title: Correlation of systemic inflammation with local inflammatory activity in non-culprit lesions: beneficial effect of statins.
abstract: BACKGROUND
  In patients with acute coronary syndromes (ACS) increased systemic and local inflammatory activation in culprit lesions is observed. It is unknown, however, whether systemic inflammation is correlated with non-culprit lesion inflammatory activation. Moreover, the effect of statins on non-culprit lesion inflammation has not been extensively investigated. The aim of the present study was to investigate in non-culprit lesions 1) the correlation between plaque temperature measurements with the levels of C-reactive protein (CRP) and 2) whether statin administration is associated with reduced heat production.
  
  
  METHODS
  We included 71 patients with ACS or stable angina (SA) undergoing percutaneous coronary intervention in culprit lesions, having an intermediate non-culprit lesion. Forty patients were treated with statin and 31 patients were not treated. Systemic inflammatory status was assessed by CRP, and local inflammatory activation by measuring the temperature difference of non-culprit lesion (deltaT), assigned as the difference between the maximal temperature of the atherosclerotic plaque from the proximal vessel wall temperature.
  
  
  RESULTS
  Mean deltaT was 0.08+/-0.07 degrees C. Patients with ACS had higher deltaT compared to patients with SA (ACS: 0.10+/-0.07 degrees C vs SA: 0.05+/-0.06, p<0.01). deltaT was less in patients treated with statin in both groups (ACS: 0.07+/-0.04 degrees C vs 0.13+/-0.08 degrees C p=0.009; SA: 0.04+/-0.05 degrees C vs 0.09+/-0.07 degrees C, p=0.04). CRP was higher in patients with ACS compared to SA (1.18+/-1.12 vs 0.47+/-0.37 mg/dL, p=0.001). There was a positive correlation of deltaT and CRP values (R=0.46, p<0.001).
  
  
  CONCLUSIONS
  Local inflammatory activation in non-culprit lesions is correlated with systemic inflammation. Moreover, statins have a beneficial effect on non-culprit lesion heat production.
authors.affiliation: ktoutouz@otenet.gr
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Toutouzas
authors.forename: Maria
authors.initials: M
authors.lastname: Drakopoulou
authors.forename: Virginia
authors.initials: V
authors.lastname: Markou
authors.forename: Ioannis
authors.initials: I
authors.lastname: Karabelas
authors.forename: Sophia
authors.initials: S
authors.lastname: Vaina
authors.forename: Manolis
authors.initials: M
authors.lastname: Vavuranakis
authors.forename: Eleftherios
authors.initials: E
authors.lastname: Tsiamis
authors.forename: Costas
authors.initials: C
authors.lastname: Tsioufis
authors.forename: Aris
authors.initials: A
authors.lastname: Androulakis
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000150:complications* / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D001831:Body Temperature; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007249:Inflammation / Q000097:blood / Q000150:complications*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications* / Q000628:therapy; D013577:Syndrome
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein