title: The particular interactions of the traditional cardiovascular risk factors with different circulating specific leukocyte subtype counts in blood: an observational study.
abstract: OBJECTIVE
  The pathogenesis of atherosclerosis is multifactorial, however the impact of inflammatory cells in this process is well known. Different traditional cardiovascular risk factors (CVRFs) may have specifically different effects on leukocyte subtype. Thus, these special interactions may induce different vascular involvement forms due to the altered endothelial damage and vascular repair mechanisms. The aim of the present study was to investigate whether there is any specific relationship between the leukocyte subtypes and the traditional CVRFs and to evaluate the independency of possible relationships.
  
  
  METHODS
  The study had a cross-sectional observational design. The study population consisted of the patients who underwent coronary angiography with a suspicion of coronary artery disease (CAD) at our institution in an outpatient manner. We enrolled 677 consecutive eligible patients with CAD or normal coronary arteries (NCA) and investigated the associations of traditional CVRFs, demographic properties and biochemical parameters including fasting plasma glucose (FPG), creatinine, serum uric acid level (SUA) and lipids with total circulating inflammatory cell (WBC, leukocytes) and subtype counts including neutrophils (N), lymphocytes (L) and monocytes (M). As a dependent variable, total leukocyte count and subtypes, and neutrophil/lymphocyte ratio (N/L ratio) which has been found to being related with increased vascular risk and events were investigated in the groups determined by the presence or absence of CVRFs and CAD by the univariate analyses and then multiple linear regression analyses.
  
  
  RESULTS
  When we performed multiple linear regression analyses to determine the independent associations of inflammatory cell subtypes, we have found that FPG had an independent incremental association with WBC (β±SE:4.2±1.4, p=0.004) and N (β±SE:4.2±1.2, p=0.001). Current smoking had an independent incremental association with WBC and all cell subtypes (for WBC, N, L, and M: β±SE: 748±161, p<0.001; β±SE: 556±136, p<0.001; β±SE: 185±69, p=0.007; β±SE: 38±20, p=0.061, respectively) and SUA had an independent incremental association with WBC (β±SE: 115±43, p=0.008), N (β±SE: 107±38, p=0.005) and M (β±SE: 26±6, p<0.001). Hypertension had an independent incremental association with WBC (β±SE: 431±140, p=0.002) and N (β±SE: 315±118, p=0.008). Male gender had an independent incremental association with only M (β±SE: 52±20, p=0.010). Family history of CAD had an independent decremental association with WBC (β±SE: -327±139, p=0.019) and N (β±SE: -326±121, p=0.007). Finally, age had an independent decremental association with WBC (β±SE: -32±7, p<0.001) and L (β±SE: -16±3, p<0.001). The N/L ratio was independently related with increased age (p<0.001), FPG (p=0.003) and SUA (p=0.012).
  
  
  CONCLUSIONS
  Our study results demonstrate that leukocyte subtypes have different specific associations with traditional CVRFs. We found that FPG affects specifically N while SUA affects specifically N and M, and current smoking affects nonspecifically on all cell subtypes. While hypertension with N and male gender with M were specifically related, age and family history of CAD were only related to L. These different interactions may lead to different endothelial damage and vascular repair mechanisms.
authors.affiliation: Department of Cardiology, Faculty of Medicine, Gazi University, Ankara-Turkey. sinanaltan@gmail.com
authors.forename: Sinan Altan
authors.initials: SA
authors.lastname: Kocaman
authors.forename: Asife
authors.initials: A
authors.lastname: Sahinarslan
authors.forename: Tolga
authors.initials: T
authors.lastname: Kunak
authors.forename: Serhat
authors.initials: S
authors.lastname: Balcioğlu
authors.forename: Mustafa
authors.initials: M
authors.lastname: Cetin
authors.forename: Mustafa
authors.initials: M
authors.lastname: Cemri
authors.forename: Timur
authors.initials: T
authors.lastname: Timurkaynak
authors.forename: Bülent
authors.initials: B
authors.lastname: Boyaci
authors.forename: Atiye
authors.initials: A
authors.lastname: Cengel
mesh_terms: D000328:Adult; D000553:Ambulatory Care; D001786:Blood Glucose; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D007962:Leukocytes / Q000166:cytology*; D008214:Lymphocytes / Q000166:cytology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000166:cytology; D012044:Regression Analysis; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D002784:Cholesterol