Comparison of Carvedilol and Metoprolol for Preventing Contrast-Induced Nephropathy after Coronary Angiography

Abstract

Aims: Contrast-induced nephropathy (CIN) is one of the most common causes of hospital-acquired acute renal failure. Oxidative stress and vasoconstriction might play key roles in its pathogenesis. In a few experimental models, antioxidant properties of carvedilol have been documented. The aim of this study was to analyze and compare the effects of carvedilol and metoprolol on the development of CIN in patients undergoing coronary angiography. Methods: One hundred patients currently taking metoprolol and 100 patients currently taking carvedilol were enrolled into the study. Venous blood samples were obtained before and 48 h after contrast administration. Cystatin C and malondialdehyde values were examined and compared. CIN was defined as a creatinine increase of at least 25% or 0.5 mg/dl from the baseline value. Results: Seven patients in the carvedilol group (7%) and 22 patients in the metoprolol group (22%) developed CIN (p = 0.003). In the metoprolol group, the median cystatin C concentration increased significantly from 978 to 1,086 ng/ml (p = 0.001) 48 h after radiocontrast administration. In the carvedilol group, the median cystatin C concentration did not change significantly (1,143 vs. 1,068 ng/ml; p = 0.94). In the metoprolol group, the mean malondialdehyde concentration increased significantly from 7.09 ± 1.48 to 8.38 ± 2.6 nmol/l (p < 0.001). In the carvedilol group, the mean serum malondialdehyde concentration did not change significantly (7.44 ± 1.21 vs. 7.56 ± 1.11 nmol/l; p = 0.59). Conclusion: When compared to metoprolol, carvedilol might decrease oxidative stress and subsequent development of CIN.

The β-Blocker Carvedilol Prevented Ultraviolet-Mediated Damage of Murine Epidermal Cells and 3D Human Reconstructed Skin

“…Two potential mechanisms for carvedilol's protective effects were examined in these experiments: β-AR blockade and ROS scavenging activity. Metoprolol was used as a control β-blocker without anti-transformation activity [9] and without proven antioxidant property [19], but is a commonly used β-blocker. 4-OHC is an intermediate compound in carvedilol synthesis that acted as a free radical scavenger (i.e., chemical antioxidant) [20].…”

“…The present study first examined whether carvedilol could protect murine epidermal cells against UV or hydrogen peroxide (H 2 O 2 )-induced oxidative damage, a known precursor event leading to skin carcinogenesis [18]. Carvedilol's protective activity was compared with metoprolol, a β-blocker without proven antioxidant property [19], and an intermediate compound for carvedilol synthesis, 4-hydroxycarbazole (4-OHC), which possesses a chemical antioxidant activity [20]. In previous studies, metoprolol and 4-OHC did not show cancer preventive efficacy when compared with carvedilol in vitro and in vivo [7,9].…”

A novel approach to contrast-induced nephrotoxicity: the melatonergic agent agomelatine

“…41 In previous studies, in which nephrotoxicity was created by glycerine and CM, increased levels of serum BUN and creatinine were shown in parallel with elevated oxidative stress and inflammation. 7 In our study, we detected large increases in serum BUN and creatinine levels in the GLY and GLY1CM groups compared with the healthy group.…”

Carvedilol – is it still the primus inter pares among b-blockers?

“…In the era of reperfusion, contrast-induced nephropathy is a frequently observed complication, especially among elderly patients with renal impairment at baseline. In a study conducted on 200 patients undergoing coronarography, of which one half received carvedilol and the other half was treated with metoprolol, contrast-induced nephropathy occurred in 7 patients (7%) treated with carvedilol and 22 (22%) patients on metoprolol (p=0.003) [24].…”