BACKGROUND: Inflammation and oxidative stress play a role in the pathophysiology of chronic heart failure (CHF). Our previous clinical trial, the Bisoprolol Improvement Group for Chronic Heart Failure Treatment Study in Dokkyo Medical University (BRIGHT-D), reported that bisoprolol is superior to carvedilol for myocardial protection in patients with CHF, as demonstrated by high-sensitivity cardiac troponin T (hsTnT) reduction. The present study was a subanalysis of the BRIGHT-D study that focused on the effects of bisoprolol vs carvedilol on inflammation and oxidative stress in CHF patients. METHODS: Of the 87 patients enrolled in the BRIGHT-D trial, the present study included 48 patients (26 in the bisoprolol group and 22 in the carvedilol group) who had baseline and follow-up measurements of derivatives of reactive oxygen metabolites (d-ROMs) as an index of oxidative stress. RESULTS: High-sensitivity C-reactive protein (hsCRP), an inflammatory marker, decreased in both groups; however, the decrease in the bisoprolol group [3.35 ± 0.78 to 2.69 ± 0.44 log (ng/ml), p = 0.001] was more significant than that in the carvedilol group [3.38 ± 0.59 to 2.85 ± 0.76 log (ng/ml), p = 0.047]. The d-ROMs also decreased in both groups; however, the decrease in the bisoprolol group (401 ± 106 to 344 ± 82 U.CARR, p = 0.015) was less significant than that in the carvedilol group (382 ± 84 to 312 ± 76 U.CARR, p = 0.006]. In all 48 patients, the change in hsTnT was correlated with that in hsCRP (R = 0.467, p = 0.003). CONCLUSIONS: Bisoprolol may be better than carvedilol for reducing inflammation, but carvedilol may be better than bisoprolol for reducing oxidative stress. Proper use of bisoprolol or carvedilol based on individual pathophysiology could be promising in patients with CHF.
BACKGROUND:Inflammation and oxidative stress play a role in the pathophysiology of chronic heart failure (CHF). Our previous clinical trial, the Bisoprolol Improvement Group for Chronic Heart Failure Treatment Study in Dokkyo Medical University (BRIGHT-D), reported that bisoprolol is superior to carvedilol for myocardial protection in patients with CHF, as demonstrated by high-sensitivity cardiac troponin T (hsTnT) reduction. The present study was a subanalysis of the BRIGHT-D study that focused on the effects of bisoprolol vs carvedilol on inflammation and oxidative stress in CHFpatients. METHODS: Of the 87 patients enrolled in the BRIGHT-D trial, the present study included 48 patients (26 in the bisoprolol group and 22 in the carvedilol group) who had baseline and follow-up measurements of derivatives of reactive oxygen metabolites (d-ROMs) as an index of oxidative stress. RESULTS: High-sensitivity C-reactive protein (hsCRP), an inflammatory marker, decreased in both groups; however, the decrease in the bisoprolol group [3.35 ± 0.78 to 2.69 ± 0.44 log (ng/ml), p = 0.001] was more significant than that in the carvedilol group [3.38 ± 0.59 to 2.85 ± 0.76 log (ng/ml), p = 0.047]. The d-ROMs also decreased in both groups; however, the decrease in the bisoprolol group (401 ± 106 to 344 ± 82 U.CARR, p = 0.015) was less significant than that in the carvedilol group (382 ± 84 to 312 ± 76 U.CARR, p = 0.006]. In all 48 patients, the change in hsTnT was correlated with that in hsCRP (R = 0.467, p = 0.003). CONCLUSIONS:Bisoprolol may be better than carvedilol for reducing inflammation, but carvedilol may be better than bisoprolol for reducing oxidative stress. Proper use of bisoprolol or carvedilol based on individual pathophysiology could be promising in patients with CHF.