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, cross-sectional study investigates the change in lipid profile and platelet activity in the different prandial states.

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). Venous blood samples for lipid profile and markers of platelet activity were collected in the fasting state and after the oral fat tolerance test (OFTT) (three and five hours later). Milkshake with a content of 90g fat was used as a fat loading. The platelet activity was measured with a Multiplate test using ADP and TRAP reagents.

Results: Total cholesterol, LDL-c, Apolipoprotein A1, and Apolipoprotein B did not change during the OFTT irrespective of the group (p=0.925). 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<0.001) with no difference in increase between the groups. Triglycerides increased significantly during the OFTT, with a peak after 5 hours (130.2 ± 14.5 mg/dL., p<0.001) irrespective of the group. Platelet activity increased after fat loading, as shown by a significantly increased thrombocyte count after three hours (p=0.111). Platelet activity measured by multiplate test with ADP (7.16±2.17 AU, p=0.005) and TRAP (11.41±3.10 AU, p=0.001) reagents showed a statistically significant increase three hours after the fat loading with no difference in growth 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.