What are the mechanisms of action for bronchial thermoplasty (BT) in the treatment of asthma?

Updated: Mar 30, 2021
  • Author: Said A Chaaban, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
  • Print

BT targets ASM through the delivery of a controlled specific amount of thermal energy (ie, RFA) to the airway wall through a dedicated catheter. RFA has been used for the treatment of cardiac arrhythmias and lung cancer. First applied to the treatment of asthma in animal studies, [24]  it was then used in the airways of patients scheduled to undergo surgery for proven lung cancer [25]  and was subsequently employed in patients with asthma. [20]

BT is performed via fiberoptic bronchoscopy in three separate procedures that treat all accessible airways located beyond the mainstem bronchi (average diameter, 3-10 mm), with the exception of the right middle lobe. The delivery of energy during bronchial thermoplasty uses continuous feedback to tightly control the degree and time of tissue heating so as to decrease ASM mass without airway perforation or stenosis. (See the image below.)

Airways and bronchial thermoplasty. Airways and bronchial thermoplasty.

AHR is invariably seen in persons with symptomatic asthma. It is widely accepted that the variable airflow obstruction characteristic of asthma is secondary to ASM contraction in response to various stimuli, including several inflammatory mediators. All of the conducting airways down to the level of the respiratory bronchioles are lined with smooth muscle, the mass of which increases asthma due to hyperplasia and hypertrophy. [26, 27]  This increased ASM mass appears to be more susceptible to stimulation, resulting in a greater degree of AHR and airway narrowing for any given contraction. [28, 29]

BT has been shown to reduce not only ASM mass but also the amount of vascular smooth muscle. In some forms of asthma, vascularization of the airway is increased. Dilation of the airway vascular bed induced by cold air may exacerbate an asthmatic attack. [30]

Animal studies have shown that the high temperature produced by BT hinders the actin-myosin interaction through denaturating of the motor proteins, thereby disrupting the ASM spasm cascade. [31]

Although studies have shown that inflammation in the small airways is a prominent contributor to the pathophysiology of asthma, [32, 33]  significant airflow obstruction and resistance occur in the first eight generations of the airway, indicating that the larger airways are involved in the disease process of asthma. [34]

The reason why BT has proved efficacious and has led to better symptom control and decrease in number of exacerbations is secondary to its targeting of ASM and the failure of current pharmacotherapy to immunomodulate ASM. In-vitro and in-vivo reports have found the glucocorticoid anti-inflammatory effects to be blunted in patients with severe asthma. [35]

One theory to explain the effect of BT is that “pacemakers” within the proximal airways control ASM contractility and that BT ablates these controlling centers, leading to the distal effect. [36]  Another theory is that a particular asthma phenotype includes a prominent component of large-airway inflammation and that modification of the adjacent structure in the airway leads to decreased mucous gland hyperplasia, reduced mucus production, and altered airway autonomic tone, which may contribute to the response to BT. Heat shock proteins may play a role. [37]

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!