Apolipoprotein, Low Density Lipoprotein Subtraction, and Insulin Associations with Familial Combined Hyperlipidemia Study of Utah Patients with Familial Dyslipidemic Hypertension

Familial dyslipidemic hypertension (FDH) Is a syndrome recently described from sibshlps selected for early familial hypertension and found to have one or more of three fasting llpld abnormalities [high trlglycerldes, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-l and B, fasting plasma Insulin (adjusted for body mass Index), and detailed anthropometries were different In two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglycerlde and/or low HDL cholesterol levels. When compared to 20 normollptdemlc hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p=0.0001), 33% higher apolipoprotein B (p=0.0002), smaller LDL particles (p=0.007), and 73% higher fasting Insulin (p=0.003), but no significant differences in body mass Index or sklnfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p=0.0001), with only 8% lower apolipoprotein A-l levels (p=0.20); significantly higher subscapular sklnfolds (p=0.02), weights (p=0.002), body mass Index (p=0.006), knee widths (p=0.0007), and wrist circumferences (p=0.0009); smaller, denser LDL subtractions (p=0.001); and Increased apolipoprotein B levels (p=0.01) compared to the normolipldemlc hypertensive group. Increased fasting Insulin levels were similar to the normollpldemlc group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting Insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and Increased fasting plasma Insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglycerlde levels. Elevated insulin levels found In both groups, but possibly originating through different physiological mechanisms, may provide the pathophyslologlcal connections between dysllpldemia, obesity, and hypertension. (Arteriosclerosis 9:335-344, May/June 1989)