B-Blockers in COPD
B-Blockers in COPD
B-Blockers in COPD
COPD
B-blockers Classification
1.Introduction
Cardiovascularcomorbidity, including coronary artery disease and
heart failure, commonly coexists in COPD due to the effects of
smoking, systemic inflammation, and hypoxaemia.
COPD may also be associated with impaired diastolic filling due to
lung hyperinflation, which may be compounded by the negative
lusitropic effects of hypoxaemia and left ventricular hypertrophy.
2.COPD and the Heart
The main accepted clinical indications for the use of beta-blockers in COPD are
Patients post-myocardial infarction
Patients with heart failure
The presence of silent cardiovascular disease may contribute to mortality in COPD
and may also be an underlying causative factor in exacerbations, which can be difficult
to separate from respiratory aetiologies
•The prevalence of left ventricular systolic dysfunction ranges between 10% and
46% in patients with COPD.
•The occurrence of heart failure with preserved left ventricular ejection fraction is
less clear, estimates in patients with severe COPD are as high as 90%
Cardiopulmonary interactions in chronic obstructive pulmonary disease.
Potential cardiac targets for beta-blockers in COPD
oThe main issue with beta-blockers in COPD is the concern regarding B2 antagonism and
associated airway smooth muscle constriction.
oThis may even occur with cardioselective agents, especially in more susceptible severe patients
with impaired respiratory reserve.
oThe risk–benefit equation in COPD becomes more favourable for patients with overt cardiac
disease such as heart failure or post-myocardial infarction.
oThere are, however, no data as to the putative beneficial effects of beta-blockers in those COPD
patients who may have concomitant silent coronary arterial disease or heart failure.
β blocker use was associated with a 22% reduction in mortality
(hazard ratio 0.78 (95% confidence interval 0.67 to 0.92))
The unmet cardiac need in COPD
•Beta-1 selective antagonists including metoprolol, bisoprolol and nebivolol exhibit dose
related beta-2 receptor blockade
•Carvedilol is a nonselective beta-antagonist that is more likely to cause
bronchoconstriction than beta-1 selective antagonists
•Slowly titrate the dose of beta-blockers at 1–2 weekly intervals up to the usual
maintenance dose
•Monitor supine and erect blood pressure, heart rate and spirometry during dose titration
blockers and alpha receptor blockers)
•Concomitant long-acting muscarinic antagonists may obviate potential
bronchoconstriction
•Symptomatic bradycardia may occur if beta-blockers are used with other rate-limiting
drugs such as calcium blockers (e.g. verapamil and diltiazem), ivabradine or anti-
arrhythmic agents (e.g. digoxin, amiodarone and flecainide)
•Symptomatic hypotension may occur when beta-blockers are used with other
vasodilatory drugs (e.g. angiotensin converting enzyme inhibitors, angiotensin receptor
blockers, calcium channel
Conclusions and the way forward
•There are compelling reasons to use cardioselective beta-blockers in patients with COPD
who have coexistent heart failure or are post-myocardial infarction.
•Further prospective medium-term safety studies are therefore required to carefully
follow the effects of cardioselective drugs on pulmonary function in patients with more
severe COPD.