The LIPL study lipid panels and platelet activity in coronary heart disease
Authors: Pogran E , Haller P H , Wegberger C W , Vujasin I V , Tscharre M T , Dick P D , Jaeger B J , Wojta J W , Huber K H 
Published: October 2022

Abstract

Introduction
Measuring lipid panel in the fasting state can be inconvenient for patients and may aggravate their compliance. Moreover, people spend most of the day in the nonfasting state. Hence, it suggests that the changes in the process of atherosclerosis happen mainly under the influence of nonfasting lipids. Up to date, the studies in the postprandial state were primarily performed in healthy subjects.

Aim
This exploratory study investigates the change in lipid profile and platelet activity in patients with different cardiovascular risk profiles in the postprandial state.

Methods
The studied population consists of 66 patients with different cardiovascular risks: patients with coronary artery disease (CAD) and diabetes mellitus type 2 (DM2) (n=20), CAD without DM2 (n=25), and a healthy control group (n=21). Lipid variables and markers of platelet function were assessed during the fasting state and 3 and 5 hours after a standardized fat meal using a standardized oral fat tolerance test (OFTT), a milkshake with 90g of fat. The platelet activity was measured with a Multiplate test using ADP, ASPI and TRAP reagents.

Results
Patients with CAD and DM2 were significantly older and had the highest BMI. All patients with CAD were on acetylsalicylic acid, and 95% of CAD patients were on high-dose statins. Total cholesterol, LDL-c, Apolipoprotein A1, and Apolipoprotein B did not change during the OFTT, irrespective of the group. However, HDL-c decreased statistically significantly three and five hours after the fat loading with a peak after five hours (3.46±0.4 mg/dL, p&lt;0.001). The lowest HDL-c was in the CAD and DM2 group (p=0.006). Triglycerides (TG) increased significantly during the OFTT, with a peak after 5 hours (130.2±14.5 mg/dL, p&lt;0.001) irrespective of the group. There was no difference in TG concentration between the groups. Differences stayed statistically significant even after adjustment for age and BMI. Platelet activity increased after fat loading, as shown by a significantly increased thrombocyte count after three hours (p&lt;0.001). Platelet activity measured by multiplate test with ADP (7.16±2.17 AU, p=0.005), ASPI (4.60±1.40 AU, p=0.005), and TRAP (11.41±3.10 AU, p=0.001) reagents increased statistically significant three hours after the fat loading. The platelet activity measured by all three reagents remained increased even after the adjustment for age and BMI (ADP: 7.14±2.10 AU, p=0.004, ASPI: 4.60±1.40 AU, p=0.006, TRAP: 11.40±3.10 AU, p=0.002). Moreover, the platelet activity measured by ADP (−13.12±4.93, p=0.030), and TRAP (−14.6±15.51, p=0.031) reagents was lower in the control group. When adjusted for age and BMI, there was no difference in the platelet activity between the three groups.

Conclusion
This study showed that fatty meal causes worsening of lipid profile and leads to increased platelet activity in subjects irrespective of cardiovascular risk profile.

Funding Acknowledgement
Type of funding sources: None.