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Background and Aim: A family history of myocardial infarction (MI) is an independent risk factor for future coronary events. Decreased plasma lipoprotein lipase (LPL) activity is associated with delayed clearance of triglyceride-rich lipoproteins (TRL) and low fasting HDL cholesterol. The aim of the study was to investigate the relations between plasma LPL activity, postprandial TRL and HDL cholesterol in offspring of MI patients., Methods and Results: A case-control study was performed in 17 healthy middle-aged offspring of MI patients and 13 healthy age-and sex-matched controls. Fasting blood samples were collected and each subject was given a standardized oral fat load (1g fat/kg body weight) with subsequent blood samples collected for an 8-h period. Offspring of MI patients had significantly lower postheparin LPL activity (62.9 mU/ml+/-22.8 mU/ml) (mean+/-SD) than healthy controls (93.0 mU/ml+/-21.7 mU/ml) (p=0.002). Decreased postheparin LPL activity was accompanied by significantly increased and delayed clearance of postprandial TRL and subsequent lower fasting HDL cholesterol in offspring of MI patients. Postheparin LPL activity was associated with HDL cholesterol (r=0.40, p=0.036) and trend analysis revealed a decrease in incremental area under the curve (AUCi) for chylomicrons with increasing LPL activity (p=0.013)., Conclusions: Offspring of MI patients had decreased postheparin LPL activity accompanied by increased postprandial TRL and subsequent decreased HDL cholesterol, an unfavourable lipid profile which may contribute to their increased risk for future coronary events.

Postprandial triglyceride-rich lipoproteins (TRL) levels are a predictor for coronary atherosclerosis. The aim of the study was to compare fasting high density lipoprotein (HDL) cholesterol, plasma lipoprotein lipase (LPL) activity, and postprandial TRL between elderly survivors of myocardial infarction (MI) and healthy controls. A case-control study was performed in 44 elderly patients 65-85 years of age with a previous history of MI and 43 age- and sex-matched healthy controls. Each participant underwent physical examination and was given a standard oral fat load with subsequent blood sampling over the next 8 h. Total and chylomicron triglycerides were assessed by area under the curve (AUC), incremental are under the curve (AUCi) and triglyceride response (TGR). Elderly MI patients had significantly lower postheparin LPL activity (87.4 +/- 36.9 mU/ml) (mean +/- 1 SD) than healthy controls (106.0 +/- 29.0 mU/ml) (P = 0.014). Decreased postheparin LPL activity was accompanied by significant increased and delayed clearance of postprandial TRL. Fasting HDL cholesterol was significantly lower in elderly MI patients than controls (1.45 +/- 0.32 and 1.66 +/- 0.47 mmol/l, respectively, P = 0.048). Multiple regression analysis revealed postheparin LPL activity as an independent predictor for postprandial TRL and fasting HDL cholesterol. Logistic regressions analysis revealed HDL cholesterol, triglycerides measured 2 h after the oral fat load, and postheparin LPL activity as independent predictors for MI. Our findings indicate that decreased fasting HDL cholesterol is associated with increased postprandial triglyceridemia which could be a target for life-style and therapeutic interventions in patients at risk for cardiovascular disease.

We examined the cross-sectional relationships between the frequency of habitual fish consumption, plasma phospholipid fatty acids, and serum lipids and hipoproteins in 152 men and women. There was a significant association between fish consumption starting from 1 dish/wk and plasma n-3, n-6, and n-9 fatty acids. Plasma eicosapentaenoic acid (EPA; 20: 5n-3) reflected fish consumption to a greater extent than did docosahexaenoic acid (DHA; 22:6n-3). Triglycerides decreased (P < 0.05) with fish consumption. In multivariate analysis in which anthropometric and lifestyle factors were controlled for, EPA correlated inversely with triglycerides (P < 0.05) and positively with high-density-lipoprotein (HDL) cholesterol and apolipoprotein A-I (both P < 0.001). In contrast, DHA did not correlate with triglycerides and showed negative associations to HDL cholesterol and apolipoprotein A-I (both P < 0.001). Platelet phospholipid EPA, but not DHA, was associated with lower triglyceride and higher HDL-cholesterol concentrations (both P < 0.05). This study suggests that hong-term intake of small amounts of fish has biological effects, and that EPA and DHA have divergent relations with lipoprotein metabolism. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Tissue factor (TF)-induced thrombin generation (TG) ex vivo has been suggested to be an important method to assess thrombotic risk. No studies have investigated the impact of postprandial lipemia on TF-induced TG. Since myocardial infarction (MI) is associated with elevated postprandial levels of triglycerides, we hypothesized a differential impact of postprandial lipemia on coagulation activation in MI-patients and healthy controls. Material and Methods: Elderly survivors of acute MI (n=44) and healthy age-and sex matched controls (n=43) underwent a fat tolerance test (1 gram per kg body weight) to assess coagulation activation during postprandial lipemia. Results: The incremental area under the curve (AUCi) for serum triglycerides was higher in MI-patients than in healthy age-and sex matched controls (5.64±0.52mmol/L⁎h and 3.94±0.39mmol/L⁎h, p=0.012) during the postprandial phase. Subsequent endogenous activation of coagulation, assessed by FVIIa and thrombin generation (F1+2), was similar among groups and not related to levels of triglycerides during the postprandial phase. Healthy individuals had a gradual decline in TF-induced thrombin generation ex vivo, assessed by endogenous thrombin potential (ETP) (AUCi=-542.4±71.4nM⁎min⁎h, p<0.001), whereas MI-patients retained their ETP (AUCi=127.4±89.0nM⁎min⁎h, p=0.47) in plasma during the postprandial phase (p for group difference=0.005). Conclusions: MI-patients had elevated postprandial lipemia and retained their ability for TF-induced TG in plasma ex vivo in the postprandial phase, whereas the capacity gradually decreased in healthy individuals. Further studies are warranted to reveal underlying mechanism(s) and clinical implications. [ABSTRACT FROM AUTHOR]