Quiz: Is Beta-blockade Safe in COPD Patients?

July 11, 2017

Beta-blockers may decrease FEV1 but have shown remarkable benefits in COPD patients. True or False?

Chronic obstructive pulmonary disease (COPD) almost never occurs in a vacuum, ie, rarely in the absence of one or more challenging comorbidities. Patients with COPD have a higher incidence of heart disease in the form of heart failure, coronary disease with acute coronary syndromes, and hypertension.1,2,3 In fact, hypertension is the most common comorbidity seen in patients with COPD.1 How is COPD, especially when accompanied by hypertension and heart disease, optimally treated? Well, herein lies a rub, so-to-speak. On one hand, beta blockers (β-blockers) are beneficial for various heart diseases; on the other, they may worsen bronchoconstriction in individuals with COPD. Let’s consider some questions.

1. Although β-blockers may decrease FEV1 in patients with COPD, which of the following are proven benefits of these agents in this population? (more than one option may be correct) 

A. Following a myocardial infarction, β-blockers reduced mortality 40% in persons with and without COPD.

B. In patients with heart failure and COPD, those taking β-blockers had fewer exacerbations and fewer emergency department visits (for both cardiovascular and respiratory complications) than those not prescribed β-blockers.

C. β-blockers should be held in COPD patients during COPD exacerbations.

Answer, discussion, and next question>

 

 

The correct answers are: A and B3

The benefits of β-blockade in the clinical settings of ischemic heart disease and heart failure do not appear to be mitigated.

 

So, given that β-blockers are beneficial in the setting of COPD, when treating hypertension or heart disease, are some agents in the class preferred over others?

2. Which one of the following statements is correct?

A. Current selective β-blockers (those targeting the β-1 cardiac receptors) are 1000-fold more selective in blocking β-1 receptors (in the heart) as opposed to β-2 (in the lung).

B. Bisoprolol, nebivolol, and metoprolol are considered β -1 selective blockers and are preferred in patients with COPD.

C. β-1 selective β-blockers do not lower FEV1.

D. Since carvedilol has α-1 blocking activity as well as β-blocking activity (both β-1 and β-2 receptors), it is favored in the treatment of COPD patients with hypertension and heart disease.

Answer, discussion, and next question>

 

 

The correct answer is: B

In reality, cardioselective β-blockers like bisoprolol have only 13- to 19-fold β-1 vs β-2 selectivity.3 In comparison, the β-2 agonist salmeterol has a β-2 selectivity of 1000-3000 times.3 As a result, even β-selective blockers lower FEV1 in COPD. Nonetheless, their evidence-based benefits in this population strongly support their use. The β-selective agents are bisoprolol, nebivolol, and metoprolol and they are favored in patients who have COPD. Since carvedilol’s β-blocking effects are non-selective, it is not recommended in people with COPD.2

Although β-blockers are not the primary therapeutic choice in patients with essential hypertension without cardiac and pulmonary comorbidities, the treatment of hypertension in patients with COPD with or without heart disease is different. β-blockers have demonstrated striking benefits in this population. But not just any β-blocker-the β-1 selective agents are preferred.


A final question.

3. The long-acting muscarinic antagonist tiotropium decreases the bronchoconstriction consequent to
 β-blockers.

A. True

B. False

Answer>

 

The correct answer is A. True

Therapeutic interventions with bronchodilators may permit β-blockade in COPD patients sensitive to β-blockers.2

References  

Di Daniele N. Therapeutic approaches of uncomplicated arterial hypertension in patients with COPD. Pulmon Pharamacol Ther. 2015; 35:1-7.

Lipworth B, Wedzicha J, Devereaux G, et al. Beta-blockers in COPD: time for reappraisal. Eur Respir J. 2016; 48:880-888.

Baker JG, Wilcox RG. B-blockers, heart disease, and COPD: current controversies and uncertainties. Thorax. 2017; 72:271-276.