Objectives
To characterize the morphological features of plaque erosion and calcified nodule in patients with acute coronary syndrome (ACS) by optical coherence tomography (OCT).
Background
Plaque erosion and calcified nodule have not been systematically investigated in vivo.
Methods
One hundred and twenty-six patients with ACS who had undergone pre-intervention OCT imaging were included. The culprit lesions were classified as plaque rupture (PR), erosion (OCT-erosion), calcified nodule (OCT-CN), or others using a new set of diagnostic criteria for OCT.
Results
The incidences of PR, OCT-erosion, and OCT-CN were 43.7%, 31.0%, and 7.9%, respectively. Patients with OCT-erosion were the youngest compared with those with PR and OCT-CN (53.8±13.1 years vs. 60.6±11.5 years, 65.1±5.0 years, p=0.005). Compared with patients with PR, presentation with non-ST-segment elevation ACS (NSTE-ACS) was more common in patients with OCT-erosion (61.5% vs. 29.1%, p=0.008) and OCT-CN (100% vs. 29.1%, p<0.001). OCT-erosion had a lower frequency of lipid plaque (43.6% vs. 100%, p<0.001), thicker fibrous cap (169.3±99.1 μm vs. 60.4±16.6 μm, p<0.001), and smaller lipid arc (202.8±73.6° vs. 275.8±60.4°, p<0.001) than PR. The diameter stenosis was least severe in OCT-erosion followed by OCT-CN and PR (55.4±14.7% vs. 66.1±13.5% vs. 68.8±12.9%, p<0.001).
Conclusions
OCT is a promising modality for identifying OCT-erosion and OCT-CN in vivo. OCT-erosion is a frequent finding in patients with ACS, especially in those with NSTE-ACS and younger patients. OCT-CN is the least common etiology for ACS and is more common in older patients.
An OCT-based calcium scoring system can help to identify lesions that would benefit from plaque modification prior to stent implantation. Lesions with calcium deposit with maximum angle >180°, maximum thickness >0.5 mm, and length >5 mm may be at risk of stent underexpansion.
Optical coherence tomography clearly demonstrated significant acute injuries and chronic intimal thickening of RA after TRI. Further study should evaluate the impact of these effects when TRI RAs are subsequently used as conduits, on long-term graft patency and on clinical outcomes after bypass surgery.
Background—
Patients with acute coronary syndrome (ACS) have a higher incidence of recurrent ischemic events. The aim of this study was to compare the plaque characteristics of nonculprit lesions between ACS and non-ACS patients using optical coherence tomography (OCT) imaging.
Methods and Results—
Patients who had 3-vessel OCT imaging were selected from the Massachusetts General Hospital (MGH) OCT Registry. MGH registry is a multicenter registry of patients undergoing OCT. The prevalence and characteristics of nonculprit plaques were compared between ACS and non-ACS patients. A total of 248 nonculprit plaques were found in 104 patients: 45 plaques in 17 ACS patients and 203 plaques in 87 non-ACS patients. Compared with plaques of non-ACS patients, plaques of ACS patients had a wider lipid arc (147.3 ± 29.5° versus 116.2 ± 33.7°,
P
<0.001), a longer lipid length (10.7 ± 5.9 mm versus 7.0 ± 3.7 mm,
P
=0.002), a larger lipid volume index [averaged lipid arc×lipid length] (1605.5 ± 1013.1 versus 853.4 ± 570.8,
P
<0.001), and a thinner fibrous cap (70.2 ± 20.2 µm versus 103.3 ± 46.8 µm,
P
<0.001). Moreover, thin-cap fibroatheroma (64.7% versus 14.9%,
P
<0.001), macrophage (82.4% versus 37.9%,
P
=0.001), and thrombus (29.4% versus 1.1%,
P
<0.001) were more frequent in ACS patients. Although the prevalence of microchannel did not differ between the groups, the closest distance from the lumen to microchannel was shorter in ACS subjects than in non-ACS (104.6 ± 67.0 µm versus 198.3 ± 133.0 µm,
P
=0.027).
Conclusions—
Nonculprit lesions in patients with ACS have more vulnerable plaque characteristics compared with those with non-ACS. Neovascularization was more frequently located close to the lumen in patients with ACS.
The presence of a CN was associated with severe calcification and larger hinge movement of the coronary artery (especially ostial and mid right coronary artery). One-third of the underlying plaque morphology of severely calcified culprit lesions in patients with ACS was caused by a CN.
Angiographic detection of target lesion coronary calcium (compared to intravascular imaging) has not changed in the past 2 decades, and angiographically invisible calcium (only detectable by IVUS or OCT) did not appear to inhibit stent expansion.
Compared with non-DM patients, DM patients have a larger LI and a higher prevalence of calcification and thrombus. The LI was larger and TCFA and macrophage infiltration were frequent in patients with A(1C) ≥8%.
In vivo critical cap thicknesses were <80 μm for the thinnest and <188 μm for most representative fibrous cap thickness. Prospective imaging studies are required to establish the significance of these values.
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