title: Effect of low-dose heparin on fibrinogen levels in patients with chronic ischemic heart disease.
abstract: Several prospective studies have demonstrated that high plasma fibrinogen levels are associated with an increased risk of ischemic heart disease. Since in most patients an increased thrombin generation has been reported, we investigated whether the control of thrombin generation could affect plasma fibrinogen levels. Forty male outpatients (20 asymptomatic with previous myocardial infarction and 20 with stable effort angina) were enrolled in a randomized medium-term (6 months) cross-over study. Clottable fibrinogen, according to Clauss, prothrombin fragment 1 + 2, thrombin-antithrombin complex, and fibrinopeptide A were evaluated in relation to treatment with low-dose heparin. After a 15-day wash-out period, during which patients had been treated only with nitrates if needed, patients were allocated to two sequential periods of treatment with standard heparin (12,500 U, subcutaneously daily) plus antianginal treatment or antianginal treatment alone, separated by a second 15-day wash-out period. At the end of the treatment period with low-dose heparin significant decreases in the plasma fibrinogen (2.5 +/- 0.6 g/l vs. 3.3 +/- 0.5 g/l, P < 0.001), prothrombin fragment 1 + 2 (1.4 +/- 0.5 nmol/l vs. 1.9 +/- 0.7 nmol/l, P < 0.001), thrombinantithrombin (4.5 +/- 2.4 ng/ml vs. 9.7 +/- 3.6 ng/ml, P < 0.001), and fibrinopeptide A (2.1 +/- 1.1 ng/ml vs. 3.5 +/- 2.1 ng/ml, P < 0.001) were observed compared with the period without heparin. The present results indicate that low-dose heparin can effectively control the increased abnormal thrombin generation and elevated fibrinogen levels in patients with ischemic heart disease, possibly decreasing the risk of cardiovascular death.
authors.affiliation: Institute of Clinica Medica Generale e Cardiologia, University of Florence, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Prisco
authors.forename: R
authors.initials: R
authors.lastname: Paniccia
authors.forename: B
authors.initials: B
authors.lastname: Bandinelli
authors.forename: A M
authors.initials: AM
authors.lastname: Gori
authors.forename: M
authors.initials: M
authors.lastname: Attanasio
authors.forename: B
authors.initials: B
authors.lastname: Giusti
authors.forename: M
authors.initials: M
authors.lastname: Comeglio
authors.forename: R
authors.initials: R
authors.lastname: Abbate
authors.forename: G F
authors.initials: GF
authors.lastname: Gensini
authors.forename: G G
authors.initials: GG
authors.lastname: Serneri
mesh_terms: D000368:Aged; D000925:Anticoagulants / Q000008:administration & dosage*; D000990:Antithrombin III / Q000378:metabolism; D002908:Chronic Disease; D018592:Cross-Over Studies; D005340:Fibrinogen / Q000378:metabolism*; D005344:Fibrinopeptide A / Q000378:metabolism; D006493:Heparin / Q000008:administration & dosage*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism*; D010446:Peptide Fragments / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D011498:Protein Precursors / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism; D013917:Thrombin / Q000378:metabolism
chemical_list: D000925:Anticoagulants; D010446:Peptide Fragments; D011498:Protein Precursors; C046193:antithrombin III-protease complex; D005344:Fibrinopeptide A; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D000990:Antithrombin III; D011516:Prothrombin; D005340:Fibrinogen; D006493:Heparin; D010447:Peptide Hydrolases; D013917:Thrombin