Abstract
Post-ischemic myocardial stunning (PIMS) is defined as a prolonged and reversible left ventricular dysfunction induced by an acute coronary ischemic insult. Takotsubo syndrome (TS) is a recognized acute cardiac disease entity, characterized by a unique pattern of transient circumferential left ventricular wall motion abnormality (LVWMA). The LVWMA in TS has all the characteristic features of myocardial stunning. Herein, the case of a 76-year-old woman with severe three-vessel coronary artery disease presented with acute coronary syndrome inducing PIMS with features identical to mid-apical pattern of TS is reported. The stunned myocardium caused incessant (throughout systole and diastole) compression of a segment of left anterior descending artery (LAD) with myocardial bridging during the acute and sub-acute stages of the disease. The systo-diastolic compression of LAD was relieved after recovery of LVWMA 26 days later. This novel observation suggests that the myocardial stunning in TS is in a cramp state during the acute and sub-acute stages of the disease. The cramp state of myocardial stunning may also explain the microvascular dysfunction seen in some patients with TS.
Highlights
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Acute coronary syndrome (ACS) induced post-ischemic myocardial stunning (PIMS).
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PIMS had all the features and course of takotsubo syndrome (TS).
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The myocardial stunning in TS caused systo-diastolic compression of a segment of left anterior descending artery (LAD) with myocardial bridging during the sub-acute stage.
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LAD compression relieved after normalization of the left ventricular dysfunction indicating that the myocardial stunning in TS was in a state of cardiac cramp.
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ACS may trigger TS, and TS may cause myocardial ischemia.
1
Introduction
Post-ischemic myocardial stunning (PIMS) is defined as a prolonged and reversible left ventricular dysfunction induced by an acute coronary ischemic insult. Takotsubo syndrome (TS) is an acute cardiac disease entity with a characteristic transient circumferential left ventricular wall motion abnormality (LVWMA) resulting in a conspicuous ballooning of the left ventricle during systole [ ]. Sato and Dote introduced the term takotsubo to describe the silhouette of the left ventricle during systole in patients with clinical signs of myocardial infarction without obstructive coronary artery disease [ , ]. TS may be triggered by innumerable emotional and physical stressors. Herein, a case of acute coronary syndrome with severe three vessel disease inducing extensive PIMS with typical features and course of TS is described. In addition, the myocardial stunning caused systo-diastolic compression of a segment of left anterior descending artery (LAD) with myocardial bridging during the acute and sub-acute stages of the disease.
2
Case presentation
A 76-year-old woman presented with acute chest pain. Three years prior to the index presentation, she was treated for pulmonary embolism. During the last few months, the patient has started to have effort-related chest pain, a history consistent with angina pectoris, of the same character of the presenting chest pain. The electrocardiogram showed flattened T waves in the anterior leads. There was modest troponin elevation (max 467 ng/L). Invasive coronary angiography revealed three-vessel coronary artery disease ( Fig. 1 A, B, C, and D ; white arrows) with a tight proximal and long distal stenoses in LAD ( Fig. 1 A, B, and C; white arrows). Left ventriculography showed mid-apical ballooning with good contractions in the basal segments ( Fig.1 E). The mid-apical ballooning was confirmed by echocardiography and cardiac magnetic resonance (CMR) imaging ( Fig. 1 F). Furthermore, CMR imaging showed myocardial edema in the hypo/akinetic segments with no late gadolinium enhancement (LGE) ( Fig. 1 G). Coronary artery bypass surgery was deemed to be inappropriate because of gracile peripheral segments of LAD. Percutaneous coronary intervention (PCI) was performed for the proximal tight stenosis of LAD ( Fig. 1 H) and the large intermediate branch stenosis 5 days after admission. A slight but not remarkable improvement was noted in the long tight peripheral LAD stenosis compared with the first angiography ( Fig. 1 H). Spontaneous coronary artery dissection was discussed. Intravascular ultrasound examination (IVUS) in LAD showed signs of myocardial bridging ( Fig. 1 I and J). After the PCI procedure, the patient improved, and her effort angina pectoris disappeared. Follow up coronary angiography 26 days later showed almost normalization of the distal long stenosis in LAD with only mild systolic compression ( Fig. 2 A, B, G and H ). Left ventriculography showed complete recovery of left ventricular dysfunction ( Fig. 2 F). The left ventricular recovery and almost normalization of the distal LAD stenosis are clearly observed in ( Fig. 2 F, G and H) compared to the mid-apical ballooning and the long LAD stenosis during index presentation in ( Fig. 2 C, D and E). The condition deemed to be: 1) Post-ischemic myocardial stunning with all features identical to takotsubo syndrome (TS) triggered by acute coronary syndrome with severe three-vessel disease; 2) the stunned myocardium in PIMS (TS) caused systolic and diastolic compression of a segment of LAD with myocardial bridging with the relief of compression after recovery of the myocardial stunning caused by TS. This indicates that the stunned myocardium in TS was in a cramp state during the acute and sub-acute stages of the disease.
2
Case presentation
A 76-year-old woman presented with acute chest pain. Three years prior to the index presentation, she was treated for pulmonary embolism. During the last few months, the patient has started to have effort-related chest pain, a history consistent with angina pectoris, of the same character of the presenting chest pain. The electrocardiogram showed flattened T waves in the anterior leads. There was modest troponin elevation (max 467 ng/L). Invasive coronary angiography revealed three-vessel coronary artery disease ( Fig. 1 A, B, C, and D ; white arrows) with a tight proximal and long distal stenoses in LAD ( Fig. 1 A, B, and C; white arrows). Left ventriculography showed mid-apical ballooning with good contractions in the basal segments ( Fig.1 E). The mid-apical ballooning was confirmed by echocardiography and cardiac magnetic resonance (CMR) imaging ( Fig. 1 F). Furthermore, CMR imaging showed myocardial edema in the hypo/akinetic segments with no late gadolinium enhancement (LGE) ( Fig. 1 G). Coronary artery bypass surgery was deemed to be inappropriate because of gracile peripheral segments of LAD. Percutaneous coronary intervention (PCI) was performed for the proximal tight stenosis of LAD ( Fig. 1 H) and the large intermediate branch stenosis 5 days after admission. A slight but not remarkable improvement was noted in the long tight peripheral LAD stenosis compared with the first angiography ( Fig. 1 H). Spontaneous coronary artery dissection was discussed. Intravascular ultrasound examination (IVUS) in LAD showed signs of myocardial bridging ( Fig. 1 I and J). After the PCI procedure, the patient improved, and her effort angina pectoris disappeared. Follow up coronary angiography 26 days later showed almost normalization of the distal long stenosis in LAD with only mild systolic compression ( Fig. 2 A, B, G and H ). Left ventriculography showed complete recovery of left ventricular dysfunction ( Fig. 2 F). The left ventricular recovery and almost normalization of the distal LAD stenosis are clearly observed in ( Fig. 2 F, G and H) compared to the mid-apical ballooning and the long LAD stenosis during index presentation in ( Fig. 2 C, D and E). The condition deemed to be: 1) Post-ischemic myocardial stunning with all features identical to takotsubo syndrome (TS) triggered by acute coronary syndrome with severe three-vessel disease; 2) the stunned myocardium in PIMS (TS) caused systolic and diastolic compression of a segment of LAD with myocardial bridging with the relief of compression after recovery of the myocardial stunning caused by TS. This indicates that the stunned myocardium in TS was in a cramp state during the acute and sub-acute stages of the disease.
