title: Beta blockers, Lp(a), hypertension, and reduced basal fibrinolytic activity.
abstract: To assess the hypothesis that beta blocker use and hypertension are associated with high lipoprotein(a) [Lp(a)] or with reduced basal fibrinolytic activity, the authors studied relationships of hypertension and beta blockers to Lp(a), lipids, lipoproteins, apolipoproteins, and basal fibrinolytic activity in 385 patients consecutively referred for diagnosis and therapy of hyperlipidemia. A second aim was to determine possible gender differences in fibrinolytic activity among patients with hypertension. Ninety-nine patients (58 women [88% post-menopausal] and 41 men) had drug-treated hypertension. In women, hypertension was a positive, independent predictor of the major inhibitors of fibrinolysis, plasminogen activator inhibitor antigen (p = 0.017), and plasminogen activator inhibitor activity (p = 0.004). In men and women, major risk factors for atherosclerosis were significant, independent predictors of reduced basal fibrinolysis. Median Lp(a) in the 99 patients with hypertension (16 mg/dL) did not differ from Lp(a) (18 mg/dL) in normotensive patients (p > 0.1). Of the 385 patients, the 39 beta blocker users had higher plasminogen activator inhibitor activity (p = 0.01), higher triglyceride (p = 0.02) levels, and higher Quetelet Indices (p = 0.01) than non-users (n = 346). After covariance adjusting for age, Quetelet Indices, sex, and triglycerides, plasminogen activator inhibitor activity was not higher in beta blocker users than in non-users (p > 0.1). Median Lp(a) did not differ in beta blocker users (16 mg/dL) and in non-users (17 mg/dL), p greater than 0.1. Hypertensive, predominantly post-menopausal women are likely to have high plasminogen activator inhibitor activity and plasminogen activator inhibitor antigen with concurrent reduced fibrinolytic activity, as well as high fibrinogen levels.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Cholesterol Center, Jewish Hospital, Cincinnati, Ohio 45229.
authors.forename: C J
authors.initials: CJ
authors.lastname: Glueck
authors.forename: H I
authors.initials: HI
authors.lastname: Glueck
authors.forename: T
authors.initials: T
authors.lastname: Hamer
authors.forename: J
authors.initials: J
authors.lastname: Speirs
authors.forename: T
authors.initials: T
authors.lastname: Tracy
authors.forename: D
authors.initials: D
authors.lastname: Stroop
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000704:Analysis of Variance; D001053:Apolipoproteins / Q000032:analysis; D001161:Arteriosclerosis / Q000453:epidemiology; D004232:Diuretics / Q000627:therapeutic use; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood*; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D008055:Lipids / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D012307:Risk Factors; D012737:Sex Factors
chemical_list: D000319:Adrenergic beta-Antagonists; D001053:Apolipoproteins; D004232:Diuretics; D008055:Lipids; D017270:Lipoprotein(a); D008074:Lipoproteins