden severe chest pain
developing after a prisoner assault. ST-segment elevation, especially on precordial leads, is the most common abnormality on the ECG obtained from those
patients. ST elevation in inferior or lateral leads, nonspecific T-wave abnormality, new bundle-branch block,
and normal ECG may be seen on admission. The ECG
findings are insufficient for differentiating TTC from
ST elevation MI. However the magnitude of ST shift is
usually less in TTC than that seen in a ST elevation MI
(1,2,4). Resolution of the ST-segment elevation, development of diffuse and often deep T-wave inversion,
and prolongation of the corrected QT interval may
commonly occur over 3 days (1).
TTC syndrome is underrecognized and often misdiagnosed. It is an important differential diagnosis of an
acute MI. The diagnostic criteria of the Mayo Clinic
is as follow (1): (a) transient hypokinesis, akinesis, or
dyskinesis in the left ventricular mid segments with
or without apical involvement; regional wall motion
abnormalities that extend beyond a single epicardial
vascular distribution; and frequently, but not always,
a stressful trigger; (b) the absence of obstructive coronary disease or angiographic evidence of acute plaque
rupture; (c) new ECG abnormalities (ST-segment elevation and/or T-wave inversion) or modest elevation
in cardiac troponin; and (d) the absence of pheochromocytoma and myocarditis. Japanese investigators
have recently presented diagnostic guidelines; however, the modified Mayo criteria are commonly used.
It is necessary to establish worldwide consensus on
diagnostic criteria for TTC.
Tako-Tsubo contraction pattern may be encountered in patients with acute MI (1,4,6). Chao et al.
reported that 14% of the patients with anterior ST
elevation MI had a classic contraction pattern of TTC
(4). Coronary angiography is the common tool to diagnose this condition, but angiography reveals only
prominent atherosclerotic plaques and may not detect lipid-rich plaques that have undergone positive
remodeling. On the other hand transient thrombosor spasm of these invisible plaques in LAD may cause
regional wall motion abnormalities as TTC (1,4).
Although the wall motion abnormalities could be
detected by echocardiography, CMR reveals subendocardial or transmural MI via myocardial delayed
enhancement even if coronary angiography does not
detect an obstructive lesion. It was reported that CMR
may be very helpful to differentiate TTC from MI (6).
In addition, CMR is more helpful to show the involvement of the right ventricular dysfunction.
In conclusion, CMR appears to be a useful imaging
modality for documenting the extent of the regional
wall motion abnormality and differentiating TTC
from MI and myocarditis in which delayed hyperenhancement is present. While TTC can mimic acute
MI, the converse is also true, that acute MI can mimic TTC. Cardiac magnetic resonance may be very
helpful to rule out TTC in this setting. The diagnosis of TTC can be easily excluded if CMR demonstrates myocardial late enhancement in consistent with
myocardial necrosis in a pattern and distribution in
consistent with acute MI