ABSTRACT
To determine possible associations between lipoprotein(a) [Lp(a)] and the severity of coronary artery lesions, we measured lipid, apolipoprotein, and Lp(a) in a large population of Belgian patients (n = 1054) undergoing coronary angiography. In both women and men, univariate analysis demonstrated significant differences in the Lp(a) concentrations according to the severity of the coronary stenosis. However, after adjustment for possible confounding factors, many of these differences were attenuated, indicating that other variables that differentiate patients from control subjects also influence Lp(a) distribution. Differences in lipid, apolipoprotein, and Lp(a) concentrations between male and female patients are discussed.
Subject(s)
Coronary Angiography , Coronary Disease/blood , Lipoprotein(a)/blood , Adult , Aged , Apolipoprotein A-I/metabolism , Apolipoproteins B/blood , Cholesterol/blood , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Coronary Disease/diagnostic imaging , Female , Humans , Male , Middle Aged , Sex Characteristics , Triglycerides/bloodABSTRACT
Using a double-blind procedure, 29 patients with a recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group receiving aspirin, 300 mg three times a day (n = 15) over 7 days. No change in renal function was observed in either treatment group. Compared with the placebo group, the 24-h urinary excretion of prostaglandin E2 (PGE2) was significantly suppressed in the aspirin group, but the urinary kallikrein activity was unchanged. These results contrast with our previous study of similar patients, in which sulfinpyrazone decreased renal function, as well as the urinary PGE2 and kallikrein excretions. These divergent effects of aspirin and sulfinpyrazone on urinary kallikrein activity could explain the different trends in renal function observed early after myocardial infarction.
Subject(s)
Aspirin/pharmacology , Kallikreins/urine , Myocardial Infarction/urine , Prostaglandins E/urine , Aged , Aspirin/therapeutic use , Clinical Trials as Topic , Dinoprostone , Double-Blind Method , Female , Humans , Kidney Function Tests , Male , Middle Aged , Myocardial Infarction/drug therapy , Myocardial Infarction/physiopathology , Random Allocation , Time FactorsABSTRACT
Twenty-nine patients with recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group (n = 15) who received sulphinpyrazone, 4 x 200 mg daily for 7 days. Renal function significantly and transiently deteriorated in the sulphinpyrazone group compared to the placebo group. In the sulphinpyrazone group the 24 hour-urinary prostaglandin E2 and kallikrein excretion were suppressed. These data suggest that the decrease in renal function caused by sulphinpyrazone early after myocardial infarction could be mediated by an inhibition of renal prostaglandin and/or kallikrein-kinin synthesis.
