METHODS: Between December 2009 and June 2010, 494 subjects were recruited from a population scheduled for diagnostic coronary angiography. Routine clinical (age, gender, BMI and treatment), cardiac (echocardiography, coronarography, carotid ultrasonography) and biochemical parameters were recorded for all patients.
Lp-PLA2 mass concentration was assessed in serum with a Plac®-test turbidimetric immunoassay. Control
Lp-PLA2 values were specifically obtained in 61 healthy subjects aged 44.5 ± 17.6 years (range: 25 to 59 years) without known cardiovascular risk factors (diabetes, smoking,
hypertension,
dyslipidemia) or cardiac treatment.
RESULTS: In healthy controls, mean
Lp-PLA2 level was 163 ± 43 μg/L (166 ± 45 μg/L in men and 159 ± 39 μg/L in women, non significant difference). In our cohort of 494 patients (69.8% men) aged 64.2 ± 16.7 years, the main etiologies of
cardiomyopathies were ischemic (40%), valvular (22%),
cardiac failure with left ventricular (
LV) dysfunction (14%),
infection (5%) and
aortic aneurysm (7%). Mean
Lp-PLA2 levels were 216 ± 17 μg/L.
Lp-PLA2 correlated with age, BMI, current smoking, history of
hypertension but not with diabetes and gender. The bivariate analysis showed a significant correlation between
Lp-PLA2, and BMI (p=0.001) but no correlation with serum
creatinine or NYHA status. A multivariate correlation showed that
Lp-PLA2 was associated with total
cholesterol, LDL-
cholesterol and
apoB (r=0.95, p<0.0001) but not with Lp(a). We observed that
Lp-PLA2 was significantly associated with treatments such as
statins and ACEi/ARA2 but not with β-blockers, antiaggregant drugs or
diuretics.
Lp-PLA2 levels were significantly higher in patients with CAD than in patients without CAD (223 ± 54 vs. 208 ± 52 μg/L, respectively; p<0.007). Moreover,
Lp-PLA2 levels were significantly higher in patients with the most extensive angiographic CAD [single (n=24)=215.2 ± 52 μg/L; two (n=55)=222 ± 53 μg/L and three vessels (n=140)=251.9 ± 53.7 μg/L, respectively; p<0.0001]. Patients with
heart failure,
sepsis or
aortic aneurysm had increased
Lp-PLA2 levels: 256.2 ± 46.8; 226.7 ± 47.3; 218.1 ± 38.9 μg/L, respectively, as compared to controls (p<0.0001). In patients with
carotid artery disease,
Lp-PLA2 significantly increased with the severity of
atherosclerosis. Mean
Lp-PLA2 levels were 218.8 ± 51 μg/L in the group without any
stenosis (n=108), 224 ± 51 μg/L in the group with mild
stenosis (n=101), and 231 ± 46 μg/L in the group with severe
stenosis (n=22); p=0.004.
CONCLUSION: This study clearly shows that interpretation of
Lp-PLA2 levels needs a good assessment of cardiac parameters and treatments, especially
statins and ACEi/ARA2.
Lp-PLA2 levels are significantly associated with
coronary heart disease and with the extension of extra
coronary disease after adjustment for age and gender.