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Lipid fractions of native plasma and of highdensity lipoprotein (HDL) were analyzed, and the clotting times of native platelet-rich and -poor plasma were recorded in patients with coronary artery disease and age-matched control subjects not taking any medication known to alter plasma lipid levels, coagulation, or platelet aggregation. Patients with coronary artery disease had lower HDL cholesterol and particularly HDL phospholipids but elevated HDL triglycerides, plasma triglycerides and diglycerides, and fibrinogen. Plasma lysolecithin was diminished. Accelerated coagulation was observed in native plasma and may be related to these changes in plasma lipids. The HDL content in cholesterol may be less relevant than that in phospholipids, which, because of their amphiphilic properties, may be essential for the removal and transport of hydrophobic cholesterol. The lower lysolecithin levels also suggest diminished esterification of cholesterol

1. Chyle lipids, labelled with (14)C, are taken up and oxidized by the isolated perfused rat heart. 2. In recirculatory perfusions, when chyle lipids are the sole exogenous energy source, about 24% of the total oxygen uptake is accounted for by their oxidation. This proportion is not changed by starvation of the rats for 48hr. and falls when an external work load is imposed on the left ventricle. 3. With albumin in the perfusion medium, the rate of (14)CO(2) output is reduced by half and there is a rise in the proportion of (14)C-labelled free fatty acids in the medium. 4. Clearing-factor lipase appears in the perfusion medium when chyle lipids are perfused through the heart. In the absence of albumin, the activity of the medium enzyme is low and only a small proportion of the (14)CO(2) output can be accounted for by the oxidation of free fatty acids released by it. In the presence of albumin, the enzyme is more active in the medium. 5. When a substantial proportion of the total clearing-factor lipase is removed from the heart by a prior perfusion with heparin, (14)C-labelled chyle lipid perfused subsequently is oxidized at only half the normal rate.

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Background: Anticardiolipin (aCl) and anti-β₂-glycoprotein I (anti-β₂-gpI) antibodies are autoantibodies associated with the antiphospholipid syndrome (APS), which is characterized by both arterial and venous thrombosis and miscarriages. The scope of this study was to explore the clinical characteristics of patients with aCl and anti-β₂-gpI antibodies. Methods: ACl were tested in 3,600 consecutive sera in our laboratory between January 1999 and June 2001. The clinical diagnosis and prevalence of thrombosis and pregnancy morbidity were retrospectively reviewed in aCl-positive patients. Furthermore, the frequency of anti-β₂-gpI antibodies, lupus anticoagulant (LA), prolonged activated partial thromboplastin time (aPTT), and thrombocytopenia were investigated in aCl-positive patients. Results: 147 aCl-positive patients, 110 women and 37 men with a mean age of 41 years (range 7.8–82.5), were identified. 42 (28.6%) aCl-positive patients fulfilled the criteria for APS which was secondary to a connective tissue disorder in 8 patients. The frequency of anti-β₂-gpI antibodies and LA, prolonged aPTT, and thrombocytopenia in aCl-positive patients was 23.8, 27.2, 25.7 and 9.2%, respectively. The presence of both aCl and anti-β₂-gpI antibodies was strongly associated with clinical symptoms of APS (p = 0.007) compared to p = 0.008 for LA. Conclusion: Our data suggest that assessment of anti-β₂-gpI antibodies in addition to aCl is a valuable diagnostic tool in the workup of patients with APS.

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Abstract. Three patients suffering from prolonged obstructive jaundice were studied after surgical removal of biliary obstruction. Four days after surgery the initial cholesterol esterification rate in the plasma rose from very low activities to values three to four times higher than those found in normal subjects. During this time lipoprotein‐X decreased in concentration. The initial cholesterol esterification rate returned to normal values when plasma lipids and lipoproteins reached normal levels. During incubation of normal plasma with lipoprotein‐X, changes in the lipid composition of the incubation mixture were observed which appeared to be catalysed by lecithin:cholesterol acyltransferase. The formation of esterified cholesterol and lysophosphatidylcholine exceeded that of control experiments when lipoprotein‐X was replaced by buffer solution in the incubation mixture. Lipoprotein‐X disappeared as monitored by electrophoresis on agar and measured after zonal ultracentrifugation, and lipoproteins with flotation behaviour of high density lipoprotein2, enriched in polar lipids, appeared. When plasma was incubated separately with lipoprotein‐X1 and lipoprotein‐X2in vitro, the T1/2 of these lipoproteins were 24 h and 9 1/2 h, respectively. Addition of lipoprotein‐X2 to normal plasma resulted in an increased initial cholesterol esterification rate with a sigmoidal response curve. Lipoprotein‐X1 increased the initial cholesterol esterification rate also but to a lesser extent. Our findings indicate that incubation of normal plasma with lipoprotein‐X results in the disappearance of this abnormal lipoprotein and the appearance of a high density lipoprotein2‐like particle mediated by enzymic cholesterol acyltransfer.

No satisfactory explanations have been offered for the smoker's paradox, the greater short-term survival of smokers after a myocardial infarction nor for the large variations in the coronary risk rate for smoking ranging between 1 and 5.9. These discrepancies as well as the smoker's paradox may be caused by different baseline characteristics of smokers and nonsmokers, whereas the usually quoted coronary risk of 2 is derived from studies based on the assumption of equal baseline characteristics. As neither this assumption nor the possibility of unequal starting conditions have been tested, we examined the main cardiovascular risk factors in smoking and nonsmoking boys as near as possible to baseline, at the age of fourteen. This age appeared to be best suited, because boys starting to smoke early are most likely to become regular and heavy smokers. Of 336 boys, 39 had smoked 8.3+/-6.0 cigarettes/day for 15.5+/-11.2 months. Compared to nonsmokers, boys who started to smoke early had lower LDL cholesterol and alpha2-antiplasmin, greater handgrip strength, vital capacity and forced expiratory volume, better perfomance on bicycle ergometry and higher testosterone. The differences in total cholesterol, LDL cholesterol, vital capacity, handgrip strength, testosterone and alpha2-antiplasmin persisted after adjustment for age, body mass, and testosterone. In addition, the differences in perfomance on bicycle ergometry and forced expiratory volume persisted after adjustment for age. These favourable baseline characteristics of those starting to smoke early can explain the smoker's paradox. In addition, they suggest that the individual coronary risk in smokers is considerably higher than 2, because the assumption of equal baseline characteristics of smokers and nonsmokers cannot be upheld.