Low-Density Lipoprotein Triglycerides Associated With Low-Grade Systemic Inflammation, Adhesion Molecules, and Angiographic Coronary Artery Disease

März, Winfried; Scharnagl, Hubert; Winkler, Karl; Tiran, A.; Nauck, Markus; Boehm, Bernhard O.; Winkelmann, Bernhard R.

doi:10.1161/01.cir.0000146898.06923.80

Cited by 132 publications

(71 citation statements)

References 33 publications

(24 reference statements)

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“…19 With this method, the LDL fraction includes particles with densities of 1.006 through 1.063 kg/L and thus comprises intermediate-density lipoproteins (IDL, 1.006 to 1.019 kg/L). 20 …”

Section: Laboratory Proceduresmentioning

confidence: 99%

Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors

et al. 2005

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Background-Platelet-activating factor acetylhydrolase (PAF-AH), also denoted as lipoprotein-associated phospholipase A2, is a lipoprotein-bound enzyme that is possibly involved in inflammation and atherosclerosis. This study investigates the relationship of PAF-AH activity to angiographic coronary artery disease (CAD), the use of cardiovascular drugs, and other established risk factors. Methods and Results-PAF-AH activity, lipoproteins, sensitive C-reactive protein (sCRP), fibrinogen, serum amyloid A, and white blood cell count were determined in 2454 subjects with angiographically confirmed CAD and in 694 control subjects. PAF-AH activity was highly correlated with LDL cholesterol (rϭ0.517), apolipoprotein B (rϭ0.644), and non-HDL cholesterol (rϭ0.648) but not with sCRP or fibrinogen. PAF-AH activity was lower in women than in men and was affected by the intake of lipid-lowering drugs (Ϫ12%; PϽ0.001), aspirin (Ϫ6%; PϽ0.001), ␤-blockers (Ϫ6%; PϽ0.001), and digitalis (ϩ7%; PϽ0.001). Unlike sCRP, fibrinogen, and serum amyloid A, PAF-AH activity was not elevated in unstable angina, non-ST-elevation myocardial infarction, or ST-elevation myocardial infarction. When nonusers of lipid-lowering drugs were examined, PAF-AH activity was associated with the severity of CAD and the number of coronary vessels with significant stenoses. In individuals not taking lipid-lowering drugs and after adjustment for use of aspirin, ␤-blocker, and digitalis, the odds ratio for CAD associated with increasing PAF-AH activity was 1.39 (95% CI 1.26 to 1.54, PϽ0.001), a finding that was robust against further adjustments. Conclusions-PAF-AH activity is not an indicator of the systemic inflammation that accompanies acute coronary syndromes. PAF-AH activity is affected by a number of cardiovascular drugs; however, after such medication use was accounted for, PAF-AH activity was associated with angiographic CAD, complementary to sCRP and independently of established risk factors such as LDL cholesterol. (Circulation. 2005;111:980-987.)

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“…19 With this method, the LDL fraction includes particles with densities of 1.006 through 1.063 kg/L and thus comprises intermediate-density lipoproteins (IDL, 1.006 to 1.019 kg/L). 20 …”

Section: Laboratory Proceduresmentioning

confidence: 99%

Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors

et al. 2005

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“…This is most likely due to a reduction in hepatic lipase activity at birth and 5 days of age. 17 Although cord TG concentration is markedly lower than that in adults, neonate cord LDL is richer in TG. 10 The present study suggests that the influence of hepatic lipase activity on LDL heterogeneity persists during at least the first 5 days of life and is greater in neonates with younger gestational age.…”

Section: Discussionmentioning

confidence: 99%

Low-density lipoprotein profile changes during the neonatal period

et al. 2008

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Objective: To investigate natural change of low-density lipoprotein (LDL) profile during the neonatal period and the impact of gestational age and birth weight on those changes.Study Design: We measured lipid composition in LDL fraction, LDL particle size and apolipoprotein B (apoB) concentration at birth, 5 days of age and 1 month of age in 63 healthy neonates that had 37 to 41-week gestational age.Result: Low-density lipoprotein cholesterol and apoB concentrations increased from birth to 5 days of age, and the concentration persisted at 1 month in breast-fed and mixed-fed infants. However, in formula-fed infants, the concentration decreased at 1 month. At 5 days of age, neonates had larger and more triglyceride (TG)-rich LDL particles than at birth. At 1 month of age, LDL particles were smaller and more cholesterol rich than at 5 days of age. Single regression analyses showed that gestational age had influenced the LDL profile at birth and 5 days of age, while at 1 month milk determined the profile. Conclusion:The number of LDL particles increased rapidly during the first 5 days of life, and the composition of LDL particles is modulated by TG content throughout the neonatal period. Gestational age and milk, rather than birth weight, determine postnatal changes in LDL profile.

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“…Recently, it was shown that alterations of LDL metabolism characterized by high LDL-triglycerides are related to coronary artery disease, systemic low-grade inflammation, and vascular damage. 51 These alterations in LDL may also contribute to an unsatisfactory vascular status. Finally, PBC patients who are candidates for liver transplantation should have no pre-existing advanced stages of atherosclerosis, which may be further aggravated by subsequent immunosuppressive therapy.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin in patients with primary biliary cirrhosis and incomplete biochemical response to ursodeoxycholic acid

et al. 2007

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Statin therapy may target both hypercholesterolemia and cholestasis in primary biliary cirrhosis (PBC). However, little is known about the efficacy and safety of statins in PBC. The aim of this single-center study was therefore to prospectively examine the effects of atorvastatin on serum markers of cholestasis, aminotransferases, and lipid and bile acid metabolism as well as inflammatory and immunological markers in patients with PBC. Fifteen patients with early-stage PBC and an incomplete biochemical response to ursodeoxycholic acid (UDCA) therapy (defined as alkaline phosphatase 1.5-fold above the upper limit of normal after 1 year) were treated with atorvastatin 10 mg/day, 20 mg/day, and 40 mg/day for 4 weeks, respectively. Serum levels of alkaline phosphatase increased during atorvastatin 20 mg and 40 mg (P < 0.05), whereas leucine aminopeptidase and ␥-glutamyltransferase remained unchanged. No statistical differences in overall serum ALT, AST, bilirubin, and IgM levels were observed. However, atorvastatin was discontinued in 1 out of 15 patients because of ALT 2-fold above baseline, and 2 patients showed ALT elevations 3-fold above the upper limit of normal at the end of the atorvastatin treatment period. Serum total cholesterol and low-density lipoprotein cholesterol levels decreased by 35% and 49%, respectively (P < 0.001). Precursors of cholesterol biosynthesis (lanosterol, desmosterol, lathosterol) showed a similar pattern. No changes in serum bile acid levels and composition were observed during treatment. Conclusion: Atorvastatin does not improve cholestasis in PBC patients with an incomplete biochemical response to UDCA but effectively reduces serum cholesterol levels. (HEPATOLOGY 2007;46:776-784.)

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Low-Density Lipoprotein Triglycerides Associated With Low-Grade Systemic Inflammation, Adhesion Molecules, and Angiographic Coronary Artery Disease

Cited by 132 publications

References 33 publications

Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors

Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors

Low-density lipoprotein profile changes during the neonatal period

Atorvastatin in patients with primary biliary cirrhosis and incomplete biochemical response to ursodeoxycholic acid

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