Winkler, Karl;
Winkelmann, Bernhard R.;
Scharnagl, Hubert;
Hoffmann, Michael M.;
Grawitz, Andrea Busse;
Nauck, Markus;
Böhm, Bernhard O.;
März, Winfried
Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors : The Ludwigshafen Risk and Cardiovascular Health Study
: The Ludwigshafen Risk and Cardiovascular Health Study
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Medientyp:
E-Artikel
Titel:
Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors : The Ludwigshafen Risk and Cardiovascular Health Study
:
The Ludwigshafen Risk and Cardiovascular Health Study
Beteiligte:
Winkler, Karl;
Winkelmann, Bernhard R.;
Scharnagl, Hubert;
Hoffmann, Michael M.;
Grawitz, Andrea Busse;
Nauck, Markus;
Böhm, Bernhard O.;
März, Winfried
Beschreibung:
<jats:p>
<jats:bold>
<jats:italic>Background—</jats:italic>
</jats:bold>
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.
</jats:p>
<jats:p>
<jats:bold>
<jats:italic>Methods and Results—</jats:italic>
</jats:bold>
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 (
<jats:italic>r</jats:italic>
=0.517), apolipoprotein B (
<jats:italic>r</jats:italic>
=0.644), and non-HDL cholesterol (
<jats:italic>r</jats:italic>
=0.648) 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 (−12%;
<jats:italic>P</jats:italic>
<0.001), aspirin (−6%;
<jats:italic>P</jats:italic>
<0.001), β-blockers (−6%;
<jats:italic>P</jats:italic>
<0.001), and digitalis (+7%;
<jats:italic>P</jats:italic>
<0.001). 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, β-blocker, and digitalis, the odds ratio for CAD associated with increasing PAF-AH activity was 1.39 (95% CI 1.26 to 1.54,
<jats:italic>P</jats:italic>
<0.001), a finding that was robust against further adjustments.
</jats:p>
<jats:p>
<jats:bold>
<jats:italic>Conclusions—</jats:italic>
</jats:bold>
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.
</jats:p>