Abstract
Although chronic sympathetic activation provides inotropic and chronotropic support to the failing heart, such activation may also have deleterious effects, including the direct cardiotoxic effects of catecholamines, activation of the renin-angiotensin-aldosterone system and an increase in myocardial oxygen demand. These observations indicate that β-blockade might be beneficial in the treatment of heart failure resulting from dilated cardiomyopathy or ischaemic heart disease. Carvedilol is a non-selective β-blocker acting on β1-, β2-, and α1-adrenoceptors. It possesses potent anti-oxidant and anti-apoptotic properties, along with neuroprotective, vasculoprotective, cardioprotective effects, and it has reduced overall mortality in patients with heart failure in controlled clinical trials. Its role in treating cardiomyopathy requires focus. The fact that anthracyclines are cardiotoxic seriously narrows their therapeutic index in cancer therapy. The cardiotoxic risk increases with the cumulative dose and may lead to congestive heart failure and dilated cardiomyopathy in adults and in children. This review focuses on recent research regarding the beneficial effects of carvedilol in the treatment of dilated cardiomyopathy and to revisit the available evidence on the cardioprotection of carvedilol when associated with anthracycline and to explain the mechanisms underlying the benefits of their co-administration.
Highlights
Cardiomyopathy is a growing public health problem
The recent introduction of angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blocker (ARB) and β-blockers greatly improved the treatment of dilated cardiomyopathy (DCM) [18]
A significant reduction in mortality was observed in favour of the group treated with carvedilol, with an absolute reduction in mortality of 5.7% over a 5 year follow up period, when used to treat congestive heart failure (CHF) mostly due to ischemic heart disease or idiopathic
Summary
The incidence of cardiomyopathy is expected to increase greatly It is a disease of the heart muscle. Hypertrophic cardiomyopathy is a genetic disorder that causes a chaotic growth of heart muscle cells within the ventricles and can cause potentially fatal cardiac arrhythmias. DCM is a cardiac muscle disorder characterized by ventricular chamber dilatation and systolic dysfunction, which often leads to HF and sudden death [6,7,8]. In DCM, normal heart muscle becomes damaged, leading to a generalized weakening of the walls of the cardiac chambers leading dilatation of the chambers (remodeling) and congestive heart failure (CHF) [9]. Anthracyclines have profound consequences on the structure and function of the heart causing with time a cardiomyopathy that leads to intractable congestive heart failure [10]. The cardiotoxicity of anthracyclines is dose-dependent and this limits its clinical implementation at optimal antitumor efficacy
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