β-Blockers, heart disease and COPD: current controversies and uncertainties

Abstract

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.

Novel selective β 1 ‐adrenoceptor antagonists for concomitant cardiovascular and respiratory disease

“…Thus, xamoterol and bucindolol, with substantial β 1 -mediated partial agonism, stimulate HR, but carvedilol (lower partial agonism in CHO-β 1 cells) and bisoprolol (no partial agonism) reduce HR (51). Of the 4 β-blockers that similarly reduce mortality in heart failure (7), carvedilol has the highest degree of partial agonism, and bisoprolol and metoprolol have no agonism or bias agonism at all. Thus, intrinsic activity that is low, equal to, or (ideally) below that of carvedilol is required, but the presence or absence of bias is not important.…”

Considerations of prescribers and pharmacists for the use of non‐selective β‐blockers in asthma and COPD patients: An explorative study

“…Receptor selectivity of β‐blockers is a dose‐dependent property, as with increasing dose, the β 1 ‐selectivity decreases . Moreover, even in cardioselective β‐blockers, β1‐selectivity was shown to be relative, and these β‐blockers can also cause β 2 ‐mediated respiratory side effects as bronchospasm or a fall in forced expiratory volume in 1 second in susceptible individuals . However, the contraindication in the guidelines is limited to NS β‐blockers; fewer hospitalizations and emergency department visits occurred with cardioselective β‐blockers, compared to NS β‐blockers .…”

Commencement of cardioselective beta‐blockers during hospitalisation for acute exacerbations of chronic obstructive pulmonary disease

“…The safety of introducing beta‐blockers during periods of acute respiratory illness, such as an acute exacerbation of COPD, remains unresolved . To examine this, we performed a retrospective cohort study to assess the safety of beta‐blocker initiation in patients admitted to hospital with an acute exacerbation of COPD.…”

“…[3][4][5] The cardiac-related morbidity and mortality has been partly attributed to the chronic inflammatory state associated with long-term COPD. [6][7][8] Acute exacerbations of COPD are particularly important periods of increased cardiac stress, with observational evidence demonstrating increased risk of acute myocardial infarction (AMI) during and following these admissions. [9][10][11][12] Additionally, pharmacotherapy used to treat COPD may increase the risk of cardiovascular events in those with pre-existing cardiovascular disease.…”

“…21,22 The safety of introducing beta-blockers during periods of acute respiratory illness, such as an acute exacerbation of COPD, remains unresolved. 8,23 To examine this, we performed a retrospective cohort study to assess the safety of beta-blocker initiation in patients admitted to hospital with an acute exacerbation of COPD. Specifically, we were interested in determining the rates of cardiovascular and respiratory adverse effects associated with beta-blocker therapy.…”