Images in Cardiovascular Medicine
Intraprocedural Stent Thrombosis Detected on Coronary Angioscopy
2016 Volume 80 Issue 6 Pages 1484-1485
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2016 Volume 80 Issue 6 Pages 1484-1485
Intraprocedural stent thrombosis (IPST) during percutaneous coronary intervention (PCI) is a rare complication leading to poor outcome,1–3 but, to date, there have been few reports on coronary angioscopy (CAS) of IPST.
A 60-year-old man was admitted to hospital due to chest pain. Four years previously he had undergone PCI for acute coronary syndrome, in the proximal left anterior descending coronary artery with 2.75×33-mm everolimus-eluting stent (EES), and in the OM with 2.5×12-mm EES. He had the coronary risk factors type 2 diabetes mellitus (HbA1c, 6.6%), and dyslipidemia (low-density lipoprotein cholesterol, 106 mg/dl), and was on aspirin 100 mg, losbastatin 5 mg, nicorandil 15 mg, bisoprorol 5 mg, famotidine D 20 mg, and ethyl icosapentate 1,800 mg. Electrocardiogram showed ST elevation in leads II, IIIaVF. Emergency coronary angiography showed no significant stenosis in the left coronary artery, but the proximal right coronary artery (RCA) was totally occluded (Figure 1-I). The patient was treated with dual antiplatelet therapy (clopidogrel 300 mg, loading dose), followed by aspiration of red thrombus (Figure 1-II). Next, on optical coherence tomography (OCT) the lumen profile was almost 3.0 mm, with multiple plaque ruptures and a large amount of red thrombus (Figure 1A–C). EES (3.0×24 mm) was deployed in the proximal RCA (Figure 2-III), but in-stent haziness developed gradually, which was thought to be due to IPST (Figure 2-IV). Activated coagulation time was 288 s. Next, the stent was dilated with a 3.5×15-mm non-compliant balloon with rated burst pressure 18 atm during 60 s (total), until the IPST disappeared. This site was then assessed on OCT and CAS. On CAS, a high yellow color-grade plaque was seen to be protruding from the stent struts, with some of the struts covered by this higher yellow plaque, with various thrombi at the stent site (Figure 2 Upper A–D). OCT showed attenuated thrombus in the stent, and the stent struts were buried in these materials (Figure 2 Lower A–D). OCT also showed adequate expansion, not under-expansion. Finally, Thrombolysis in Myocardial Infarction Trial (TIMI)-flow grade 3 was achieved without stenosis. After the intervention therapy, hemodynamic condition was dramatically improved. The patient received anti-coagulation therapy for approximately 1 week to prevent stent thrombosis.
(I) Emergency coronary angiography showing total occlusion of the proximal right coronary artery. (II) Aspiration of red thrombus. (A–C) On optical coherence tomography the lumen profile was almost 3.0 mm, with multiple plaque ruptures and a large amount of red thrombus.
(III) Deployment of everolimus-eluting stent (3.0×24 mm) in the proximal right coronary artery. (IV) Gradual development of in-stent haziness due to intraprocedural stent thrombosis. (Upper A–D) Coronary angioscopy showing high yellow color-grade plaque protruding from the stent struts, with some of the struts covered by this higher yellow plaque, and various thrombi at the stent site. (Lower A–D) Optical coherence tomography showing attenuated thrombus in the stent, and the stent strut buried in these materials.
Maximum creatine kinase/creatine kinase-MB concentration was 1283/106 IU/L. Major adverse cardiac events were not seen.
IPST is a risk factor for major adverse cardiovascular events.1 The reported frequency of IPST ranges from 0.5 to 1.2%.2,3 Morofuji et al reported that IPST patients had higher frequency of multiple ruptures with larger cavities on intravascular ultrasound.4 In the present case, multiple ruptures and a large amount of thrombus were detected on OCT. Absolutely yellow plaque and neointima on CAS are associated with various types of thrombosis,5 therefore yellow dense plaque may be associated with the cause of thrombosis. Another possible factor is poor effect of antiplatelet therapy. In the present case the patient received clopidogrel at admission, and also prior to PCI, but he did not develop stent thrombosis. This suggests a low potential for clopidogrel resistance.
IPST may be associated with early phase of stent thrombosis. It was reported that the incidence of major adverse cardiac events, target lesion revascularization, 5-year mortality in early stent thrombosis and late stent thrombosis was higher than in very late thrombosis.6
The present case suggests that IPST is related to dense yellow plaque, and to thrombosis. If IPST is seen on coronary angiography, anti-coagulation therapy and aggressive lipid lowering therapy should be continued.
