Clinical implications of airway hyperresponsiveness in COPD

Abstract

COPD represents one of the leading causes of mortality in the general population. This study aimed at evaluating the relationship between airway hyperresponsiveness (AHR) and COPD and its relevance for clinical practice. We performed a MEDLINE search that yielded a total of 1919 articles. Eligible studies were defined as articles that addressed specific aspects of AHR in COPD, such as prevalence, pathogenesis, or prognosis. AHR appears to be present in at least one out of two individuals with COPD. The occurrence of AHR in COPD is influenced by multiple mechanisms, among which impairment of factors that oppose airway narrowing plays an important role. The main determinants of AHR are reduction in lung function and smoking status. We envision a dual role of AHR: in suspected COPD, specific determinants of AHR, such as reactivity and the plateau response, may help the physician to discriminate COPD from asthma; in definite COPD, AHR may be relevant for the prognosis. Indeed, AHR is an independent predictor of mortality in COPD patients. Smoking cessation has been shown to reduce AHR. Further studies are needed to elucidate whether this functional change is associated with improvement in lung function and respiratory symptoms.

Figure 1

Schematic of the potential mechanisms underlying the relationship between AHR and COPD. Abbreviations: AHR, airway hyperresponsiveness; ASM, airway smooth muscle; AW, airway wall; DI, deep inspiration.

Figure 2

Schematic of the interdependence between the airway and the surrounding parenchyma, showing the opposing forces, ie, those distending the airway and those causing narrowing. The former are sustained by increased lung volumes and mediated by the connective tissue; the latter are induced by airway smooth muscle contraction. The bronchodilatory effect of deep inspiration, which is mediated by the tethering forces that are applied to the airway walls, can be affected by two mechanisms: thickness of the airway wall due to remodeling changes (1), or structural damage to the parenchymal tissue (2).