Neoatherosclerosis is an unsolved problem with Drug-Eluting Stent (DES) and is the results of atherosclerosis progression; however, the contribution of stent itself to the process has not been clarified, especially among the second-generation DES. We found an interesting case in which neoatherosclerosis was formed only in the area very close to the stent struts suggesting that stent itself may play an important role for the formation of neoatherosclerosis still in the second-generation DES.
Background: Population science has shown similar outcomes between cobalt–chromium everolimus-eluting stent (CoCr-EES) and platinum–chromium everolimus-eluting stent (PtCr-EES). However, subclinical intracoronary thrombus following implantation of CoCr-EES or PtCr-EES in acute myocardial infarction (AMI) has not been explored.
Methods: We performed coronary angioscopy (CAS) 13 ± 2 days after stent implantation: 47 stents in 46 lesions from 42 patients with AMI (male 90%, mean age 64 ± 13 years). The degree of thrombus adhesion and yellow plaque severity were compared between CoCr-EES (26 stents from 22 patients) and PtCr-EES (21 stents from 20 patients). The degree of thrombus adhesion was graded: grade 0 (none), no thrombus; grade 1 (focal), several spotty thrombi; grade 2 (diffuse), thrombus extending between the struts. Yellow plaque severity was graded: grade 0, white; grade 1, light yellow; grade 2, yellow; grade 3, intensive yellow.
Results: Thrombus grade was similar (CoCr-EES: grade 0, 4%; grade 1, 50%; grade 2, 46%; PtCr-EES: grade 0, 19%; grade 1, 38%; grade 2, 43%, P = 0.46). Yellows plaque grade was also similar between CoCr-EES (grade 0, 0%; grade 1, 23%; grade 2, 19%; grade 3, 58%) and PtCr-EES (grade 0, 0%; grade 1, 19%; grade 2, 29%; grade 3, 52%, P = 0.88).
Conclusions: Extent of subclinical intracoronary thrombus was comparable between CoCr-EES and PtCr-EES in the subacute phase of AMI, associated with equally severe yellow plaque lesions. Thrombogenicity of PtCr-EES may be similarly low to that of CoCr-EES in patients with AMI.
The existence of aortoiliac atheroma is highly associated with aortoiliac aneurysm, dissection, and peripheral arterial embolism. Accordingly, it is crucial to clarify the mechanism and process of the atherosclerotic plaque progression in the aorta and iliac arteries. Here, we report visualization of various plaques along with the entire aorta and iliac artery by non-obstructive angioscopy in a 45-year-old man with coronary artery disease (CAD). Especially, the significant ulcerative lesions below the infra renal aortoiliac wall were observed, one of which was like a tiny fish mouth opening and closing with the heartbeats. The angioscopic observation on the aortoiliac wall may provide the clue of the atherosclerotic plaque progression.
Very late stent thrombosis (VLST) is a potentially life-threatening complication in coronary angioplasty patients. The patient was a 95-year-old man who had been implanted with a durable polymer everolimus-eluting stent (DP-EES, 3.5 × 23 mm) at the restenosis site in the proximal part of the left descending artery using only plain balloon angioplasty for acute coronary syndrome (ACS) 27 months earlier. Final intravascular ultrasound (IVUS) evaluation had shown no stent malapposition and adequate stent expansion. However, he presented to our hospital due to vomiting and fatigue 89 months after the implantation. An electrocardiogram showed ST-elevation in V2-6 leads, we therefore suspected ACS and emergent coronary angiography (CAG) revealed total occlusion of DP-EES site, which was diagnosed as VLST. Percutaneous coronary intervention (PCI) was subsequently carried out and complete recovery of blood flow was obtained by thrombus aspiration. Optical coherence tomography (OCT) demonstrated uncovered struts, stent malapposition, and some thrombi in the proximal part of DP-EES. Yellow chemogram was not detected in the DP-EES site by near-infrared spectroscopy (NIRS). Coronary angioscopy (CAS) showed exposed stent struts with red thrombus adhesion in the proximal part of the DP-EES. Judging from intravascular images, the main cause of VLST was stent malapposition and uncovered struts. Here, we report a case with VLST due to late acquired stent malapposition and uncovered struts 89 months after DP-EES implantation.