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Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
Lipoprotein(a) is associated with coronary atheroma progression: analysis from a serial coronary computed tomography
Xi Wang1,2, Dong-Kai Shan2, Guan-Hua Dou3
1Medical School of Chinese PLA, Beijing, China.
Insights
Elevated Lipoprotein(a) [Lp(a)] is linked to coronary atheroma progression. Perivascular fat attenuation index did not show association, suggesting Lp(a) is an independent risk factor for plaque advancement.
Area of Science:
- Cardiology
- Radiology
- Biochemistry
Background:
- Lipoprotein(a) [Lp(a)] is associated with coronary atherosclerosis and may influence perivascular inflammation.
- Limited data exists on the relationship between Lp(a), perivascular inflammation, and coronary atheroma progression.
Purpose of the Study:
- To investigate the association between Lp(a) and perivascular fat attenuation index (FAI) with coronary atheroma progression.
- Utilize coronary computed tomography angiography (CCTA) for detecting coronary atheroma progression.
Main Methods:
- Serial CCTA scans were analyzed for patients with available Lp(a) data.
- Quantitative CCTA analysis measured total plaque volume (TPV) and perivascular FAI.
- Coronary plaque progression (PP) defined as ≥10% TPV increase or new lesions; associations examined via multivariate logistic regression.
Main Results:
- 116 patients (mean age 53.49 years) were included; 32 showed PP over a mean 30.8-month interval.
- Baseline and follow-up Lp(a) levels were significantly higher in the PP group.
- No significant difference in perivascular FAI between groups; elevated baseline Lp(a) was an independent risk factor for PP (OR=1.031).
Conclusions:
- Lp(a) is independently associated with coronary atheroma progression, exceeding the impact of LDL cholesterol and conventional risk factors.
- Further research is needed to clarify the role of perivascular inflammation, as indicated by FAI, in coronary atheroma progression.
Background:
Lipoprotein(a) [Lp(a)] has been closely related to coronary atherosclerosis and might affect perivascular inflammation due to its proinflammatory properties. However, there are limited data about Lp(a) and related perivascular inflammation on coronary atheroma progression. Therefore, this study aimed to investigate the associations between Lp(a) and the perivascular fat attenuation index (FAI) with coronary atheroma progression detected by coronary computed tomography angiography (CCTA).
Methods:
Patients who underwent serial CCTA examinations without a history of revascularization and with available data for Lp(a) within one month before or after baseline and follow-up CCTA imaging scans were considered to be included. CCTA quantitative analyses were performed to obtain the total plaque volume (TPV) and the perivascular FAI. Coronary plaque progression (PP) was defined as a ≥ 10% increase in the change of the TPV at the patient level or the presence of new-onset coronary atheroma lesions. The associations between Lp(a) or the perivascular FAI with PP were examined by multivariate logistic regression.
Results:
A total of 116 patients were ultimately enrolled in the present study with a mean CCTA interscan interval of 30.80 ± 13.50 months. Among the 116 patients (mean age: 53.49 ± 10.21 years, males: 83.6%), 32 patients presented PP during the follow-up interval. Lp(a) levels were significantly higher among PP patients than those among non-PP patients at both baseline [15.80 (9.09-33.60) mg/dLvs. 10.50 (4.75-19.71) mg/dL,P = 0.029] and follow-up [20.60 (10.45-34.55) mg/dLvs. 8.77 (5.00-18.78) mg/dL,P = 0.004]. However, there were no differences in the perivascular FAI between PP group and non-PP group at either baseline or follow-up. Multivariate logistic regression analysis showed that elevated baseline Lp(a) level (OR = 1.031, 95% CI: 1.005-1.058,P = 0.019) was an independent risk factor for PP after adjustment for other conventional variables.
Conclusions:
Lp(a) was independently associated with coronary atheroma progression beyond low-density lipoprotein cholesterol and other conventional risk factors. Further studies are warranted to identify the inflammation effect exhibited as the perivascular FAI on coronary atheroma progression.
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