“…ND denotes not detected, RCA right coronary artery, Mg1 first marginal branch of the circumflex coronary artery, and Dg1 first diagonal branch of the left anterior descending coronary artery. reduced levels of circulating remnant lipoproteins [30][31][32][33] and very low levels of LDL cholesterol. 33 These patients usually also have low body-mass indexes and follow a low-fat diet -both of which are associated with a reduced risk of atherosclerosis.…”
Premature atherosclerosis can occur in patients with familiar chylomicronemia as a result of mutations in the lipoprotein lipase gene. Defective lipolysis may increase susceptibility to atherosclerosis in humans.
“…ND denotes not detected, RCA right coronary artery, Mg1 first marginal branch of the circumflex coronary artery, and Dg1 first diagonal branch of the left anterior descending coronary artery. reduced levels of circulating remnant lipoproteins [30][31][32][33] and very low levels of LDL cholesterol. 33 These patients usually also have low body-mass indexes and follow a low-fat diet -both of which are associated with a reduced risk of atherosclerosis.…”
Premature atherosclerosis can occur in patients with familiar chylomicronemia as a result of mutations in the lipoprotein lipase gene. Defective lipolysis may increase susceptibility to atherosclerosis in humans.
“…A possible explanation for the discrepancy between this and our study could relate to an analytical artifact. Triglyceride-rich lipoproteins can undergo ex vivo hydrolysis unless tubes containing an inhibitor of lipoprotein lipase are used for blood collection; this phenomenon occurs in proportion to the triglyceride content in the blood sample [32]. Because atorvastatin markedly lowered plasma triglyceride concentrations in the DALI study, the amount of FFA generated by the ex vivo hydrolysis of triglycerides might likewise have been reduced, resulting in lower apparent FFA concentrations on atorvastatin.…”
“…18 Table 2 summarizes the major lipid/lipoprotein abnormalities that are associated with elevated apo B or sdLDL. 6,[31][32][33][34][35] A snapshot review of the previous work in light of the findings presented here suggests that sdLDL concurrent with elevated apo B levels [with normal levels of Lp(a)] represent a phenotype characteristic to FCHL independent of the macrocomposition of plasma lipoproteins.…”
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