title: Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis--influence on IP-10, TNF-α and MCP-1.
abstract: BACKGROUND
  Hypertension is one of the most prominent risk factors for coronary artery disease (CAD). Treatment of hypertension is therefore important for reducing cardiovascular events and the progression of atherosclerosis. Several treatment strategies are common in clinical practice for example the use of ACE-blockers or angiotensin receptor II blockers (ARBs), so called sartans. Telmisartan, belonging to the class of ARBs, was shown to exert anti-inflammatory effects besides the blood pressure lowering.
  
  
  METHODS
  In this work, two separate substudy groups of hypertensives were compared. 16 patients with arterial hypertension have been treated with telmisartan (initial 40 mg Kinzalmono®) for 7.3 ± 4.4 months. The telmisartan group was compared to a matched control group including 31 hypertensive patients without telmisartan treatment with a follow up period of 1.9 ± 0.5 years. Serum samples from the beginning and the end of follow up were analyzed with Luminex® technology for 26 cytokines and chemokines. The baseline scores of coronary artery calcification (CAC) were gathered by multislice detector computer tomography.
  
  
  RESULTS
  After 7 months of telmisartan treatment and 2 years in control patients most of the measured analytes did not change significantly. MCP-1 (P=0.001; P<0.001) was increased significantly in both telmisartan and control group. The relative decrease in IP-10 and TNF-α levels was observed in telmisartan group, as opposed to the increase in control (telmisartan vs. control P=0.048; P=0.01). No linear rank-correlation between measured analytes and the initial CAC was found.
  
  
  CONCLUSIONS
  Telmisartan reduced blood pressure in patients with atherosclerosis and arterial hypertension within a short time period, whereas the inflammatory status of these patients remained largely unchanged. An involvement of telmisartan in the regulation of inflammatory and anti-inflammatory mediators in the context of CAD and CAC is possible, but cannot clearly be assumed based on the present findings.
authors.affiliation: Department of Cardiology and Angiology, University Hospital Erlangen, Germany.
authors.forename: Lutz
authors.initials: L
authors.lastname: Klinghammer
authors.forename: Katharina
authors.initials: K
authors.lastname: Urschel
authors.forename: Iwona
authors.initials: I
authors.lastname: Cicha
authors.forename: Piotr
authors.initials: P
authors.lastname: Lewczuk
authors.forename: Dorette
authors.initials: D
authors.lastname: Raaz-Schrauder
authors.forename: Stephan
authors.initials: S
authors.lastname: Achenbach
authors.forename: Christoph D
authors.initials: CD
authors.lastname: Garlichs
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D050197:Atherosclerosis / Q000188:drug therapy; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D018932:Chemokine CCL2 / Q000097:blood*; D054357:Chemokine CXCL10 / Q000097:blood*; D003324:Coronary Artery Disease / Q000188:drug therapy*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D007249:Inflammation / Q000188:drug therapy; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D000077333:Telmisartan; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001565:Benzoates; C111835:CCL2 protein, human; C114753:CXCL10 protein, human; D018932:Chemokine CCL2; D054357:Chemokine CXCL10; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D000077333:Telmisartan