Key result
Maternal ApoAV variants linked to ~16% higher fasting triglycerides during pregnancy.
Why the study?
The direct role of elevated triglyceride levels in plasma on premature coronary artery atherosclerosis and pancreatitis remains to be determined.
Observational (n=483)
No
Effect estimate: 16.2% increase (95% CI 7.6%-25.9%)
Absolute Event Rate: 2.29% vs 1.97%
p-value: p=<0.001
Maternal ApoAV variants may elevate gestational triglycerides; leaves open whether they influence pregnancy-related cardiovascular or pancreatic risk.
Available data suggest that elevated triglyceride levels in plasma, associated with increased VLDL or chylomicron remnants, are associated with premature coronary artery atherosclerosis. Whether this is a direct effect or as a result of the association of hypertriglyceridemia with decreased HDL as well as decreased LDL particle size remains to be determined. Many families with premature coronary disease have a genetic form of hypertriglyceridemia associated with decreased HDL, or with both decreased HDL and increased LDL cholesterol concentrations. In addition, subjects with severe hypertriglyceridemia in excess of 1000 mg/dl associated with elevation of plasma chylomicrons are at increased risk of developing recurrent pancreatitis. Therefore, triglycerides have been implicated in the pathogenesis of both atherosclerosis and pancreatitis.
No takes yet. Share an insight, caveat, or question.
Schaefer et al. (1988) conducted an observational in Pregnancy (n=483). ApoAV S19W and -1131T>C gene variants vs. Non-carriers (wild-type homozygotes) was evaluated on Fasting Triglycerides at 28 weeks gestation (S19W variant analysis) (16.2% increase, 95% CI 7.6%-25.9%, p=<0.001). Maternal carriage of the ApoAV S19W or -1131T>C gene variants significantly increased fasting triglyceride concentrations during pregnancy by 16.2% and 11.0%, respectively, compared to non-carriers.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: