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Beta-blockers have traditionally been considered contraindicated in patients with heart failure because they may block the compensatory actions of the sympathetic nervous system with potential to worsening of symptoms. However, chronically failing heart is adrenergically activated and persistent elevations of catecholamines and sympathetic nervous system activity cause progressive myocardial damage, leading to worsening left ventricular function and dilation. Several large clinical trials have demonstrated that beta-blockers decrease mortality in patients who are already receiving standard heart failure therapy (i.e., angiotensin-converting enzyme [ACE] inhibitors and diuretics with or without digoxin). Hence the role of beta blockade in heart failure management.
Beneficial effects of beta-blockers in heart failure include improvement in LV ejection fraction over a period of 3-6 months decrease in LV end-systolic and end-diastolic volumes and mass in 4 to 12 months ('reversed remodeling').
Large randomized trials have shown mortality reduction to the tune of 35 per cent with beta-blocker therapy.
Current guidelines recommend that beta-blockers be used in patients with systolic dysfunction, ejection fraction less than 40 per cent, and mild to moderate heart failure as judged by New York Heart Association (NYHA) (10) class II or III symptoms. Beta-blockers should be started at low doses and gradually increased to the target goals. Effective beta blockade can be reached progressively by increasing doses of beta-blocker agents every 2 to 3 weeks.
Agents found useful in heart failure are second generation selective B 1 agents or third generation agents with vasodilatory action. There is evidence for the usefulness of metoprolol, bisoprolol, and cardvedilol in heart failure.
The plasma membrane is the outer membrane of the cell it delimits the cell itself and a cell interior with particular conditions for the cellular function. As it is selectively per
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