Rapid Plaque Progression Possibly Due to Intraplaque Hemorrhage in a Patient With Coronary Artery Spasm

A 75-year-old man underwent emergency coronary angiography (CAG) for the diagnosis of acute coronary syndrome. A subtotal occlusion of the right coronary artery (RCA) was identified (Figure A) and successfully treated with implantation of a drug-eluting stent (Figure B,C). Post-procedural intracoronary optical coherence tomography (OCT; Terumo Corporation) showed non-flow-limiting fibrolipidic plaque with macrophage infiltration proximal to the stented segment (Figure D; Supplementary Movie 1). One year later, CAG and an acetylcholine provocation test were performed because of multiple episodes of resting angina, showing the progression of luminal stenosis in the RCA proximal to the stent segment (Figure E). Intracoronary injection of 20 μg acetylcholine induced severe focal vasospasm at the segment and diffuse spasm in the distal RCA (Figure F) with accompanying chest pain and ST-segment depression, leading to the diagnosis of coronary spastic angina. Injection of nitrates resolved the spasm (Figure G). Subsequent OCT demonstrated new development of layered plaque with luminal stenosis, which consisted of low-intensity areas with low signal attenuation, suggesting healing after intraplaque hemorrhage (IPH) or plaque rupture (Figure H; Supplementary Movie 2).

Figure.

Images at (A–C) the index procedure and (E–G) 1 year. (D,H) OCT frames 1.25 mm (5 frames) proximal to the stent at the time of index procedure (D) and at 1 year (H). Asterisks (*) indicate macrophage accumulation. Other symbols (†, ‡, §) indicate layers of the layered plaque, with the latter two symbols (‡, §) indicating low-intensity areas with low signal attenuation.

Layered plaque results from one or multiple silent episodes of a non-occlusive thrombotic event and is associated with a rapid stepwise progression. The low-intensity area without connection to the luminal surface observed in this case indicates likely involvement of IPH in the progression of layered plaque, although plaque erosion and rupture are other potential underlying mechanisms and may have also occurred. It is conceivable that mechanical force produced by coronary spasm may induce IPH or plaque rupture within the pre-existing lipidic plaque, which rapidly enlarged plaque volume and led to the development of a layered feature on OCT examination.

Disclosures

S.U. is a member of Circulation Journal’s Editorial Team and has received remuneration from Abbott Vascular Japan, Daiichi-Sankyo, Novartis Pharma, Bayer, and Amgen, as well as scholarship funds from Abbott Vascular Japan. T.K. has received remuneration from Abbott Vascular Japan. All the other authors have no conflicts of interest to disclose.

IRB Information

This study was approved by the Institutional Ethics Committee at Kawasaki Medical School (Approval no. 5455).

Supplementary Files

Supplementary Movie 1. Baseline OCT immediately after percutaneous coronary intervention.

Supplementary Movie 2. Follow-up OCT at 1 year.

Please find supplementary file(s);

http://dx.doi.org/10.1253/circj.CJ-22-0004