Atherosclerosis as a disease entity remains an intensely researched field, given the tendency for considerable morbidity and mortality. This attention has given rise to exciting opportunities in developing tools aimed at early detection and possible targeting of specific therapeutic interventions. One such modality is optical coherence tomography (OCT) that permits high-resolution visualization of backscattered light. This has given unique insights into disease processes and with greater detail than traditional grey scale intravascular ultrasound (IVUS). We present a 69-year-old man with 1 week crescendo angina 9 months following stent implantation to the left anterior descending (LAD) artery. Angiography demonstrated a new lesion in the mid LAD and diagonal branches. Assessment of the region with OCT revealed a high lipid content plaque with a thin fibrous cap (maximal thickness = 20 µm). In association, rupture of the thin cap was apparent, occurring at both shoulders of the plaque with associated mural thrombus. The patient was treated with further stent implantation and remains symptom-free at 3 months follow-up.
The predilection for plaque to rupture at the shoulder region is interesting. Pathological studies have shown that this region demonstrates intense inflammatory cell infiltrate, particularly with macrophage cells and lymphocytes. When activated, macrophages release matrix metalloproteinases in the vessel wall, which, in turn, can induce ‘weak spots’ that become susceptible to rupture. Other factors also implicated in this increased vulnerability at the plaque shoulder include neovascularization with expression of adhesion molecules and increased biomechanical stresses occurring around cellular microcalcifications within the thin cap.
Several imaging modalities have been used to assess and identify vulnerable plaque (VP) including coronary angioscopy, IVUS, and magnetic resonance imaging. Recently, there has been significant interest in the field of VP detection using OCT. This modality permits high-resolution imaging (10–20 µm), in the vicinity of 10 times greater than IVUS and has become a key tool to detect and quantify thin cap fibroatheroma and macrophage distribution. This individual clinical observation supports the evidence gained from post-mortem observations pointing to the plaque ‘shoulder’ as a site of vulnerability for rupture.
Panel A. Angiography in the right cranial view demonstrated stenosis in the mid left anterior descending artery involving both small diagonal branches. The previously proximally implanted left anterior descending artery stent was widely patent. The region corresponding to the optical coherence tomography images is shown with the black arrow.
Panels B–C. Intravascular optical coherence tomography (LightLab Imaging, Westford, MA, USA) was acquired using a non-occlusive technique with a 3.0 mm/s pullback. Optical coherence tomography clearly demonstrated the presence of a lipid-rich plaque in the 6–9'o clock position characterized by low reflectivity, speckled appearance with diffuse margins. This was covered with a bright rim of fibrous tissue corresponding to thin-cap fibroatheroma. Mural thrombus was evident in all optical coherence tomography cross sections. The thin-cap fibroatheroma measured was 20 µm thick, and was found to be ruptured at each of the two shoulders of the plaque (arrows).