Key result
Postprandial lipemia similarly increases VIIaAT in post-MI patients and controls despite persistent baseline hypercoagulability.
Why the study?
The effects of postprandial lipemia on circulating VIIaAT, procoagulant phospholipid activity, and thrombin generation in postmyocardial infarction patients were unclear.
Does postprandial lipemia affect circulating VIIaAT, PPL activity, and thrombin generation in post-MI patients compared to controls?
Case-Control (n=296)
Does postprandial lipemia affect circulating VIIaAT, PPL activity, and thrombin generation in post-MI patients compared to controls?
Postprandial lipemia increases VIIaAT levels, potentially adding to cardiovascular risk, though its impact on PPL activity and thrombin generation appears minor.
Postprandial lipemia may augment hypercoagulability via VIIaAT in post-MI patients; leaves open its role in recurrent events.
INTRODUCTION: Factor VII activation occurs postprandially. A proportion of activated factor VII (VIIa) circulates in complex with antithrombin (VIIaAT). Our primary objective was to assess the effects of postprandial lipemia on circulating VIIaAT, procoagulant phospholipid (PPL) activity, and thrombin generation. METHODS: Plasma samples from postmyocardial infarction patients (n = 40) and controls (n = 39) were taken before and at 3 and 6 hours during a standardized oral fat tolerance test (OFTT). Fasting PPL activity measurements were also made in a second cohort of 108 postinfarction patients and 109 controls. VIIaAT was analyzed with the Asserachrom VIIaAT ELISA, PPL activity with the STA-Procoag-PPL kit, and thrombin generation with calibrated automated thrombogram with PRP-Reagent as trigger (all Diagnostica Stago products). RESULTS: Postprandially, VIIaAT increased in all samples without significant case-control differences in the overall response during the OFTT. Thrombin generation measures peak height and velocity, and PPL activity, were marginally affected by the test meal in the controls. Levels of all patient baseline measures were significantly different from controls, indicating a more hypercoagulable state, and these differences were maintained throughout the OFTT. Fasting samples from cases showed higher PPL activity than control samples. CONCLUSION: Viewing VIIaAT quantitation as a surrogate for TF activity measurement, postprandial increase in VIIaAT may reflect a mechanism that adds to the cardiovascular risk associated with postprandial lipemia. On the other hand, the impact of postprandial lipemia on PPL activity and thrombin generation seems to be minor.
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Silveira et al. (2018) conducted a case-control in Post-myocardial infarction (n=296). Standardized oral fat tolerance test (postprandial lipemia) vs. Controls was evaluated on Circulating VIIaAT, procoagulant phospholipid (PPL) activity, and thrombin generation. Postprandial lipemia increased VIIaAT levels similarly in post-myocardial infarction patients and controls, though patients maintained a more hypercoagulable baseline state throughout the test.
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