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Published on: October 12, 2017
Elevated plasma lipoprotein-associated phospholipase A₂ activity is associated with plaque rupture in patients with
Chuan-Fen Liu1, Li Qin, Jing-Yi Ren
1Department of Cardiology, Peking University People's Hospital, Beijing 100044, China.
Insights
Elevated lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is linked to plaque rupture in coronary artery disease (CAD) patients. This finding suggests Lp-PLA2 may serve as a valuable biomarker for identifying vulnerable plaques.
Area of Science:
- Cardiology
- Biomarkers
- Vascular Biology
Background:
- Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is associated with coronary events in patients with coronary artery disease (CAD).
- Direct evidence linking Lp-PLA2 activity to vulnerable plaque characteristics in CAD patients was previously lacking.
Purpose of the Study:
- To investigate the association between plasma Lp-PLA2 activity and vulnerable plaque features in patients with CAD.
- To determine if Lp-PLA2 activity is an independent predictor of plaque rupture.
Main Methods:
- Plasma Lp-PLA2 activity was measured in 146 consecutive CAD patients undergoing coronary angiography and intravascular ultrasound (IVUS).
- Patients were analyzed for plaque rupture, positive remodeling, and soft plaque characteristics using IVUS.
- Multivariate logistic regression was employed to assess independent associations.
Main Results:
- Of 83 analyzed patients, 47% had plaque rupture, predominantly in acute coronary syndrome (ACS) patients.
- Patients with plaque rupture showed significantly more positive remodeling and soft plaques.
- Plasma Lp-PLA2 activity was independently associated with plaque rupture (OR 1.13-1.11) after adjusting for clinical and IVUS parameters.
Conclusions:
- Plasma Lp-PLA2 activity is significantly associated with plaque rupture in CAD patients.
- Lp-PLA2 activity is an independent predictor of plaque rupture, beyond traditional risk factors, hs-CRP, and IVUS findings.
- Lp-PLA2 may serve as a potential risk marker for vulnerable plaques in coronary artery disease.
Background:
Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) has recently been shown to be positively related to coronary events in patients with coronary artery disease (CAD). However, direct evidence about the relationship between circulation Lp-PLA(2) activity and vulnerable plaque in patients with CAD remains lacking.
Methods:
Plasma Lp-PLA(2) activity was determined in 146 consecutive patients with CAD who underwent clinically-indicated coronary angiography and preinterventional intravascular ultrasound (IVUS).
Results:
Eighty-three patients were included in the final analysis after the initial screening. Sixty (72.3%) were acute coronary syndrome (ACS) patients and 23 (27.7%) were stable angina pectoris (SAP) patients. Plaque rupture occurred in 39 (47.0%) patients, and 34 (87.2%) were from ACS patients and 5 (12.8%) from SAP patients. There were no significant differences in clinical and angiographic characteristics between patients with plaque rupture and those without plaque rupture, except for smoking, high-sensitive C-reactive protein (hs-CRP) level and Lp-PLA(2) activity (all P < 0.05). IVUS measurement uncovered that patients with plaque rupture had more frequent positive remodeling (74.4% vs. 43.2%, P = 0.004), soft plaques (64.1% vs. 36.4%, P = 0.012) and higher remodeling index (1.13 ± 0.16 vs. 0.99 ± 0.11, P = 0.041) as compared with those without plaque rupture. Multivariate Logistic regression analysis showed that plasma Lp-PLA(2) activity was independently associated with plaque rupture after adjusting for smoking, positive remodeling and soft plaque (Model 1: odds ratio (OR) 1.13, 95% confidence interval (CI): 1.06 - 1.20) or adjusting for smoking, hs-CRP level, positive remodeling and soft plaque (Model 2: OR 1.11, 95%CI: 1.04 - 1.19).
Conclusions:
Plasma Lp-PLA(2) activity is associated with plaque rupture in patients with CAD, independently of traditional CAD risk factors, hs-CRP level and IVUS parameters. Lp-PLA(2) may be a risk marker for vulnerable plaques.
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