Abstract
The circulating levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) can be a simple, but practical and useful marker of cardiovascular disease (CVD). As limited studies are available in patients with diabetes mellitus (DM), further studies are needed to establish the clinical application of Lp-PLA2 in DM practice. The present study investigated the correlation between Lp-PLA2 and the cardio-ankle vascular index (CAVI), a recent marker of arterial stiffness, in DM patients according to their diabetes duration. Clinical data, including the plasma Lp-PLA2 mass and CAVI values, were collected from CVD-free type 2 DM female patients (n = 65, mean age 62 years, mean hemoglobin A1c 7.0%). The Lp-PLA2 level of patients with a diabetes duration of <10 years (n = 40:20.2 IU/mL) was not significantly different from that of patients with a diabetes duration of ≥10 years (n = 25:20.5 IU/mL), while the CAVI level was significantly higher in patients with ≥10 years (9.0) than in those with <10 years (8.1; p < 0.05). A stepwise multiple regression analysis found a positive correlation between the Lp-PLA2 and CAVI levels (β = 0.43, p < 0.01) in patients with a diabetes duration of ≥10 years. This correlation between Lp-PLA2 and CVAI suggests the possible use of Lp-PLA2 in DM patients with long-term disease. Further studies on Lp-PLA2 are warranted in DM practice in relation to the disease duration.
Highlights
Hyperglycemia causes endothelial dysfunction, vascular inflammation, arterial wall hypertrophy and fibrosis, which are all interrelated processes that lead to vascular damage with arterial stiffness [1,2]
A study using a meta-analysis [5] has reported that an increase of lipoprotein-associated phospholipase A2 (Lp-PLA2) mass/activity can predict the development of Cardiovascular disease (CVD)
The Lp-PLA2 level of patients with a diabetes duration of ě10 years did not significantly differ from that of patients with a duration of
Summary
Hyperglycemia causes endothelial dysfunction, vascular inflammation, arterial wall hypertrophy and fibrosis, which are all interrelated processes that lead to vascular damage with arterial stiffness [1,2]. Blood markers for CVD risks in DM patients remain to be explored. A study using a meta-analysis [5] has reported that an increase of Lp-PLA2 mass/activity can predict the development of CVD (even though there are some differences in the prediction ability of CVD between the Lp-PLA2 activity and mass [6,7]). The guidelines of several societies advocate the use of Lp-PLA2 when evaluating CVD risks [8,9]; the results of Mendelian randomization and phase III randomized control trials on inhibitors of Lp-PLA2 do not always support the causal involvement of Lp-PLA2 in the development of CVD [10]. Lp-PLA2 is currently regarded as a simple (non-causal), but practical marker for CVD [5,10], and we must further consider how to use Lp-PLA2 in the clinical setting
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