Why the study?
Does a fat load reveal abnormal postprandial lipemia in CAD patients and their progeny compared to controls?
Does a fat load reveal abnormal postprandial lipemia in CAD patients and their progeny compared to controls?
Patients with CAD and their adult progeny exhibit delayed and elevated postprandial triglyceride metabolism, suggesting a familial genetic disorder of triglyceride metabolism.
Fat-load testing may flag heritable triglyceride defects in CAD families; hypothesis-generating and should not yet change practice.
OBJECTIVE: To assess the postprandial response to a fat load in patients with coronary artery disease (CAD) and age-matched controls. METHODS: Postprandial lipemia was assessed in patients with CAD confirmed by angiography (study group, n = 44) and in patients without coronary lesions (control group, n = 20). Family members of patients with CAD were also included (spouses group, n = 22; progeny group, n = 33). Fasting triglyceride and cholesterol concentrations in the control and study groups were less than 2.3 and 6.47 mmol/l, respectively. After initial blood sampling, the patients consumed 30% cream (200 ml/m2 body area). Repeat measurements of triglycerides, total cholesterol and high-density lipoprotein were made after 2, 4, 6, and 8 h. RESULTS: Changes were most marked in triglyceride concentrations. Peak values were observed after 4 h in the spouses, progeny, and control groups, and after 6 h in the study group. To compensate for the large age span (8-40 years) of the progeny, two subgroups were formed, taking 25 years as the cut-off value. Triglycerides continued to increase until the 4th hour in both subgroups, but the subgroups differed as to the absolute concentration of triglycerides. During the first 6 h of the test, the concentrations were significantly greater in the subgroup of older progeny than in their fathers with CAD. CONCLUSIONS: These findings indicate that triglycerides are metabolized at a slower rate and remain longer in the circulation of patients with CAD, as compared with patients without CAD. A significantly greater level of postprandial lipemia has been observed in adult progeny of patients with CAD, suggesting a genetic disorder of triglyceride metabolism in these individuals.
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Przybycień et al. (2000) studied this question.
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