Platelet function in the postprandial period

Abstract

BackgroundPostprandial hyperlipidemia and hyperglycemia have been related to cardiovascular events. Among different underlying mechanisms platelet activation seems to be responsible too. No comparable data between various tests in normo- vs. hyperlipidemics before and at different time intervals are available after a fat meal. We aimed to compare 9 of them within the same patients at several time points in postprandial hyperlipidemia.ResultsFor some tests baseline values between the groups were significantly different (TXB2, platelet sensitivity, sedimentation and WU-test). However, hyperlipidemia revealed a variable influence on the tests examined. Some of the available tests apparently sensitive to show platelet activation reflect the increase in triglycerides (TG), such as the sedimentation index. ADP-induced platelet aggregatory activity in count adjusted washed isolated platelet samples during postprandial hyperlipidemia indicates mildly enhanced platelet activity, but does not seem to induce significant changes in aggregation. In patients with severe hypertriglyceridemia (> 400 mg/dl fasting) changes in platelet function are more pronounced due to delayed decay and may last up to 16 hours paralleling TG reaching the prevalue. The overwhelming majority of platelet function tests do not significantly respond to postprandial hyperlipidemia. The correlation between the tests applied is poor. For standardization purpose, platelet aggregation tests, aimed to examine proaggregatory capacity in atherosclerosis, should only be performed at the same time of the day after a fasting period > 6 hours. The great variation in preanalytical work-up on comparison of various tests, large number of platelet tests available and their respective potential value are discussed.ConclusionsAt present, the suspicion that platelet function is significantly activated in the postprandial period cannot be supported by any of the tests used. The information provided is valuable to know for which test and group of patients a fasting period of which duration is recommendable.

Dietary Macronutrients Do Not Differently Influence Postprandial Serum and Plasma Brain-Derived Neurotrophic Factor Concentrations: A Randomized, Double-Blind, Controlled Cross-Over Trial

“…Therefore, it could be that either there may be less platelets in the postprandial state or the clotting process, in which BDNF is released from platelets, is less efficient in the samples collected during the postprandial state. In this context, it was found that a high-fat meal elevated platelet count ( Sinzinger and Berent, 2012 ), but a high-carbohydrate meal did not ( Ahuja et al, 2009 ). Regarding the clotting process, it has been shown that meals rich in fats seem to activate coagulation factor VII which stimulates the clotting process ( Silveira, 2001 ).…”

Apolipoprotein A-IV binds αIIbβ3 integrin and inhibits thrombosis

“…Gel- filtered platelets (2.5 × 10 8 /mL) and PPP were prepared respectively. To minimize interference in the light transmission of PRP, which is commonly caused by postprandial chylomicrons and other lipid particles 69 , 125 µL gel-filtered platelets were incubated with its PPP (125 µL) for 20 min under 37 °C. The same volume of PPP and PIPES buffer were used as blank control.…”

The LIPL study: Postprandial lipid profile, inflammation, and platelet activity in patients with chronic coronary syndrome

“…Prior investigations examining the platelet activity in the postprandial state show conflicting evidence [ 15 , 16 , 20 , 36 , 37 ]. The reason for these discrepancies includes differences in methodology, different types of meals with different fat concentrations, as well as different measuring methods or various concentrations of agonists used in the tests, respectively.…”

“…Therefore, no exact sample size calculation could be performed on the given co-primary outcome variables. Alternatively, sample size estimation was performed according to the results on ADP-response of platelet-rich plasma after OFTT in patients with metabolic syndrome by Sinzinger et al [ 15 ]. Accordingly, 21 patients would be needed to show a significant difference in platelet activation (given a desired power of 0.8 and a p-value of 0.05) per group.…”

“…Most studies on postprandial lipemia were performed in healthy subjects or in individuals with diabetes mellitus type 2 (DM2) without CVD. Accordingly, little is known about the lipid profile during a postprandial state in patients with established CVD [ 2 , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] ]. Therefore, our study aimed to investigate postprandial lipid profiles and markers of inflammation and platelet activation in high-risk chronic coronary syndrome (CCS) patients with/without DM2 and to compare these results with a healthy population.…”