Meng Wang1, James Corsetti2, Scott McNitt3, David Q Rich1, Charles E Sparks2, Arthur J Moss3, Wojciech Zareba4. 1. Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA. 2. Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA. 3. Heart Research Follow-up Program, University of Rochester Medical Center, Rochester, NY, USA. 4. Heart Research Follow-up Program, University of Rochester Medical Center, Rochester, NY, USA. Electronic address: wojciech_zareba@urmc.rochester.edu.
Abstract
BACKGROUND: Laboratory findings have suggested that systemic and vascular inflammation can impair the antiatherogenic function of high-density lipoproteins (HDLs). However, evidence from population studies is sparse. OBJECTIVE: The objective of the study was to assess if blood inflammatory markers modify the risk of recurrent coronary events associated with apolipoprotein A-I (apoA-I) and HDL cholesterol (HDL-C) among postinfarction patients. METHODS: ApoA-I, HDL-C, and inflammatory markers (C-reactive protein [CRP], serum amyloid A (SAA), fibrinogen, von Willebrand factor [vWF], and D-dimer) were measured from blood samples of 1028 patients drawn 2 months after an index myocardial infarction (MI). Patients were followed up for the composite coronary endpoint (nonfatal MI, coronary death, or unstable angina) for an average of 26 months. Cox proportional hazard models were used to assess effect modifications for the association of apoA-I and HDL-C with coronary risk by each inflammatory marker. RESULTS: CRP significantly modified the risk of recurrent coronary events associated with apoA-I. Among the entire population, multivariable-adjusted hazard ratios associated with each standard deviation increase in apoA-I for those with low and high CRP levels were 0.89 and 1.35, respectively (P value for interaction = .008). vWF was a significant effect modifier of the apoA-I/coronary risk association only among diabetic patients (hazard ratios were 0.56 and 1.43, for diabetic patients with low and high vWF levels, respectively; P value for interaction = .002). No effect modification was observed for the HDL-C/coronary risk association. CONCLUSION: Among stable post-MI patients, CRP modified the risk of recurrent coronary events associated with apoA-I. VWF modified this association only among the diabetic subgroup.
BACKGROUND: Laboratory findings have suggested that systemic and vascular inflammation can impair the antiatherogenic function of high-density lipoproteins (HDLs). However, evidence from population studies is sparse. OBJECTIVE: The objective of the study was to assess if blood inflammatory markers modify the risk of recurrent coronary events associated with apolipoprotein A-I (apoA-I) and HDL cholesterol (HDL-C) among postinfarction patients. METHODS:ApoA-I, HDL-C, and inflammatory markers (C-reactive protein [CRP], serum amyloid A (SAA), fibrinogen, von Willebrand factor [vWF], and D-dimer) were measured from blood samples of 1028 patients drawn 2 months after an index myocardial infarction (MI). Patients were followed up for the composite coronary endpoint (nonfatal MI, coronary death, or unstable angina) for an average of 26 months. Cox proportional hazard models were used to assess effect modifications for the association of apoA-I and HDL-C with coronary risk by each inflammatory marker. RESULTS:CRP significantly modified the risk of recurrent coronary events associated with apoA-I. Among the entire population, multivariable-adjusted hazard ratios associated with each standard deviation increase in apoA-I for those with low and high CRP levels were 0.89 and 1.35, respectively (P value for interaction = .008). vWF was a significant effect modifier of the apoA-I/coronary risk association only among diabeticpatients (hazard ratios were 0.56 and 1.43, for diabeticpatients with low and high vWF levels, respectively; P value for interaction = .002). No effect modification was observed for the HDL-C/coronary risk association. CONCLUSION: Among stable post-MI patients, CRP modified the risk of recurrent coronary events associated with apoA-I. VWF modified this association only among the diabetic subgroup.
Authors: Tareq S Harb; Wojciech Zareba; Arthur J Moss; Paul M Ridker; Nader Rifai; Victor J Marder; Luc Miller-Watelet Journal: Am J Cardiol Date: 2003-05-01 Impact factor: 2.778
Authors: A J Moss; R E Goldstein; V J Marder; C E Sparks; D Oakes; H Greenberg; H J Weiss; W Zareba; M W Brown; C S Liang; E Lichstein; W C Little; J A Gillespie; L Van Voorhees; R J Krone; M M Bodenheimer; J Hochman; E M Dwyer; R Arora; F I Marcus; L F Watelet; R B Case Journal: Circulation Date: 1999-05-18 Impact factor: 29.690
Authors: James P Corsetti; Wojciech Zareba; Arthur J Moss; David L Rainwater; Charles E Sparks Journal: Atherosclerosis Date: 2005-10-20 Impact factor: 5.162
Authors: W Zareba; G Pancio; A J Moss; V G Kalaria; V J Marder; H J Weiss; L F Watelet; C E Sparks Journal: Thromb Haemost Date: 2001-09 Impact factor: 5.249
Authors: Baohai Shao; Constanze Bergt; Xiaoyun Fu; Pattie Green; John C Voss; Michael N Oda; John F Oram; Jay W Heinecke Journal: J Biol Chem Date: 2004-11-30 Impact factor: 5.157
Authors: Constanze Bergt; Subramaniam Pennathur; Xiaoyun Fu; Jaeman Byun; Kevin O'Brien; Thomas O McDonald; Pragya Singh; G M Anantharamaiah; Alan Chait; John Brunzell; Randolph L Geary; John F Oram; Jay W Heinecke Journal: Proc Natl Acad Sci U S A Date: 2004-08-23 Impact factor: 11.205
Authors: Lemin Zheng; Benedicta Nukuna; Marie-Luise Brennan; Mingjiang Sun; Marlene Goormastic; Megan Settle; Dave Schmitt; Xiaoming Fu; Leonor Thomson; Paul L Fox; Harry Ischiropoulos; Jonathan D Smith; Michael Kinter; Stanley L Hazen Journal: J Clin Invest Date: 2004-08 Impact factor: 14.808
Authors: James P Corsetti; Wojciech Zareba; Arthur J Moss; Paul M Ridker; Victor J Marder; David L Rainwater; Charles E Sparks Journal: Atherosclerosis Date: 2003-12 Impact factor: 5.162