PMC6458957_01
Electrocardiography (ECG), coronary angiography (CAG), and cardiac magnetic resonance imaging (C-MRI) on the first admission. (a) ECG on admission revealed no significant change except a left axis deviation. (b) CAG revealed no coronary artery occlusion either in the right coronary artery (RCA: left anterior oblique 50  view) or the left coronary arteries (LCA: caudal 30  view). (c) C-MRI of short and long axis view. The arrows indicate the delayed enhancement of the myocardium.
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He was immediately relieved of chest pain after admission, and there was no significant finding on a 12-lead electrocardiogram except a left axis deviation (Figure 1(a)). Although coronary angiography (CAG) revealed no artery occlusion (Figure 1(b)), left ventriculography showed mild hypokinesis in the posterior wall, and cardiac magnetic resonance imaging exhibited a delayed gadolinium enhancement in the posterior wall area (Figure 1(c)), suggesting myocardial infarction in the territory of the left circumflex coronary artery (LCX).
Second CAG and adenosine stress myocardial perfusion scintigraphy. (a) The second CAG was performed to investigate the acetylcholine-induced vasospasm. Although the coronary arteries did not exhibit vasospasm induced by acetylcholine, CAG revealed de novo stenosis in #12. (b) The adenosine stress myocardial perfusion scintigraphy (Tc-99m tetrofosmin) showed the myocardial ischemia in the posterior wall area, suggesting myocardial ischemia in #12.
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CAG was performed 3 months after the discharge. CAG revealed de novo stenosis in the obtuse marginal branches (#12: 75% with haziness, Figure 2(a)), and adenosine stress myocardial perfusion scintigraphy (Tc-99m tetrofosmin) showed myocardial ischemia in the posterior wall area (Figure 2(b)), where the tracer uptake was reduced at stress and restored at rest.
CAG and intravascular ultrasound images during PCI. In the first PCI, a zotarolimus-eluting stent (3.0 x 12 mm) was implanted in #12 (a, between white arrows). Emergent CAG, which was performed 3 hours after the first PCI, revealed massive thrombus in the stent lesion (b, white arrows). The intravascular ultrasound study (c) showed the new lining thrombus (white arrows) in the stent proximal (A and B), whereas not in the distal (C).
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The first PCI toward #12 was successfully performed by implantation of a zotarolimus-eluting stent (3.0 x 12 mm) and CAG revealed no residual stenosis (Figure 3(a)). The emergent CAG demonstrated a stent thrombosis at the proximal edge of the stent (Figure 3(b)). Although the intravascular ultrasound imaging exhibited neither the underexpansion of the prior-implanted stent nor the coronary artery dissection around the stent, it showed new lining thrombus (white arrows) at the proximal edge of the stent (Figure 3(c)).
CAG findings after second PCI. Although an additional drug-eluting stent sized 3.0 x 12 mm was implanted in #12 (a), CAG performed 3 days after the second PCI revealed the recurrence of thrombus (white arrow) with 75% haziness stenosis in #12 (b). Another CAG performed 14 days after the third PCI again revealed recurrence of stent thrombosis with 75% stenosis in #12 (c). The final CAG, which was performed after the fourth PCI, showed 50% of residual stenosis with thrombus, and we decided not to perform further PCI to #12 (d).
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An additional drug-eluting stent (3.0 x 12 mm, everolimus-eluting stent) was implanted at the proximal edge of the prior stent lesion of #12 (Figure 4(a), second PCI) under the support of an intra-aortic balloon pumping. However, CAG, performed 3 days after the second PCI, revealed a massive thrombus with 75% stenosis in #12 (Figure 4(b)). The follow-up CAG, which was performed 14 days after the third PCI, again revealed the recurrence of stent thrombosis with 75% stenosis in #12 (Figure 4(c)). CAG, after the cessation of eltrombopag, showed 50% of residual stenosis with thrombus; hence, we did not perform further PCI to #12 (Figure 4(d)).