OBJECTIVE: Increasing evidence indicates that the Fas/Fas ligand interaction is involved in atherogenesis. We sought to analyze soluble Fas (sFas) and soluble Fas ligand (sFasL) concentrations in subjects at high cardiovascular risk and their modulation by atorvastatin treatment. METHODS AND RESULTS: ACTFAST was a 12-week, prospective, multicenter, open-label trial which enrolled subjects (statin-free or statin-treated at baseline) with coronary heart disease (CHD), CHD-equivalent, or 10-year CHD risk > 20%. Subjects with LDL-C between 100 to 220 mg/dL (2.6 to 5.7 mmol/L) and triglycerides < or = 600 mg/dL (6.8 mmol/L) were assigned to a starting dose of atorvastatin (10 to 80 mg/d) based on LDL-C at screening. Of the 2117 subjects enrolled in ACTFAST, AIM sub-study included the 1078 statin-free patients. At study end, 85% of these subjects reached LDL-C target. Mean sFas levels were increased and sFasL were reduced in subjects at high cardiovascular risk compared with healthy subjects. Atorvastatin reduced sFas in the whole population as well as in patients with metabolic syndrome or diabetes. Minimal changes were observed in sFasL. CONCLUSIONS:sFas concentrations are increased and sFasL are decreased in subjects at high cardiovascular risk, suggesting that these proteins may be novel markers of vascular injury. Atorvastatin reduces sFas, indicating that short-term treatment with atorvastatin exhibits antiinflammatory effects in these subjects.
RCT Entities:
OBJECTIVE: Increasing evidence indicates that the Fas/Fas ligand interaction is involved in atherogenesis. We sought to analyze soluble Fas (sFas) and soluble Fas ligand (sFasL) concentrations in subjects at high cardiovascular risk and their modulation by atorvastatin treatment. METHODS AND RESULTS: ACTFAST was a 12-week, prospective, multicenter, open-label trial which enrolled subjects (statin-free or statin-treated at baseline) with coronary heart disease (CHD), CHD-equivalent, or 10-year CHD risk > 20%. Subjects with LDL-C between 100 to 220 mg/dL (2.6 to 5.7 mmol/L) and triglycerides < or = 600 mg/dL (6.8 mmol/L) were assigned to a starting dose of atorvastatin (10 to 80 mg/d) based on LDL-C at screening. Of the 2117 subjects enrolled in ACTFAST, AIM sub-study included the 1078 statin-free patients. At study end, 85% of these subjects reached LDL-C target. Mean sFas levels were increased and sFasL were reduced in subjects at high cardiovascular risk compared with healthy subjects. Atorvastatin reduced sFas in the whole population as well as in patients with metabolic syndrome or diabetes. Minimal changes were observed in sFasL. CONCLUSIONS: sFas concentrations are increased and sFasL are decreased in subjects at high cardiovascular risk, suggesting that these proteins may be novel markers of vascular injury. Atorvastatin reduces sFas, indicating that short-term treatment with atorvastatin exhibits antiinflammatory effects in these subjects.
Authors: M Guzmán-Fulgencio; J Berenguer; M García-Álvarez; D Micheloud; J C López; J Cosín; I Fernández de Castro; P Catalán; P Miralles; S Resino Journal: Eur J Clin Microbiol Infect Dis Date: 2011-03-26 Impact factor: 3.267
Authors: Rosalyn Baker; Joseph G Dauner; Ana Cecilia Rodriguez; Marcus C Williams; Troy J Kemp; Allan Hildesheim; Ligia A Pinto Journal: Cytokine Date: 2010-12-16 Impact factor: 3.861
Authors: D S Cross; C A McCarty; E Hytopoulos; M Beggs; N Nolan; D S Harrington; T Hastie; R Tibshirani; R P Tracy; B M Psaty; R McClelland; P S Tsao; T Quertermous Journal: Curr Med Res Opin Date: 2012-11 Impact factor: 2.580
Authors: Mahmut Ilker Yilmaz; Juan Jesús Carrero; Alberto Ortiz; Jose Luis Martín-Ventura; Alper Sonmez; Mutlu Saglam; Halil Yaman; Mujdat Yenicesu; Jesús Egido; Luis Miguel Blanco-Colio Journal: Clin J Am Soc Nephrol Date: 2009-10-09 Impact factor: 8.237