Advanced Asthma Clinic
Plantation, FL — Personalized Pulmonary & Asthma Care
A bronchoscopic procedure that physically reduces airway smooth muscle — offering a structural solution when inhaled medications and biologics are not enough.
Severe asthma that does not respond adequately to inhaled corticosteroids, long-acting bronchodilators, and even biologic therapies presents a clinical challenge that has historically had few options. Bronchial thermoplasty (BT) represents a fundamentally different approach: rather than modulating the inflammatory or immunological drivers of asthma, it addresses the structural problem of excessive bronchial smooth muscle — the tissue whose contraction causes the airway narrowing at the core of every asthma attack.
FDA-approved in 2010, BT is the only bronchoscopic procedure available for severe asthma. Understanding when it is appropriate, what the evidence supports, and how it compares or combines with modern biologic therapies requires careful evaluation with a pulmonologist who specializes in severe, refractory disease.
To understand bronchial thermoplasty, it helps to understand what happens to the airway wall in severe asthma over years of persistent inflammation.
Normal bronchial smooth muscle (BSM) wraps around the airway in a helical pattern. When it contracts — in response to allergens, cold air, exercise, or infections — the airway narrows. In healthy lungs, this response is modest and quickly reversible. In severe asthma, three pathological changes occur:
The net result is a mechanical liability: even if airway inflammation is controlled pharmacologically, the enlarged smooth muscle layer can still produce life-threatening bronchoconstriction. No currently available inhaled or systemic medication selectively reduces smooth muscle mass. This is the gap bronchial thermoplasty was developed to fill.
BT is performed using the Alair Bronchial Thermoplasty System (Boston Scientific), the only device FDA-approved for this indication. The system consists of a radiofrequency (RF) generator and a flexible catheter with an expandable basket electrode at its tip. The catheter is passed through the working channel of a standard flexible bronchoscope.
Once positioned in a target airway segment, the basket electrode expands to contact the bronchial wall circumferentially. A controlled burst of RF energy (nominally 10 watts) heats the tissue to approximately 65°C (149°F) for 10 seconds. This temperature is sufficient to denature contractile smooth muscle proteins and reduce smooth muscle mass without causing mucosal sloughing or significant damage to cartilaginous airway structures at the parameters used. Each activation treats a 5 mm segment of airway. The catheter is repositioned and re-activated methodically, working from distal to proximal airways in each target lobe.
BT treats the airways visible and accessible by flexible bronchoscopy — the segmental and subsegmental bronchi. Airways smaller than approximately 3 mm in diameter cannot be reached by the catheter. Upper lobe airways are included in the third session. The upper lobes were excluded from treatment in the original sessions of the AIR and AIR2 trials due to anatomical access concerns but were incorporated into the third session protocol in standard clinical use.
BT is delivered across three outpatient bronchoscopy sessions to distribute the procedural stress on the airways and allow recovery between sessions. Performing all airways in a single session would produce unacceptable peri-procedural inflammation.
All accessible segmental and subsegmental airways of the right lower lobe are treated. Performed under conscious sedation or general anesthesia as an outpatient procedure. Duration approximately 45–75 minutes. Patient observed for 2–4 hours post-procedure before discharge.
Left lower lobe airways treated after confirmation that any peri-procedural symptoms from Session 1 have resolved. Spirometry is obtained before proceeding to confirm stable lung function.
Upper lobe airways on both sides are treated in a single session. This is typically the most technically demanding session due to upper lobe anatomy. Patient is cleared from spirometry before proceeding.
To minimize peri-procedural airway inflammation, patients typically receive prednisone 50 mg orally once daily for 3 days starting the day before each BT session. This protocol was used in the AIR2 trial and is standard clinical practice. Continue all maintenance asthma medications during the treatment period unless specifically directed otherwise by your physician. Consult your physician for your individualized pre-procedure regimen.
