There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
<p class="first" id="d6182046e69">Treating people with cardiovascular disease and
COPD causes significant clinician
anxiety. β-Blockers save lives in people with heart disease, specifically postinfarction
and heart failure. COPD and heart disease frequently coexist and people with both
disorders have particularly high cardiovascular mortality. There are concerns about
giving β-blockers to people with concomitant COPD that include reduced basal lung
function, diminished effectiveness of emergency β-agonist treatments, reduced benefit
of long-acting β-agonist treatment and difficulty in discriminating between asthma
and COPD. β-Blockers appear to reduce lung function in both the general population
and those with COPD because they are poorly selective for cardiac β1-adrenoceptors
over respiratory β2-adrenoceptors, and studies have shown that higher β-agonist doses
are required to overcome the β-blockade. COPD and cardiovascular disease share similar
environmental risks and both disease states have high adrenergic and inflammatory
activation. β-Blockers may therefore be particularly helpful in reducing cardiovascular
events in this high-risk group. They may reduce the background inflammatory state,
and inhibit the tachycardia and hypertension associated with both the endogenous adrenaline
and high-dose β-agonist treatment associated with acute exacerbations of COPD. Some
studies have suggested no increased and, at times, reduced mortality in patients with
COPD taking β-blockers for heart disease. However, these are all observational studies
and there are no randomised controlled trials. Potential ways to improve this dilemma
include the development of highly β1-selective β-blockers or the use of non-β-blocking
heart rate reducing agents, such as ivabridine, if these are proven to be beneficial
in randomised controlled trials.
</p>