Detrimental Effects of β-Blockers in COPD

Woude, H. J. van der; Zaagsma, Johan; Postma, Dirkje S.; Winter, Trea H; Hulst, Marinus van; Aalbers, Rick

doi:10.1378/chest.127.3.818

Cited by 131 publications

(42 citation statements)

References 27 publications

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“…In fact, bronchial hyper-reactivity is a predictor of asthma and a risk factor for mortality in selected populations, e. g. in COPD populations [54,55]. Unfortunately, only one study has so far assessed the relationship between β-AR antagonists and bronchial hyper-reactivity, and its results are consistent with a β-AR antagonists related increased risk of hyperreactivity [56]. The available evidence does not support the routine measurement of the bronchial response to methacholine before and after β-AR antagonists use, but this topic seems worthy of both clinical and epidemiological studies, since hyper-reactivity is not exclusively found in subjects with a definite diagnosis of asthma or COPD, but it has an average prevalence of 15% in the general population [57].…”

Section: -Ar Modulation In Clinical Practicementioning

confidence: 99%

Respiratory Effects of β-Adrenergic Receptor Blockers

Incalzi¹,

Pedone

2007

CMC

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Antagonists of the beta-adrenergic receptor (beta-AR antagonists) are a heterogeneous class of drugs. Selected members of this class are highly recommended in congestive heart failure (HF) and after acute myocardial infarction. Hydrosolubility, half life and prevalent route of excretion define the pharmacokinetic profile of individual drugs, whereas the respective degree of affinity for beta1-AR and beta2-AR, the level of coexistent agonist properties and several beta-AR independent properties (e. g. antioxidant, direct vasodilating effect) contribute to shape the pharmacodynamic profile. Genetically determined differences in the response to beta-AR antagonists and, probably, age-related changes in the neuroautonomic system are further source of variability in the effect of beta-AR antagonists on bronchial tone. Patients with chronic obstructive pulmonary disease (COPD) are theoretically at risk of worsening respiratory flows and symptoms caused by beta-AR antagonists prescribed for concurrent HF or myocardial infarction. Most of these patients, however, do not experience side effects, maybe because the improved haemodynamic due to beta-AR antagonists therapy may in turn improve the respiratory function. Occasional patients can develop untoward respiratory effects of beta-AR antagonists, and this risk is higher for those with severe COPD or active asthma. We provide some simple common sense rules for selecting patients with COPD or asthma that are suitable for beta-AR antagonists therapy while minimizing the risk of adverse respiratory effects.

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Section: -Ar Modulation In Clinical Practicementioning

confidence: 99%

Respiratory Effects of β-Adrenergic Receptor Blockers

Incalzi¹,

Pedone

2007

CMC

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“…carvedilol, sotalol and timolol, have a higher β 2 selectivity. This finding could explain why the effects of metoprolol, a β 1 -selective blocker, on bronchial hyperresponsiveness are the same as those of propranolol, a non-selective β-blocker, in patients with COPD [77]. However, to our knowledge, effectiveness of the drugs in humans depends on more than just receptor affinity.…”

Section: β-Blockers In Copdmentioning

confidence: 99%

“…A recent, controlled, crossover trial reported that the short-term administration of non-selective β-blockers increases bronchial hyperresponsiveness in irreversible COPD [77]. It is well known that bronchial hyperresponsiveness is associated with a tendency to a more rapid decline in FEV 1 in COPD patients and with increased mortality.…”

Section: β-Blockers In Copdmentioning

confidence: 99%

“…It is well known that bronchial hyperresponsiveness is associated with a tendency to a more rapid decline in FEV 1 in COPD patients and with increased mortality. However, the long-term effect of β-blockers was not examined; few patients were studied, some patients treated with placebo show an unexpectedly high bronchial hyperresponsiveness, suggesting selection bias, and mean changes in responsiveness – although significant – were within the range of variability [77]. However, the effect could be time dependent.…”

Section: β-Blockers In Copdmentioning

confidence: 99%

“…However, a large proportion of COPD patients (up to 70%) may also show bronchial hyperresponsiveness [96]. Alternatively, methacholine responsiveness has been measured during short-term treatment with β-blockers [77]. Indeed, methacholine response increased more following the administration of non-selective β-blockers.…”

Section: Principles Of β-Blocker Treatment In Copdmentioning

confidence: 99%

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Is the Use of β-Blockers in COPD Still an Unresolved Dilemma?

Foresi

Cavigioli²,

Signorelli³

et al. 2010

Respiration

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β-Blockers are competitive antagonists at β-adrenergic receptors (β-AR) and are a life-saving form of treatment in different cardiovascular diseases (CVD). Despite current guidelines supporting the use of selective β₁-blockers in patients with CVD and especially in heart failure (HF), they are still largely underused, mostly as a consequence of the presence of chronic obstructive pulmonary disease (COPD). In primary care, prevalence of COPD in patients with HF is approximately 25%, and it will rise in the next years. In the general population, only 20% of COPD patients with HF are treated with β-blockers. β-Blockers may result in pulmonary adverse effects that are relevant to COPD patients. Bronchoconstriction may be the consequence of: absence of cardioselectivity; loss of cardioselectivity at high doses, and unopposed stimulation of cholinergic muscarinic M₂ receptors. The concern of inducing bronchospasm is the more likely explanation of a poor prescription of β-blockers in patients with CVD also suffering from COPD. However, under carefully controlled conditions, which include close monitoring of lung function and appropriate selection of the drug and titration of the dose on a case-by-case basis, selective β₁-blockers can be safely administered to most patients with COPD. Pneumologists and cardiologists should develop a detailed and standardized protocol to guide the use of selective β₁-blockers in everyday practice, which could significantly reduce the physicians’ mistrust of β-blockers in COPD patients.

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