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Comparison of Lp-PLA2 Activity, Lp-PLA2 Mass and Lp-PLA2 mRNA in Acute Coronary Syndrome Patients
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Background: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a risk predictor for cardiovascular diseases (CVD). Generally, plasma Lp-PLA2 was thought to be secreted by circulatory inflammatory cells. Lp-PLA2 mRNA expression of PBMC may also be a risk predictor.
Methods: A total of 104 subjects angiographically verified ACS patients were enrolled, including 73 unstable angina pectoris (UAP) patients and 31 acute myocardial infarction (AMI) patients. Plasma lipids, Lp-PLA2 activity and Lp-PLA2 mass were measured. Lp-PLA2 mRNA expression of PBMC was relatively quantified by real-time fluorescence PCR.
Results: Plasma Lp-PLA2 activity was increased in AMI patients compared to UAP patients (395.21±145.91 vs. 328.53±127.03 U/L, p=0.024). Lp-PLA2 mass of AMI patients was also higher than UAP patients (136.43±45.46 vs. 119.16±44.19 ng/mL, p=0.093), while PBMC mRNA expression was not statistically different [1.07 (0.74, 1.57) vs. 0.88(0.49, 1.99), p=0.453]. Comparing Lp-PLA2 mRNA by groups, Lp-PLA2 mRNA level was higher in male ACS patients and smoking ACS patients (p=0.008, p=0.048, respectively). Multivariate logistic regression analysis showed that Lp-PLA2 activity was an AMI risk predictor (OR=5.224, 95% CI 1.687-16.181, p=0.004), after smoking, systolic blood pressure, diabetes and hyperlipidemia were adjusted. Recurrent ACS patients were older (p=0.035), but they showed lower levels of Lp-PLA2 mass and Lp-PLA2 activity (p=0.014, p=0.045, respectively), compared to primary ACS patients.
Conclusion: Smoking may be an important regulatory factor for Lp-PLA2 mRNA expression in PBMC. Among three Lp-PLA2 indexes, Lp-PLA2 activity was the best marker indicating AMI risk, while Lp-PLA2 mass maybe play better role as a predictor in avoiding ACS recurrence.
Title: Comparison of Lp-PLA2 Activity, Lp-PLA2 Mass and Lp-PLA2 mRNA in Acute Coronary Syndrome Patients
Description:
Background: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a risk predictor for cardiovascular diseases (CVD).
Generally, plasma Lp-PLA2 was thought to be secreted by circulatory inflammatory cells.
Lp-PLA2 mRNA expression of PBMC may also be a risk predictor.
Methods: A total of 104 subjects angiographically verified ACS patients were enrolled, including 73 unstable angina pectoris (UAP) patients and 31 acute myocardial infarction (AMI) patients.
Plasma lipids, Lp-PLA2 activity and Lp-PLA2 mass were measured.
Lp-PLA2 mRNA expression of PBMC was relatively quantified by real-time fluorescence PCR.
Results: Plasma Lp-PLA2 activity was increased in AMI patients compared to UAP patients (395.
21±145.
91 vs.
328.
53±127.
03 U/L, p=0.
024).
Lp-PLA2 mass of AMI patients was also higher than UAP patients (136.
43±45.
46 vs.
119.
16±44.
19 ng/mL, p=0.
093), while PBMC mRNA expression was not statistically different [1.
07 (0.
74, 1.
57) vs.
0.
88(0.
49, 1.
99), p=0.
453].
Comparing Lp-PLA2 mRNA by groups, Lp-PLA2 mRNA level was higher in male ACS patients and smoking ACS patients (p=0.
008, p=0.
048, respectively).
Multivariate logistic regression analysis showed that Lp-PLA2 activity was an AMI risk predictor (OR=5.
224, 95% CI 1.
687-16.
181, p=0.
004), after smoking, systolic blood pressure, diabetes and hyperlipidemia were adjusted.
Recurrent ACS patients were older (p=0.
035), but they showed lower levels of Lp-PLA2 mass and Lp-PLA2 activity (p=0.
014, p=0.
045, respectively), compared to primary ACS patients.
Conclusion: Smoking may be an important regulatory factor for Lp-PLA2 mRNA expression in PBMC.
Among three Lp-PLA2 indexes, Lp-PLA2 activity was the best marker indicating AMI risk, while Lp-PLA2 mass maybe play better role as a predictor in avoiding ACS recurrence.
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