| Trial | Year | Design | n | Primary Finding |
|---|---|---|---|---|
| AIR (Asthma Intervention Research) | 2006 | RCT vs. medical management | 112 | 32% reduction in mild exacerbation days; improved morning PEF and ACQ score vs. control |
| RISA (Research in Severe Asthma) | 2007 | RCT — steroid-dependent patients | 34 | Significant reduction in rescue oral corticosteroid requirement; improved ACQ and AQLQ scores |
| AIR2 (NEJM 2010) | 2010 | Double-blind, sham-controlled RCT | 297 | 32% reduction in severe exacerbations; 84% reduction in ED visits; improved AQLQ score; benefits sustained at 1 year |
| Post-BT Study | 2011–2016 | 5-year prospective follow-up of AIR2 BT cohort | 162 | Clinical benefits maintained at 5 years; stable spirometry; no progressive airway injury on imaging or biopsy |
| PRISM registry | Ongoing | Real-world registry (US centers) | ~400+ | Real-world exacerbation and hospitalization reductions consistent with trial data; broader phenotype range than trials |
| Criterion | Requirement | Rationale |
|---|---|---|
| Age | 18 years or older | FDA approval covers adults only; pediatric data absent |
| Asthma severity | Severe persistent, uncontrolled on ICS + LABA | BT is a third-line or beyond procedure; not indicated for mild/moderate disease |
| FEV1 | ≥60% predicted during stable phase | AIR2 inclusion criterion; very low FEV1 increases peri-procedural risk |
| Smoking | Non-smoker for ≥1 year | Smoking confounds response and increases bronchoscopic risk |
| Respiratory status at procedure | No active infection or exacerbation | Procedure must be delayed until respiratory status is stable |
| Implanted devices | No pacemaker or ICD | RF energy may interfere with cardiac device function — absolute contraindication |
| Prior BT | Not previously treated with BT | Re-treatment is not currently supported by evidence or FDA labeling |
BT targets smooth muscle hypertrophy. Certain asthma phenotypes may have less to gain:
The majority of BT patients experience some degree of expected, temporary worsening of respiratory symptoms in the days following each session. This reflects normal tissue response to the RF energy and resolves within approximately one week in most patients:
In the AIR2 trial, the proportion of patients who experienced treatment-related hospitalizations was approximately 8.4% in the BT group during the active treatment phase, compared to 2.7% in the sham group — primarily driven by peri-procedural respiratory exacerbations. This risk differential resolved after the treatment phase; during the 12-month post-treatment follow-up, hospitalization rates were lower in the BT group. Reported serious adverse events have included: lower respiratory tract infections, atelectasis requiring intervention, and post-procedural bronchospasm. Deaths directly attributable to BT have not been reported in trial populations, but the procedure carries the risks inherent to flexible bronchoscopy under sedation.
The Post-BT Study — a 5-year follow-up of AIR2 participants — found no evidence of progressive or cumulative airway damage from the procedure. CT chest imaging at 5 years showed no bronchiectasis, no worsening of airway wall thickness, and no new pulmonary infiltrates attributable to BT. Spirometry remained stable relative to pre-procedure values. These findings provide important reassurance about the long-term structural safety of the treatment.
For patients with severe asthma, the question of whether to pursue BT, biologic therapy, or both is one of the central decisions in advanced asthma management. The two approaches are not mutually exclusive, but they have different indications, mechanisms, and evidence profiles.
| Feature | Bronchial Thermoplasty | Biologic Therapy |
|---|---|---|
| Mechanism | Reduces smooth muscle mass (structural) | Blocks inflammatory cytokines (pharmacological) |
| Target population | Severe asthma uncontrolled on ICS/LABA, any phenotype if smooth muscle hypertrophy is present | Phenotype-specific: eosinophilic (anti-IL-5, IL-4/13), allergic (anti-IgE), or broad type 2 (anti-TSLP) |
| Administration | Three outpatient bronchoscopy sessions; one-time treatment | Subcutaneous injection every 2–8 weeks, ongoing |
| Onset | Gradual improvement over weeks to months post-procedure | Exacerbation reduction often seen within weeks; full benefit at 3–6 months |
| Durability | Structural change; 5-year data shows maintained benefit | Benefit maintained while on therapy; some loss with discontinuation |
| Key biomarker requirement | None — phenotype-agnostic for smooth muscle component | Required: eosinophils, IgE, or other type 2 markers for most agents |
| Ongoing cost | One-time procedural cost; no ongoing medication cost from BT | High ongoing medication cost; biologic access requires PA and may need financial assistance |
| Combination | Can be combined with biologics in appropriate patients | Can be used before, after, or alongside BT |
In current clinical practice, most centers use biologic therapy first in patients with a clear eosinophilic or allergic phenotype and adequate biomarker profile. Bronchial thermoplasty is often considered when:
Some specialists sequence BT before biologics in specific cases, particularly when the patient's eosinophil profile is borderline and smooth muscle disease is suspected as dominant. Others use BT and biologics concurrently in patients with both structural and inflammatory components. There is no universally adopted algorithm, and decisions require individualized assessment. Always consult your physician.
