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Optical coherence tomography assessment of macrophages accumulation in non-ST-segment elevation acute coronary syndromes
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Aims
To investigate in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) the prevalence and the features of optical coherence tomography (OCT)-detected macrophages accumulation in culprit plaques as compared with nonculprit plaques (NCP).
Methods
The study is a post-hoc analysis of a prospective study aimed at evaluating the relationship between aortic inflammation as assessed by 18F-fluorodeoxyglucose-PET and features of coronary plaque vulnerability as assessed by OCT. We enrolled 32 patients with first NSTE-ACS who successfully underwent three-vessel OCT.
Results
The median age was 65 (54–72) years and 27 patients (84%) were men. Culprit plaques were clinically defined. Overall, the rate of lipid plaques and lipid plaques containing macrophages were 6.4 and 4.2 per patient, respectively. Culprit plaques had a smaller minimal luminal area, a higher extension of lipid component and a thinner fibrous cap than NCPs. Macrophages accumulations were more likely found in culprit plaque (84 vs. 61%, P = 0.015) in which they had also a higher circumferential extension. On univariable analysis, macrophages accumulation extension had a higher association with culprit plaques (odds ratio = 4.42; 95% confidence interval; 2.54–9.15, P < 0.001) than the mere presence of macrophages accumulation (odds ratio = 3.36; 95% confidence interval; 1.30–8.66, P = 0.012). Culprit plaques with thrombus had a lower distance between macrophages accumulation and the luminal surface than culprit plaque with no thrombus (0.06 vs. 0.1 mm; P = 0.04).
Conclusion
In patients with NSTE-ACS, macrophages accumulations are more likely present in culprit plaque in which they disclose also a greater extension compared with those observed in NCP. The distance between macrophages accumulation and the luminal surface is lower in thrombotic culprit plaque than that in nonthrombotic culprit plaque.
Ovid Technologies (Wolters Kluwer Health)
Title: Optical coherence tomography assessment of macrophages accumulation in non-ST-segment elevation acute coronary syndromes
Description:
Aims
To investigate in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) the prevalence and the features of optical coherence tomography (OCT)-detected macrophages accumulation in culprit plaques as compared with nonculprit plaques (NCP).
Methods
The study is a post-hoc analysis of a prospective study aimed at evaluating the relationship between aortic inflammation as assessed by 18F-fluorodeoxyglucose-PET and features of coronary plaque vulnerability as assessed by OCT.
We enrolled 32 patients with first NSTE-ACS who successfully underwent three-vessel OCT.
Results
The median age was 65 (54–72) years and 27 patients (84%) were men.
Culprit plaques were clinically defined.
Overall, the rate of lipid plaques and lipid plaques containing macrophages were 6.
4 and 4.
2 per patient, respectively.
Culprit plaques had a smaller minimal luminal area, a higher extension of lipid component and a thinner fibrous cap than NCPs.
Macrophages accumulations were more likely found in culprit plaque (84 vs.
61%, P = 0.
015) in which they had also a higher circumferential extension.
On univariable analysis, macrophages accumulation extension had a higher association with culprit plaques (odds ratio = 4.
42; 95% confidence interval; 2.
54–9.
15, P < 0.
001) than the mere presence of macrophages accumulation (odds ratio = 3.
36; 95% confidence interval; 1.
30–8.
66, P = 0.
012).
Culprit plaques with thrombus had a lower distance between macrophages accumulation and the luminal surface than culprit plaque with no thrombus (0.
06 vs.
0.
1 mm; P = 0.
04).
Conclusion
In patients with NSTE-ACS, macrophages accumulations are more likely present in culprit plaque in which they disclose also a greater extension compared with those observed in NCP.
The distance between macrophages accumulation and the luminal surface is lower in thrombotic culprit plaque than that in nonthrombotic culprit plaque.
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