Effect of long-term diltiazem administration on serum lipids in post-myocardial infarction survivors. Multicenter Diltiazem Post-Infarction Trial Research Group.
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Biomedical subjects
Publications and source records attributed to A Saritelli.
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We compared the clearance rate (K2) of plasma triglycerides (TG) following the intravenous (IV) infusion of a fat emulsion in 13 male endurance athletes (age 33 +/- 5.6 years, mean +/- SD) and 12 sedentary men (33 +/- 5.6 years). The athletes had lower fasting triglycerides (TG) (75 +/- 30.4 mg/dL v 125 +/- 52.5 mg/dL) and higher high-density lipoprotein (HDL) cholesterol concentrations (64 +/- 16.2 mg/dL v 42 +/- 9.4 mg/dL) than the sedentary subjects (P less than .01 for all). The higher HDL concentrations were due to increases in both the HDL2 and HDL3 subfractions. K2 in the athletes was 92% higher than that in the sedentary men (4.8 +/- 2.3%/min v 2.5 +/- 0.7%/min, P less than .01), but there was no difference in postheparin lipoprotein lipase activity (LPLA) between the groups (P greater than .05). K2 was positively correlated with LPLA (r = .51) and inversely related to fasting TG concentrations (r = -.73, P less than .01 for both). Furthermore, K2 was directly related to HDL (r = .75), HDL2 (r = .72), and HDL3 (r = .60) cholesterol concentrations (P less than .01 for all). These data suggest that the low TG levels in endurance athletes result at least in part from increased TG removal and that the elevated HDL concentrations of endurance athletes are related to enhanced fat clearance.
The metabolism and toxicity of the ubiquitous plasticizer, bis-(2-ethylhexyl) phthalate (DEHP), and its principal metabolite, mono-(2-ethylhexyl) phthalate (MEHP), have been extensively investigated. In an attempt to understand their disposition in man, we studied the in vitro serum protein-binding characteristics of these compounds, using ultracentrifugation and agarose gel electrophoresis. The association of DEHP and lipoproteins was shown to be highly dependent upon, and proportional to, the lipid concentration of the serum. It appears that more than half of the serum DEHP is bound to proteins with density greater than 1.21 g/mL when the concentration of cholesterol is below 300 mg/dL or the cholesterol and triglyceride total concentration is less than 600 mg/dL. As the cholesterol and triglyceride concentrations increase, the percent DEHP bound to VLDL, IDL, and LDL increases. MEHP is bound principally to nonlipoprotein constituents in the serum, and this binding distribution is unaffected by lipid concentration. The percent binding of DEHP and MEHP to individual proteins was also found to be unaffected by their concentrations in serum. These data indicate that the protein-binding characteristics of these compounds, in vitro, is somewhat more complex than previously reported.
Two hundred twenty-one first-year medical students participated in a voluntary coronary heart disease risk factor self-change project designed to teach the principles of behavioral change. Blood pressure, serum lipids, percentage body fat, cardiovascular fitness, and smoking status were measured prior to the project. Students designed their own programs of behavior modification and, after 8 weeks, repeat measurements were obtained in students whose projects related to coronary heart disease risk (56% of entire group). Despite generally low initial coronary heart disease risk factors, most risk factor groups successfully altered the targeted risk factors. The subgroup attempting to lower serum cholesterol (n = 49) reduced total cholesterol 15 +/- 24 mg/dl (mean +/- SD) and low-density lipoprotein cholesterol 11 +/- 20 mg/dl (P less than 0.001 for both). The blood pressure group (n = 9) decreased systolic blood pressure 8 +/- 10 mm Hg (P less than 0.05), and the weight-loss group (n = 33) lost 3.0 +/- 2.9 kg (P less than 0.001), reducing estimated percentage body fat 1.7 +/- 1.8 (P less than 0.001). The self-change project was well received by the students and appears to be a useful technique for introducing the principles of behavioral medicine to first-year medical students.
We sought to determine the optimal dose of heparin for evaluating the activities of lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase (HTGLA) in postheparin plasma. Nine physically active and ten sedentary men (age 30 +/- 5 yr, mean +/- SD) received 30, 50, 75, and 100 IU/kg of heparin in random order during a 2-week period. Based on all the samples, the average LPLA in the athletes was 43% higher (P less than 0.001) and HTGLA was 19% lower than in the untrained subjects (NS). The greatest LPLA was obtained after a heparin dose of 75 IU/kg, but LPLA after the three highest doses were not significantly different. There was also a dose effect on HTGLA (P less than 0.001) with greatest activities following doses of 75 and 100 IU/kg. Despite these dose effects, subjects maintained their rank order for both postheparin lipase activities regardless of the heparin dose. The only exception was for LPLA in the sedentary men probably because of lower LPLA and a smaller range of values. We also examined the effect of repeated daily injections of 75 IU/kg heparin on LPLA, HTGLA, and serum lipids. Repeated heparin administration on three consecutive days produced no significant effects on the apparent lipase activities. When all subjects were combined, HDL-cholesterol was increased over time (P less than 0.05) due to increases in both the HDL2 (P less than 0.05) and HDL3-cholesterol (NS) subfractions. Infusion of heparin or saline on three consecutive days into 18 additional men, however, had no effect on any lipid parameter.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of propranolol on lipids and lipoproteins were investigated in survivors of a recent myocardial infarction who were enrolled in the double-blind Beta-Blocker Heart Attack Trial. Nonfasting serum samples were obtained in more than 2800 patients assigned randomly to either propranolol or placebo. The propranolol-treated group had high-density lipoprotein cholesterol levels 3-4 mg/dl less and triglyceride concentrations 30-40 mg/dl higher than the placebo group. These effects occurred in men and women in all age categories.
Acute reductions in triglycerides and low density lipoprotein (LDL) cholesterol concentrations have been demonstrated in endurance athletes after prolonged exercise. To determine if similar changes occur in untrained subjects and to determine the duration of exercise necessary for such changes, we measured serum lipids and lipoproteins in 10 sedentary men after 1 hour of exercise at their anaerobic threshold. Findings in sedentary men were compared with those of 9 competitive cyclists after 1 and 2 hr of exercise. LDL cholesterol increased in the cyclists immediately after 1 and 2 hours of exercise. Total cholesterol and high density lipoprotein (HDL) cholesterol also increased in the cyclists immediately after the 2 hr session. These increases were transient and not significant when corrected for changes in plasma volume. Serum triglycerides were unchanged for 4 hr after exercise. By 24 hr, however, triglycerides had decreased in both the trained (17%) and untrained men (22%) after the 1 hr session and in the trained men (33% p less than 0.01) after the 2 hr session. These results demonstrate a delayed decrease in triglyceride concentration that is related to the duration of exercise and probably has no distinct threshold. The lower level of triglycerides in endurance athletes and in sedentary subjects after exercise training is due at least in part to an acute exercise effect.