Continuous 1-Month Release of Cholesterol Crystals in a Patient With Acute Coronary Syndrome After Stenting.

Coronary stenting was performed for a 76-year-old patient with acute coronary syndrome with severe stenosis of the right coronary artery. Puff rupture including cholesterol crystals was detected on nonobstructive general angioscopy. One month after intervention, continuous release of cholesterol crystals was found despite successful percutaneous coronary intervention. (Level of Difficulty: Intermediate.).

Case Report

A 76-year-old man with a history of hypertension, dyslipidemia, and diabetes mellitus was referred to us for worsening effort angina. On admission, electrocardiography and blood tests revealed no significant abnormalities. Acute coronary syndrome was suspected because emergency coronary computed tomographic angiography revealed severe stenosis in the proximal right coronary artery. Invasive coronary angiography indicated 90% stenosis. Puff-chandelier rupture, presenting as puff-like materials glistening against the light from the angioscopy fiber catheter, was detected and sampled at the stenotic site by means of nonobstructive general angioscopy (NOGA) (Figure 1A, Video 1). Percutaneous coronary intervention (PCI) was successfully performed. Through the original methods, cholesterol crystals (CCs) were detected as 27,727 counts/10 mL, suggesting plaque including atheroma rupture on site (Figures 1B and 1C) The maximum serum troponin T level was 0.015 ng/mL (normal 0.002-0.016 ng/mL) within 1 month after PCI. NOGA of the right coronary artery was performed 1 month after the intervention for residual significant stenosis in the left anterior descending artery. Invasive coronary angiography did not reveal evidence of stenosis or reduced flow in the right coronary artery; however, NOGA showed protrusions of ruptured plaque debris from stent struts (Figure 1D, Video 1). Free CCs were obtained on coronary sampling of the stented ruptured plaque (Figures 1E and 1F). CCs are reportedly released from disrupted plaques, leading to ischemic and inflammatory organ injury. Despite successful PCI, asymptomatic embolization of CCs, which potentially caused myocardial injury, continued for 1 month. Thus, asymptomatic and preclinical myocardial injuries due to embolization continued during embolization of CCs.

Figure 1

Angioscopic Images and Histopathological Images of the Ruptured Plaque in the Right Coronary Artery

(A) Angioscopic image of ruptured plaque in the right coronary artery at baseline. (B) Cholesterol crystals and (C) atheroma stained with hematoxylin-eosin of sampled puff-chandelier rupture. (D) Angioscopic image of ruptured plaque in the right coronary artery 1 month after intervention. (E) Cholesterol crystals and (F) atheroma stained with hematoxylin-eosin of the same site. Scale bar = 20 μm.

Funding Support and Author Disclosures

Dr Komatsu is a technical consultant for Nemoto Kyorin-do Co. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.