A comprehensive evaluation for BT candidacy at our Plantation clinic typically includes:
Bronchial thermoplasty is not a cure for asthma. Patients who respond well typically experience:
Most patients continue all maintenance medications after BT — the procedure reduces the structural capacity for bronchoconstriction but does not eliminate the underlying inflammatory disease. In some patients with high ongoing type 2 inflammation, biologic therapy remains necessary alongside or after BT.
A proportion of patients — estimated at 15–25% based on trial response distributions — experience minimal benefit from BT. Current research is focused on identifying imaging or biomarker predictors of BT response to better select patients prospectively. Consult your physician to discuss whether your clinical and biomarker profile suggests likely benefit.
Dr. Frank Hull evaluates patients for bronchial thermoplasty, biologic therapies, and combined approaches for severe persistent asthma. Lung function testing, phenotyping biomarkers, and prior authorization management are available at our Broward County clinic.
Schedule an Evaluation — 954-522-7226This article is for educational purposes and does not constitute medical advice, diagnosis, or treatment. Always consult your physician or a qualified pulmonologist for decisions specific to your clinical situation.
Bronchial thermoplasty (BT) is an FDA-approved (2010) bronchoscopic procedure for severe persistent asthma in adults. A physician delivers controlled radiofrequency energy to the bronchial wall through a catheter passed via bronchoscope, heating airway smooth muscle to approximately 65°C to reduce the excess smooth muscle mass that causes excessive airway narrowing in severe asthma. It is performed in three outpatient sessions approximately three weeks apart.
In severe asthma, bronchial smooth muscle becomes hypertrophied (enlarged) and hyperplastic (increased in number), creating a structural capacity for excessive bronchoconstriction that medications cannot reverse. BT uses RF energy to reduce this smooth muscle mass. Less smooth muscle means the airway cannot narrow as severely during triggers, reducing the frequency and intensity of attacks. Post-procedure biopsies confirm persistent smooth muscle reduction for up to 5 years.
Adults 18+ with severe persistent asthma uncontrolled on maximized ICS/LABA therapy, with FEV1 ≥60% predicted during stable phase, non-smoking status ≥1 year, no active respiratory infection at time of procedure, and no implanted cardiac devices (pacemakers, ICDs). A thorough pulmonologist evaluation including spirometry and CT chest is required before scheduling. Consult your physician.
AIR2 (NEJM 2010, n=297) was a double-blind, sham-controlled RCT — the most rigorous design for a procedural intervention. BT patients showed a 32% reduction in severe exacerbations requiring systemic corticosteroids and an 84% reduction in emergency department visits compared to sham bronchoscopy, with significantly improved asthma quality-of-life scores. Five-year follow-up confirmed these benefits were durable with no evidence of airway damage.
Yes. BT reduces smooth muscle mass (structural); biologics reduce inflammatory signaling (pharmacological). In patients with both structural smooth muscle disease and active type 2 eosinophilic inflammation, the two approaches can be complementary. Sequencing — BT before or after biologic trial — depends on phenotype, eosinophil levels, and treatment response history. Consult your physician for individualized guidance.
BT has an established safety profile in appropriately selected patients. Temporary worsening of respiratory symptoms for up to one week after each session is expected and managed with a pre-procedure prednisone course. In the AIR2 trial, treatment-related hospitalizations occurred in ~8% of BT patients during the treatment phase, resolving to lower rates post-treatment. Five-year data show no progressive airway damage. Serious risks include post-procedural respiratory infections and bronchospasm. A cardiac device (pacemaker/ICD) is an absolute contraindication. Consult your physician to review your individual risk.