title: Haemorheological and endothelial-dependent alterations in heart failure after ACE inhibitor, calcium antagonist and beta blocker.
abstract: The aim of our study was to evaluate endothelium-dependent dilatation induced by an ACE-inhibitor, calcium antagonist and beta blocker in patients suffering from heart failure (NYHA class II and III). We studied 34 patients (19M, 15F, mean age 76.96+/-8.82) in pharmacological wash-out for at least one week, divided into 3 groups: Group A (15 patients, 9M and 6F) taking ramipril (5 mg/die); Group B (10 patients, 6M and 4F) taking amlodipine (10 mg/die), Group C: (9 patients, 4M and 5F) taking carvedilole (25 mg/die). The groups were homologous for NYHA class and instrumental echographic parameters (mean EF=22.5+/-6.7 and mean sAPP 38.4+/-8.7). At the beginning and after 3 weeks of therapy, we performed a clinical and instrumental assessment; we studied endothelial function by determination of L-arginine and L-citrulline (amino acids of the nitric oxide metabolic pathway), the L-citrulline/L-arginine ratio (an index of NOS activity) and VCAM-1 (endothelial dysfunction index); haemorheological parameters (blood viscosity, plasma fibrinogen and erythrocyte morphology); coagulative/fibrinolytic parameters (PT, aPTT, fibrinogen and PAI-1). The results show that L-citrulline and L-arginine increase, while VCAM-1 decreases. The L-citrulline/L-arginine ratio increases in a statistically significant way. This trend is maintained in each group. These results demonstrate that the drugs used induce an improvement of endothelium-dependent dilatation. In addition, there is progressive haemorheological and fibrinolytic improvement, with a reduction of PAI-1 and blood viscosity.
authors.affiliation: Department of Internal, Vascular and Geriatric Medicine, University of Siena, Italy. turchetti@unisi.it
authors.forename: V
authors.initials: V
authors.lastname: Turchetti
authors.forename: M A
authors.initials: MA
authors.lastname: Bellini
authors.forename: L
authors.initials: L
authors.lastname: Boschi
authors.forename: G
authors.initials: G
authors.lastname: Postorino
authors.forename: A
authors.initials: A
authors.lastname: Pallassini
authors.forename: M G
authors.initials: MG
authors.lastname: Richichi
authors.forename: L
authors.initials: L
authors.lastname: Trabalzini
authors.forename: M
authors.initials: M
authors.lastname: Guerrini
authors.forename: S
authors.initials: S
authors.lastname: Forconi
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000368:Aged; D017311:Amlodipine / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D001120:Arginine / Q000378:metabolism; D001809:Blood Viscosity; D002118:Calcium / Q000037:antagonists & inhibitors*; D002227:Carbazoles / Q000494:pharmacology; D000077261:Carvedilol; D002956:Citrulline / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000096:biosynthesis; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000378:metabolism; D011412:Propanolamines / Q000494:pharmacology; D017257:Ramipril / Q000494:pharmacology; D013997:Time Factors; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002227:Carbazoles; D011412:Propanolamines; D019010:Vascular Cell Adhesion Molecule-1; D014665:Vasodilator Agents; D000077261:Carvedilol; D017311:Amlodipine; D002956:Citrulline; D005340:Fibrinogen; D001120:Arginine; D019001:Nitric Oxide Synthase; D017257:Ramipril; D002118:Calcium