279 LAYERED PLAQUES: NOT ALL ARE HEALED


 Layered plaques are the effect of a previous plaque event. They are associated with coronary spasm and found in more than 50% of patients with stable angina and a quarter of those with an acute coronary syndrome. Nevertheless, it is not clear whether their presence is indicative of a healing process or rather is predictive of an increased risk of future events. A 71-year-old male, heavy smoker and hypertensive, presented with episodes of angina at rest that resolved spontaneously in less than 5 minutes, with evidence of ST-segment elevation (STE) in the lower leads during one of these episodes. Coronary angiography showed an intermediate stenosis at the end of the mid segment of the dominant right coronary artery (RCA) (Figure A). Optical coherence tomography (OCT) revealed a layered plaque, consisting of high backscattering layers alternated with low reflection layers (Figures A1-3). Given the minimum luminal area of 3.65 mm2 and the absence of other criteria for plaque instability (erosion, thin-cap, etc.), we treated the patient conservatively with medical therapy alone, consisting of a single antiplatelet agent and a high-dose statin with ezetimibe. A non-dihydropyridine calcium antagonist and a long-acting nitrate were started given the suspicion of coronary spasm. Four months later the patient returned to the emergency department for persistent oppressive chest pain unresponsive to sublingual nitrates with evidence of STE in the lower leads. Emergency coronary angiography showed an acute occlusion of RCA with TIMI 0 flow in correspondence to the layered plaque highlighted 4 months earlier on OCT (Figure B). Antegrade flow was restored with manual thrombus aspiration (Figure C) and OCT showed lesion progression with many new layers, together with a cavity suggestive of plaque rupture (Figures C1-3). A 3.5×38 mm everolimus eluting stent was deployed – based on OCT sizing – and post-dilated with a 4.0×8 mm non-compliant balloon, obtaining an excellent angiographic result with TIMI 3 flow (Figure D). Low-reflecting layers within layered plaques are generally considered to be lipid deposits, but they could also represent intraplaque haemorrhages, generated by coronary spasm. The haematoma can be reorganised within the plaque to create a new layer, leading to lesion progression without necessarily requiring a loss of endothelial integrity. The progressive increase of the haematoma may lead to plaque rupture when the pressure exceeds the resistance of superficial layers. This case reveals a new possible mechanism of plaque progression in patients with coronary spasm and explains how layered plaques can be ambivalently considered to be either stable or vulnerable. Their treatment should be meticulously tailored not only based on classical criteria of plaque instability but also according to the underlying trigger mechanism.