title: Concomitant coronary and peripheral arterial disease: relationship between the inflammatory status of the affected limb and the severity of coronary artery disease.
abstract: OBJECTIVE
  In coronary artery disease (CAD), concomitant peripheral arterial disease (PAD) entails increased systemic inflammatory profile and more severe coronary atherosclerosis. We investigated the relationship between the inflammatory status in the affected limb and CAD severity.
  
  
  METHODS
  In 46 CAD+PAD and 31 CAD-alone patients, the inflammatory status of the leg circulation was measured by the transfemoral gradients of neutrophil myeloperoxidase (MPOx) content and interleukin-6 (IL-6). CAD severity was defined by evaluating coronary artery endothelial function, number of significant coronary stenoses, and prevalence of three-vessel CAD and myocardial infarction (MI).
  
  
  RESULTS
  In the affected limb of CAD+PAD patients, the transfemoral gradients of neutrophil MPOx content and IL-6 were higher (P < .01, for both) than in the healthy leg of CAD-only patients. At multivariate analysis, CAD+PAD patients with transfemoral gradients of MPOx and IL-6 > median had a more compromised coronary artery endothelial function (P < .05, for both). Furthermore, CAD+PAD patients with transfemoral gradients of neutrophil MPOx content > median showed an independent association with a greater number of significant coronary stenoses, and a greater prevalence of three-vessel CAD and previous MI (P < .01, for all). A more severe coronary atherosclerosis was observed also in CAD+PAD patients with transfemoral gradients of IL-6 > median vs those with IL-6 < median, although differences were not statistically significant.
  
  
  CONCLUSIONS
  In CAD patients, the coexistence of PAD does not necessarily entail a more severe coronary atherosclerosis. Only those with an inflammatory status of the affected limb presents more severe CAD. Future studies will clarify whether the presence of peripheral inflammation plays a mechanistic role in CAD evolution.
authors.affiliation: Department of Clinical Medicine, Cardiovascular, and Immunological Sciences, University of Naples Federico II, Naples, Italy. brevetti@unina.it
authors.forename: Gregorio
authors.initials: G
authors.lastname: Brevetti
authors.forename: Federico
authors.initials: F
authors.lastname: Piscione
authors.forename: Vittorio
authors.initials: V
authors.lastname: Schiano
authors.forename: Gennaro
authors.initials: G
authors.lastname: Galasso
authors.forename: Francesco
authors.initials: F
authors.lastname: Scopacasa
authors.forename: Massimo
authors.initials: M
authors.lastname: Chiariello
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D003080:Cold Temperature; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000150:complications* / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000276:immunology / Q000503:physiopathology; D005260:Female; D005263:Femoral Artery; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D016015:Logistic Models; D035002:Lower Extremity / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000276:immunology; D058729:Peripheral Arterial Disease / Q000150:complications* / Q000276:immunology; D009195:Peroxidase / Q000097:blood; D012720:Severity of Illness Index; D014661:Vasoconstriction
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D009195:Peroxidase