title: Inflammatory and hemostatic markers in relation to cardiovascular prognosis in patients with stable angina pectoris. Results from the APSIS study. The Angina Prognosis Study in Stockholm.
abstract: Increased inflammatory activity and platelet activation have been associated with an increased risk of cardiovascular (CV) events in epidemiological studies, but their prognostic importance in patients with stable angina pectoris is less well established. The Angina Prognosis Study in Stockholm (APSIS), comprised 809 patients (2766 patient years) with stable angina pectoris on double-blind treatment with verapamil or metoprolol. Plasma levels of fibrinogen and orosomucoid (an acute phase reactant), white blood cell counts (WBC), platelet counts and the urinary excretion of beta-thromboglobulin (reflecting platelet secretion), were related to the risk of CV death (n=36), non-fatal myocardial infarction (MI) (n=30) or revascularization (n=99) in a subgroup of 782 patients. Verapamil and metoprolol had only minor effects on the inflammatory variables. In multivariate Cox regression analyses (adjusted for previous MI, hypertension, diabetes mellitus and smoking), fibrinogen and WBC were independent predictors of CV death or non-fatal MI, as well as the risk of revascularization. Orosomucoid did not carry any independent information. Platelet counts and urinary beta-thromboglobulin were not significantly related to CV prognosis. The treatment given did not significantly influence the prognostic impact of either fibrinogen or WBC. Fibrinogen and WBC were independent predictors of CV death or non-fatal MI as well as disease progression leading to revascularization in patients with stable angina pectoris. As fibrinogen is also an acute-phase reactant, the present findings indicate that inflammatory activity is involved in disease progression in stable angina pectoris.
authors.affiliation: Department of Internal Medicine, Danderyd Hospital, 182 88, Danderyd, Sweden. claes.held@med.ds.sll.se
authors.forename: C
authors.initials: C
authors.lastname: Held
authors.forename: P
authors.initials: P
authors.lastname: Hjemdahl
authors.forename: N
authors.initials: N
authors.lastname: Håkan Wallén
authors.forename: I
authors.initials: I
authors.lastname: Björkander
authors.forename: L
authors.initials: L
authors.lastname: Forslund
authors.forename: B
authors.initials: B
authors.lastname: Wiman
authors.forename: N
authors.initials: N
authors.lastname: Rehnqvist
mesh_terms: D000318:Adrenergic beta-Agonists / Q000627:therapeutic use; D000368:Aged; D000787:Angina Pectoris / Q000097:blood* / Q000188:drug therapy; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000401:mortality*; D004311:Double-Blind Method; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D006487:Hemostasis; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007958:Leukocyte Count; D008297:Male; D008790:Metoprolol / Q000627:therapeutic use; D008875:Middle Aged; D015999:Multivariate Analysis; D009961:Orosomucoid / Q000032:analysis*; D011379:Prognosis; D014700:Verapamil / Q000627:therapeutic use; D001620:beta-Thromboglobulin / Q000032:analysis
chemical_list: D000318:Adrenergic beta-Agonists; D002121:Calcium Channel Blockers; D009961:Orosomucoid; D001620:beta-Thromboglobulin; D005340:Fibrinogen; D014700:Verapamil; D008790:Metoprolol