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In this article, we discuss the different selectivity of β-blockers in the subset of HF patients with compromised respiratory physiology, such as those with chronic obstructive pulmonary disease (COPD), or restrictive lung disease.
Introduction
β-blockers are effective in the treatment of heart failure (HF) and have shown to improve clinical outcomes. However, HF patients with respiratory comorbidities remain undertreated with β-blockers despite recent consensus that HF treatment with β-blockers should be considered even in the presence of respiratory comorbidities, with the sole exception of true severe asthma.
Pharmacologically, the different β-blockers that have been clinically shown to be effective in HF, often differ in their selectivity of the β-receptor subtypes. For instance, carvedilol has high affinity to bind with both β1 and β2 receptors (β1β2 blocker); in contrast, bisoprolol has higher β1 selectivity.
Notably, the β1 receptors are predominantly located in cardiac tissues, while the β2 receptors are predominantly expressed in the respiratory tissues. An important clinical significance of this differential expression is that, while β1 blockade, via reduced sympathetic activity, provides a therapeutic effect in heart failure; conversely, the β2 stimulation, via bronchodilation, provides the therapeutic effect in airway/respiratory diseases.
This distinction among β-blockers based on their selectivity to bind with β1 or β2 receptor might not be very important in all patients with HF. However, in the subset of HF patients with compromised respiratory physiology, such as those with chronic obstructive pulmonary disease (COPD), or restrictive lung disease, the different selectivity of β-blockers may show clinically meaningful differences. However, the current clinical guidelines do not address this aspect satisfactorily. The present study, a narrative review by Sinagra et al.,1 attempted to address this knowledge gap.
Aims
This review aimed to evaluate the differences between β1-selective and β1-β2 blockers in the context of HF, and propose an algorithm for optimal β-blocker selection in patients with HF based on the β-selectivity of different β-blockers.
β Selectivity and Heart-Lung Interactions
HF can worsen the respiratory function by restricting the lung function and diffusion capacity (DLCO), and by increasing the inefficient ventilation and the slope of ventilation (VE/VCO2). These negative effects of HF on the respiratory system seem to be compensated by the body via β2 receptors. Therefore, using a β1β2-blocker, but not a β1-blocker, in HF might worsen the DLCO and VE/VCO2 (Figure 1).
Figure 1: β1 vs β1β2 Blockade in Heart Failure
