Effects of carvedilol vs bisoprolol on inflammation and oxidative stress in patients with chronic heart failure

Abstract

The effects of beta-blockers on long-term morbidity and mortality have been established in patients with chronic heart failure (CHF) with reduced left ventricular function [1][2][3][4]. Among various beta-blockers, only carvedilol and bisoprolol are approved by Japanese guidelines for the treatment of patients with CHF [5]. Bisoprolol is highly selective for the beta-1 receptor, whereas carvedilol is a non-selective beta-blocker with simultaneous alpha-receptor antagonism [6]. However, there is no established clinical evidence on how to properly use these two agents. 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 a greater reduction in high-sensitivity cardiac troponin T (hsTnT) [7].

Metabolic effects of carvedilol through β‐arrestin proteins: investigations in a streptozotocin‐induced diabetes rat model and in C2C12 myoblasts

“…The authors concluded that both compounds have beneficial effects. They concluded that carvedilol was more effective in reducing oxidative stress, an effect repeatedly shown for carvedilol treatment (Toyoda et al, 2020).…”

Multifactorial Basis and Therapeutic Strategies in Metabolism-Related Diseases

“…Mitochondrial dysfunctions play an important role in CVDs pathogenesis [ 355 ]; however, there are no medications to modulate mitochondrial functions available in clinical practice [ 406 ]. However, therapeutic agents have been investigated to target mitochondrial, including the mitochondria-targeted antioxidant MitoQ1, that decreases ROS production and has shown protective effect in hypertensive rat models [ 407 ], and carvedilol or antidiabetic drugs that prevent cardiac mitochondrial oxidative damage [ 408 ]. Therapies targeting endothelial NO synthase (eNOS) activity and function, using statins, ACE inhibitors, and AT1-receptor blockers, have been shown to improve cardiovascular prognosis by decreasing the level of oxidative stress, inflammation, and mediators of vascular dysfunctions [ 409 , 410 ].…”

Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure

“…Carvedilol shifts the heart energy substrate usage from fatty acids to glucose oxidation [ 315 , 368 ] by decreasing free fatty acids, inhibiting fatty acid oxidation, resulting in increased glycolysis, oxidation and energy efficiency [ 364 , 395 , 414 , 415 ] ( Figure 2 ). Mechanisms of cardioprotective effects of carvedilol are linked to oxidative metabolism and decreases in oxidative stress [ 102 , 327 , 363 , 414 , 415 , 416 , 417 , 418 ], which reduces the impairment of mitochondrial metabolism during HF [ 419 ]. Carvedilol can also improve insulin sensitivity and plasma lipid profile [ 419 , 420 , 421 ].…”

“…Mechanisms of cardioprotective effects of carvedilol are linked to oxidative metabolism and decreases in oxidative stress [ 102 , 327 , 363 , 414 , 415 , 416 , 417 , 418 ], which reduces the impairment of mitochondrial metabolism during HF [ 419 ]. Carvedilol can also improve insulin sensitivity and plasma lipid profile [ 419 , 420 , 421 ]. The net effect of these metabolic changes are favorable effects on glucose metabolism [ 412 , 421 ], by improving myocardial energy efficiency through increased carbohydrate utilization [ 395 , 422 , 423 ], similar to α 1A -AR agonism.…”