Key result
Standard low-fat diet linked to ~/dL postprandial triglyceride spike in statin-treated CVD patients.
Why the study?
Does a standard low fat diet induce postprandial lipemia in patients with cardiovascular diseases who have normal fasting lipid profiles and are on statin therapy?
Observational (n=12)
No
Does a standard low fat diet induce postprandial lipemia in patients with cardiovascular diseases who have normal fasting lipid profiles and are on statin therapy?
Patients with cardiovascular disease on statin therapy with normal fasting lipids still experience significant, prolonged postprandial elevations in triglycerides and VLDL, suggesting fasting lipids may be insufficient for assessing residual risk.
Answers are grounded in this paper and cite their sources.
Postprandial lipemia may signal residual risk despite normal fasting lipids in CVD; leaves open whether testing should guide care.
BACKGROUND: Dyslipidemia is associated with cardiovascular morbidities and mortality. Currently, fasting lipid profile determination is used to monitor treatment response. Recently, postprandial lipemia is of increasing interest because of its atherogenic and thrombogenic potential and also was found to be more predictive for cardiovascular diseases. OBJECTIVES: To demonstrate postprandial lipemia among patients with cardiovascular diseases despite low fat diet, normal fasting lipid profile and even statin regimen. PATIENTS AND METHODS: Patients aged 40-80 years old with cardiovascular diseases (i.e. coronary artery disease and cerebrovascular disease) more than 6 months, on statin treatment for more than 6 months and normal fasting lipid profile (according to NCEP ATP III guidelines) were included. Study exclusion criteria were pregnancy, acute cardiovascular events < 6 months, hepatic or renal failure. Finally, twelve patients were included. RESULTS: The triglyceride level showed a significant rise from fasting to 2 hours after breakfast with a mean difference of 23.86 mg/dL (P =0.012). The level peaked at 4 hours after breakfast with a mean difference (MD) of 72.02 mg/dL (P =0.002). Subsequent triglyceride levels plateaued and were significantly higher than the baseline (P <0.05) until the 12th hour of observation. VLDL levels showed a similar pattern. Levels increased significantly from fasting to 2h after breakfast (mean difference: 4.49 mg/dL, P = 0.007), then plateaued and further increased 4 hours after breakfast (MD: 14.01 mg/dL, P = 0.002). VLDL levels were significantly higher than fasting (P < 0.05) and did not return to baseline until the 12th hour of observation. In contrast, the levels of total cholesterol, HDL and LDL decreased postprandially. CONCLUSIONS: Triglyceride and VLDL peaking and plateauing were observed in patients with cardiovascular diseases despite low fat diet, normal fasting lipid profile and statin regimen. These findings may raise more attentions in monitoring and management of dyslipidemia in patients with cardiovascular and cerebrovascular events.
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Samson et al. (2012) conducted an observational in Cardiovascular diseases (coronary artery disease or cerebrovascular disease) (n=12). Standardized low fat diet vs. Fasting baseline was evaluated on Change in triglyceride levels from fasting to 4 hours postprandial (MD 72.02 mg/dL, p=0.002). A standardized low-fat diet induced significant postprandial peaking of triglycerides at 4 hours in patients with cardiovascular disease despite statin therapy.
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