Is abnormal postprandial lipemia a familial risk factor for coronary artery disease in individuals with normal fasting concentrations of triglycerides and cholesterol?
K. Przybycien et al., Is abnormal postprandial lipemia a familial risk factor for coronary artery disease in individuals with normal fasting concentrations of triglycerides and cholesterol?, CORON ART D, 11(5), 2000, pp. 377-381
Objective To assess the postprandial response to a fat load in patients wit
h coronary artery disease (CAD) and age-matched controls.
Methods Postprandial lipemia was assessed in patients with GAD 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 inc
luded (spouses group, n=22; progeny group, n = 33). Pasting triglyceride an
d cholesterol concentrations in the control and study groups were less than
2.3 and 6.47 mmol/l, respectively. After initial blood sampling, the patie
nts consumed 30% cream (200 ml/m(2) body area). Repeat measurements of trig
lycerides, total cholesterol and high-density lipoprotein were made after 2
, 4, 6, and 8 h.
Results Changes were most marked in triglyceride concentrations. Peak value
s 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 ye
ars) 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 s
ubgroups, but the subgroups differed as to the absolute concentration of tr
iglycerides. During the first 6 h of the test, the concentrations were sign
ificantly greater in the subgroup of older progeny than in their fathers wi
th 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 postpr
andial lipemia has been observed in adult progeny of patients with CAD, sug
gesting a genetic disorder of triglyceride metabolism in these individuals.
Coron Artery Dis 11 :377-381 (C) 2000 Lippincott Williams & Wilkins.