title: Effects of atorvastatin on reactive hyperemia and inflammatory process in patients with congestive heart failure.
abstract: Purpose of the study was to investigate whether short-term atorvastatin treatment improves endothelial function and affects inflammatory process in patients with heart failure (HF) and normal cholesterol levels. HF is characterized by endothelial dysfunction and increased inflammatory process, while statins restore endothelial function having also anti-inflammatory effects in hypercholesterolemic patients. We investigated the effect of 4-week atorvastatin treatment (10 mg/day) on endothelial function and inflammatory markers in patients with HF and cholesterol levels <220 mg/dl. Patients were randomly allocated into groups and received atorvastatin (n=19) or no statin (n=19). Forearm blood flow was measured using gauge-strain plethysmography. Serum levels of tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and soluble vascular cell adhesion molecule (sVCAM-1) were determined with ELISA. Data are expressed as median [25th-75th percentile]. Forearm vasodilatory response to reactive hyperemia was significantly improved in atorvastatin-treated patients (from 38.1% [32.0-59.1] to 70.0% [61.1-106.3], P<0.01), while it remained unaffected in the control group. Levels of IL-6, TNF-alpha and sVCAM-1 were decreased in atorvastatin-treated group (from 7.8 pg/ml [4.8-9.5], 3.2 pg/ml [2.7-4.8] and 595 ng/ml [440-810] to 5.6 pg/ml [2.5-9.0], 2.8 pg/ml [2.0-3.6] and 289 ng/ml [169-368], respectively, P<0.05 for all) but not in the control group. These findings indicate that atorvastatin may improve forearm vasodilatory response to reactive hyperemia and depress inflammatory process in patients with heart failure and normal baseline cholesterol levels.
authors.affiliation: Cardiology Unit, Hippokration Hospital, Athens University Medical School, 69 S. Karagiorga, 16675 Athens, Greece. tousouli@med.uoa.gr
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Charalambos
authors.initials: C
authors.lastname: Antoniades
authors.forename: Eirini
authors.initials: E
authors.lastname: Bosinakou
authors.forename: Maria
authors.initials: M
authors.lastname: Kotsopoulou
authors.forename: Christos
authors.initials: C
authors.lastname: Pitsavos
authors.forename: Charalambos
authors.initials: C
authors.lastname: Vlachopoulos
authors.forename: Demosthenis
authors.initials: D
authors.lastname: Panagiotakos
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D000069059:Atorvastatin; D015415:Biomarkers / Q000032:analysis; D016207:Cytokines / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005542:Forearm / Q000098:blood supply; D006333:Heart Failure / Q000188:drug therapy*; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D006940:Hyperemia / Q000209:etiology*; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use*; D012039:Regional Blood Flow; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D015415:Biomarkers; D016207:Cytokines; D006538:Heptanoic Acids; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D000069059:Atorvastatin