Abstract
An acute coronary ischemic insult may “cause” prolonged post-ischemic myocardial stunning. In spite of being a major stress factor, acute coronary syndrome is regarded as an exclusion criterion for takotsubo syndrome. We describe the case of a 39-year-old female patient presented with anterior ST-elevation myocardial infarction. Emergency coronary angiography revealed spontaneous coronary artery dissection confirmed with intravascular ultrasound examination. The patient developed clinical, angiographic and cardiac image features consistent with both post-ischemic myocardial stunning and takotsubo syndrome. Complete healing of the coronary dissection occurred with conservative treatment. There was also resolution of the greatest part of the left ventricular dysfunction. The findings in the present case indicate that the post-ischemic myocardial stunning and takotsubo syndrome are two different names for the same clinical condition and that the acute coronary syndrome triggers rather than excludes takotsubo syndrome.
1
Introduction
Spontaneous coronary artery dissection (SCAD) is a fatal disease with a high mortality in the acute stage. It occurs most often in young women, age < 40 years, and frequently in the peripartum period. SCAD is usually presenting with acute coronary syndrome caused by acute coronary stenosis or occlusion, which may necessitate emergency coronary revascularization . An acute ischemic attack caused by acute coronary syndrome may induce prolonged post-ischemic myocardial stunning . In spite of being a major physical stress factor, acute coronary syndrome is still erroneously regarded as an exclusion criterion for takotsubo syndrome . Herein, we present a case of SCAD in a young woman, treated successfully with conservative measures. She developed prolonged post-ischemic myocardial stunning and had at the same time all the clinical signs of takotsubo syndrome .
2
Case presentation
A 39-year-old female patient presented with acute severe chest pain of one hour duration. Her past history was unremarkable. The patient was not in the peri-partum period during presentation. The electrocardiogram (ECG) revealed ST-elevations over the anterior chest leads ( Fig. 1 A ). Because of the correlation of the chest pain to respiration, computed tomography of the thorax was performed. It did not show any evidence for pulmonary embolism or aortic dissection. The chest pain disappeared about one hour after admission and there was regress of the ST-elevations ( Fig. 1 B). Echocardiography showed akinesia and ballooning of the mid-apical parts of the left ventricle ( Fig. 1 C). Emergency coronary angiography revealed stenosis in a long segment of the middle part of the left anterior descending artery (LAD) with haziness at the distal part of the stenosis ( Fig. 2 A and B arrows). Left ventriculography confirmed the findings of left ventricular mid-apical ballooning ( Fig. 2 C and D). On suspicion of spontaneous LAD dissection, intravascular ultrasound examination (IVUS) of LAD was performed, and revealed signs of SCAD ( Fig. 2 E and F). Because of her stable clinical condition and open coronary artery with normal blood flow, the patient was treated conservatively. The ECG showed T-wave inversions on anterior chest leads and biphasic T-waves inferolaterally with prolongation of the corrected QT time (491 msec) ( Fig. 1 D) 2 days after admission. Follow-up echocardiography (3 weeks after presentation) showed normalization of greater part of the akinetic region of the left ventricle apart from a small region in the septal apical part ( Fig. 3 A and B ). Coronary angiography 5 months after the index presentation revealed complete normalization of the dissected LAD segment ( Fig. 3 C arrows). Left ventriculography showed signs of almost normalization of the left ventricular function. Cardiac magnetic resonance imaging 4 months after the illness showed also almost normalization of the left ventricular function ( Fig. 3 D). There was delayed gadolinium enhancement only in a limited area of the mid-apical part of the septum and no delayed enhancement in the remaining part of the left ventricle ( Fig. 3 E and F white arrows).
2
Case presentation
A 39-year-old female patient presented with acute severe chest pain of one hour duration. Her past history was unremarkable. The patient was not in the peri-partum period during presentation. The electrocardiogram (ECG) revealed ST-elevations over the anterior chest leads ( Fig. 1 A ). Because of the correlation of the chest pain to respiration, computed tomography of the thorax was performed. It did not show any evidence for pulmonary embolism or aortic dissection. The chest pain disappeared about one hour after admission and there was regress of the ST-elevations ( Fig. 1 B). Echocardiography showed akinesia and ballooning of the mid-apical parts of the left ventricle ( Fig. 1 C). Emergency coronary angiography revealed stenosis in a long segment of the middle part of the left anterior descending artery (LAD) with haziness at the distal part of the stenosis ( Fig. 2 A and B arrows). Left ventriculography confirmed the findings of left ventricular mid-apical ballooning ( Fig. 2 C and D). On suspicion of spontaneous LAD dissection, intravascular ultrasound examination (IVUS) of LAD was performed, and revealed signs of SCAD ( Fig. 2 E and F). Because of her stable clinical condition and open coronary artery with normal blood flow, the patient was treated conservatively. The ECG showed T-wave inversions on anterior chest leads and biphasic T-waves inferolaterally with prolongation of the corrected QT time (491 msec) ( Fig. 1 D) 2 days after admission. Follow-up echocardiography (3 weeks after presentation) showed normalization of greater part of the akinetic region of the left ventricle apart from a small region in the septal apical part ( Fig. 3 A and B ). Coronary angiography 5 months after the index presentation revealed complete normalization of the dissected LAD segment ( Fig. 3 C arrows). Left ventriculography showed signs of almost normalization of the left ventricular function. Cardiac magnetic resonance imaging 4 months after the illness showed also almost normalization of the left ventricular function ( Fig. 3 D). There was delayed gadolinium enhancement only in a limited area of the mid-apical part of the septum and no delayed enhancement in the remaining part of the left ventricle ( Fig. 3 E and F white arrows).
