Why the study?
Does salbutamol inhalation decrease augmentation index primarily through increased heart rate rather than endothelial function in subjects without cardiovascular medications?
Does salbutamol inhalation decrease augmentation index primarily through increased heart rate rather than endothelial function in subjects without cardiovascular medications?
The decrease in augmentation index following salbutamol inhalation is largely explained by an increase in heart rate, suggesting it may not predominantly reflect endothelial function.
HR increase confounds salbutamol AIx changes; leaves open its validity as an endothelial marker without correction.
The change in augmentation index following salbutamol inhalation has been applied to evaluate endothelial function. We examined the contribution of salbutamol‐induced increase in heart rate to the observed decrease in augmentation index. Haemodynamics were recorded using whole‐body impedance cardiography and continuous pulse wave analysis from tonometric radial blood pressure. All subjects (n = 335, mean age 46, body mass index 26, 48% men) were without medications with cardiovascular influences. The effects of salbutamol inhalation (0.4 mg) versus the endothelium‐independent agent nitroglycerin resoriblet (0.25 mg) were examined during passive head‐up tilt, as the haemodynamic influences of these compounds depend on body position. Salbutamol decreased augmentation index by ~3‐4% units in supine and upright positions. Although salbutamol moderately increased cardiac index (+4.5%) and decreased systemic vascular resistance (−8.5%), the significant haemodynamic explanatory factors for decreased augmentation index in multivariate analysis were increased supine heart rate, and increased upright heart rate and decreased ejection duration ( p < 0.001 for all, r 2 = 0.36–0.37). Sublingual nitroglycerin decreased supine and upright augmentation index by ~15% units and ~23% units, respectively. The haemodynamic explanatory factors for these changes in multivariate analysis were increased heart rate, reduced ejection duration and reduced systemic vascular resistance ( p ≤ 0.021 for all, r 2 = 0.22–0.34). In conclusion, the lowering influence of salbutamol on augmentation index may be largely explained by increased heart rate, suggesting that this effect may not predominantly reflect endothelial function.
No takes yet. Share an insight, caveat, or question.
Tikkakoski et al. (2018) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: