Poor Subpleural Perfusion May Predict Balloon Pulmonary Angioplasty Failure

The presence of poor subpleural perfusion (PSP) may be suggestive of small vessel disease with diffuse distal thrombosis, which may predict balloon pulmonary angioplasty (BPA) failure, according to a study published in Chest.

Researchers conducted a retrospective observational study in patients who underwent BPA in French hospitals from February 2014 to August 2016 to assess whether there was an association between PSP and patient outcomes after BPA in nonoperable chronic thromboembolic pulmonary hypertension (CTEPH).

The researchers hypothesized that worse outcome hemodynamic responses to BPA would be associated with PSP based upon its relationship with small pulmonary vessel disease with diffuse distal thrombosis. A total of 101 individuals were classified into two groups: BPA success (n=86) and BPA failure (n=15). 

BPA failure was defined as a mean pulmonary arterial pressure (PAP) >30 mm Hg and PVR decrease <30% at re-evaluation despite sufficient BPA sessions, whereas BPA success was defined as a mean PAP at re-evaluation of >30mmHg but a decrease in pulmonary vascular resistance (PVR) ≥30%, or a mean PAP of ≤30 mm Hg but a PVR decrease of <30%. 

PSP was present in 13.9% of individuals in the BPA success group compared with 46.7% in the BPA failure group (P <.003), while hemodynamically, 62% and 28% of individuals in the BPA success and failure groups achieved a mean PAP of ≤30 mm Hg and ≤25% after BPA, respectively. Compared with patients in the BPA failure group, individuals in the success group had higher diffusing capacity for carbon monoxide (DLCO; P =.035) and more developed bronchial arteries with a larger total cross-section (P =.043). 

When compared with individuals with normal perfusion (n=82), individuals classified as having PSP (n=19) had higher diastolic PAP (P =.019), lower DLCO (P =.037), lower mixed oxygen saturation (P =.046), higher percentage of New York Heart Association function class III and IV (94.7% vs 68.0%; P =.018), and less well developed bronchial arteries (P =.032). 

There was an improvement (decrease) in PAP and PVR in the poorly perfused group (48.6±9.7 mm Hg to 39.0±10.2 mm Hg; P =.002 and 9.03±2.99 Wood units to 5.89±3.10 Wood units; P =.002, respectively). However, a much more significant decrease in the mean PAP and PVR was observed in individuals with normal perfusion (44.9±10.3 mm Hg to 29.4±7.5 mm Hg; P <.0001 and 8.12±3.20 Wood units to 3.61±1.57 Wood units; P <.0001, respectively). An improvement in arterial O₂ pressure (PaO₂) was also seen in the normally perfused group, with 9 of 20 patients (45%) able to discontinue oxygen therapy compared with no significant change in PaO₂ pressures in patients in the poorly perfused group, and only one out of 6 patients (16.7%) was able to discontinue oxygen therapy.

After a stepwise multivariate analysis, PSP was found to be the only factor independently associated with BPA failure (adjusted odds ratio, 4.02; 95% CI, 1.17-13.89; P =.028).

Researchers concluded that PSP was able to predict BPA failure based upon specific hemodynamic criteria despite the similar baseline hemodynamics observed in patients with PSP and patients with normal subpleural perfusion. Approximately 15% of nonoperable CTEPH demonstrated a poor response to BPA in this study. Therefore, it is recommended that clinicians consider discontinuing BPA procedures and initiating other medical treatments in individuals who demonstrate a poor hemodynamic response to BPA after several sessions. Researchers also suggested that the development of diffuse distal thrombosis in patients with CEPTH may be related to poorly developed bronchial arteries.

Disclosures: Several researchers disclosed financial relationships with pharmaceutical companies, including Actelion, Bayer, GlaxoSmithKline, and Merck Sharp & Dohme.

Reference

Taniguchi Y, Brenot P, Jais X, et al. Poor subpleural perfusion predicts failure after balloon pulmonary angioplasty for non-operable chronic thromboembolic pulmonary hypertension [published online May 3, 2018]. CHEST. doi:10.1016/j.chest.2018.03.059