Traditionally, beta-blockers have been contraindicated in patients with heart failure. However, there are some patients with systolic heart failure who benefit from a beta-blocker (24). Early evidence was strongest for idio-pathic dilated cardiomyopathy rather than ischemic heart disease (25). However, several randomized controlled trials of beta-blockers in patients with mild to moderate heart failure have been published. These include the CIBIS II trial with bisoprolol (26), the MERIT-HF trial with metoprolol (27), and the PRECISE trial with carve-dilol (28). These have shown that cardiac mortality in these patients can be reduced by one-third, despite concurrent treatment with conventional therapies of proven benefit (that is ACE inhibitors).
Diastolic dysfunction can lead to congestive heart failure, even when systolic function is normal (29,30). Since ventricular filling occurs during diastole, failure of intra-ventricular pressure to fall appropriately during diastole leads to increased atrial pressure, which eventually leads to increased pulmonary and systemic venous pressures, causing a syndrome of congestive heart failure indistinguishable clinically from that caused by systolic pump failure (31). Diastolic dysfunction occurs in systemic arterial hypertension, hypertrophic obstructive cardio-myopathy, and infiltrative heart diseases, which reduce ventricular compliance or increase ventricular stiffness (32). As energy is required for active diastolic myocardial relaxation, a relative shortage of adenosine triphosphate in ischemic heart disease also often leads to co-existing diastolic and systolic dysfunction (33). Beta-blockers improve diastolic function in general, and this may be beneficial in patients with congestive heart failure associated with poor diastolic but normal systolic function.
Beta-blockade reduces mortality in patients with heart failure by at least a third when initiated carefully, with gradual dose titration, in those with stable heart failure (34,35). Similarly, beta-blocker prescribing should be encouraged in people with diabetes, since they have a worse outcome after cardiac events and beta-blockade has an independent secondary protective effect (36,37). The small risk of masking metabolic and autonomic responses to hypoglycemia, which was only a problem with non-selective agents in type I diabetes, is a very small price worth paying in diabetics with coronary heart disease.
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