title: The comparative effects of valsartan and amlodipine on vascular microinflammation in newly diagnosed hypertensive patients.
abstract: Pentraxin 3 (PTX3) is a new candidate immunoinflammatory marker that has been reported to be associated with cardiometabolic risk factors. We aimed to investigate the effects of valsartan and amlodipine on the PTX3 and C-reactive protein (CRP) levels in patients with essential hypertension. Patients with a newly diagnosed essential hypertension were admitted to our internal medicine outpatient clinic. Patients were randomized to one of the following intervention protocols: calcium channel blocker (amlodipine, 5-10 mg/day) as group A (n = 22; mean age ± standard deviation [SD]: 52 ± 11 year) and angiotensine II receptor blocker (valsartan, 80-320 mg/day) as group B (n = 28; mean age ± SD: 50 ± 14 year). Endothelial dysfunction and systemic inflammation were evaluated with PTX3 and CRP. There was a significant decrease in the level of PTX3 after treatment in two groups (P < .05). Although there was a significant decrease in the level of CRP after treatment in amlodipine group, there was no significant decrease in the levels of PTX3 and CRP after treatment in two groups. There were no significant differences in the systolic and diastolic blood pressure reduction between the two treatment groups. In the treatment of hypertension, prior knowledge of the level of plasma PTX3 could be important in antihypertensive drug choice. C-reactive protein and PTX3 are the markers that have role in vascular inflammation and are found associated with the prognosis of cardiovascular outcomes in many trials. In our study, PTX and CRP levels were decreased when compared to baseline levels.
authors.affiliation: Department of Cardiology, Beytepe Hospital , Ankara , Turkey.
authors.forename: Murat
authors.initials: M
authors.lastname: Unlu
authors.forename: Murat
authors.initials: M
authors.lastname: Karaman
authors.forename: Seyit Ahmet
authors.initials: SA
authors.lastname: Ay
authors.forename: Sevket
authors.initials: S
authors.lastname: Balta
authors.forename: Mustafa
authors.initials: M
authors.lastname: Cakar
authors.forename: Sait
authors.initials: S
authors.lastname: Demirkol
authors.forename: Turgay
authors.initials: T
authors.lastname: Celik
authors.forename: Erol
authors.initials: E
authors.lastname: Arslan
authors.forename: Seref
authors.initials: S
authors.lastname: Demirbas
authors.forename: Turker
authors.initials: T
authors.lastname: Turker
authors.forename: Halil
authors.initials: H
authors.lastname: Yaman
authors.forename: Fatih
authors.initials: F
authors.lastname: Bulucu
authors.forename: Kenan
authors.initials: K
authors.lastname: Sağlam
mesh_terms: D000328:Adult; D017311:Amlodipine / Q000627:therapeutic use*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002097:C-Reactive Protein / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors; D000683:Serum Amyloid P-Component / Q000378:metabolism; D013777:Tetrazoles / Q000627:therapeutic use*; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068756:Valsartan; D014657:Vasculitis / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D000099153:Pentraxins
chemical_list: D017311:Amlodipine; D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D002097:C-Reactive Protein; D002121:Calcium Channel Blockers; D018836:Inflammation Mediators; D000683:Serum Amyloid P-Component; D013777:Tetrazoles; D014633:Valine; D000068756:Valsartan; D000099153:Pentraxins