3 research outputs found
Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail
Congress of the European-Society-of-Cardiology (ESC), Aug 29-Sep 02, 2015, London, Englan
Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail
C reactive protein (CRP) is a biomarker indicating systemic inflammation. Elevated levels of this biomarker are associated with increased rates of cardiovascular disease, including chronic heart failure (HF). Highāsensitivity CRP assays were developed in order to measure lower levels of CRP, down to 0.3mg/l (hsāCRP). Up to now, very little is known about the effects of betaāblocker titration on hsāCRP levels in ischemic and nonāischemic HF patients. Also, little is known if this effect differs between selective and unselective blockers. Purpose: This research explored the trajectories of hsāCRP before and after betaāblocker (carvedilol vs bisoprolol) titration in elderly HF patients depending on the type of betaāblocker used and the etiology of the disease (ischemic vs nonāischemic). Methods: We measured plasma levels of hsāCRP and NTāproBNP in 520 HF patients ā„ 65 years (72.06Ā±5.24 years, 38%f, LVEF 41.8Ā±13.8%; ischemic n=243; nonischemic n=277) of the Cardiac Insufficiency Bisoprolol Study in ELDerly (CIBISāELD). In this trial, patients were randomized to bisoprolol vs. carvedilol and doses were uptitrated to the target or maximally tolerated dose. hsāCRP and NTāproBNP levels were assessed at baseline (BL) and at followāup (FU), after 12 weeks. Results: In patients with ischemic HF, hsāCRP levels decreased in the bisoprolol group (BL=0.60Ā±0.94 mg/ dl, n=166; FU=0.43Ā±0.694mg/dl, n=131; p=0.010), and were without a change in the carvedilol group (BL=0.60Ā±1.69mg/dl, n=181; FU=0.57Ā±0.982mg/ dl, n=136; p=0.731). There was also no change of hsāCRP levels in nonāischemic HF patients in both groups (bisoprolol: BL=0.64Ā±1.175 mg/dl, n=197; FU=0.470Ā±0.81mg/dl, n=152, p=0.069; carvedilol: BL=0.45Ā±0.78mg/dl, n=198; FU=0.41Ā±0.701 mg/ dl, n=152, p=0.420). Plasma levels of NTāproBNP decreased in ischemic patients treated with bisoprolol, (BL=1594Ā±2146 pg/ml, n=169; FU=1468Ā±2110pg/ ml, n=133, p=0.04), while changes in the carvedilol group were not significant (BL=1648Ā±1991 pg/ml, n=188; FU=1567Ā±2119pg/ml, n=135, p=0.556). In the nonāischemic group NTāpro levels did not change significantly in the carvedilol group, while there was an increase in nonāischemic patients in the bisoprolol group (BL=1427Ā±3113 pg/ml, n=208; FU=1533Ā±5385 pg/ml, n=166, p=0.017). Conclusion: Results indicate that bisoprolol might be associated with a decrease of hsāCRP and NTāproBNP levels only in ischemic HF patients, while in nonischemic HF patients there was no change of hsāCRP and an increase of NTāproBNP levels. In carvedilol treated patients no significant changes were shown in neither group