Abstract
Balloon pulmonary angioplasty (BPA) is an effective treatment for patients with chronic thromboembolic pulmonary hypertension (CTEPH) who are ineligible for pulmonary endarterectomy. However, the treatment approach for patients with cardiogenic shock or refractory heart failure due to low cardiac output syndrome (LCOS) remains unclear, with limited studies on the efficacy and safety of rescue BPA in this population. Between 2011 and 2023, we performed rescue BPA on nine patients with CTEPH: two experienced severe CTEPH requiring extracorporeal membrane oxygenation or ventilator support due to complications from acute pulmonary embolism. Three had progressively worsening or drug-resistant right heart failure, three had syncope, and one had frequent ventricular tachycardia. Prior to BPA, cardiac indexes were below 2.0 L/min/m 2 without mechanical and inotropic support, and symptoms were likely related to LCOS. Although one patient died following BPA, the others experienced immediate hemodynamic improvements after the first BPA and were discharged alive. Rescue BPA may be a safe and effective treatment option for hemodynamically compromised patients with CTEPH and concomitant LCOS.
Learning objectives
Rescue balloon pulmonary angioplasty (BPA) improves hemodynamics and facilitates the withdrawal of mechanical and inotropic support for cardiogenic shock or worsening right heart failure in patients with chronic thromboembolic pulmonary hypertension. Rescue BPA may be a viable treatment option for hemodynamically compromised patients due to low cardiac output syndrome. However, given that these patients are at higher risk for complications, rescue BPA should be performed in specialized centers.
Introduction
Balloon pulmonary angioplasty (BPA) is an effective and established treatment for chronic thromboembolic pulmonary hypertension (CTEPH), demonstrating safety in improving both hemodynamics and symptoms. However, evidence about the efficacy and safety of BPA in patients with cardiogenic shock or refractory heart failure due to low cardiac output syndrome (LCOS) remains largely limited to individual case reports. To better understand the clinical benefits and safety of rescue BPA, we reviewed and summarized data from nine patients with CTEPH who underwent rescue BPA for severely compromised hemodynamics.
Case report
At our center, nine patients with CETPH underwent rescue BPA between 2011 and 2023. Rescue BPA was defined as the entire series of BPAs performed urgently, rather than on standby, during a single hospitalization to achieve immediate hemodynamic improvement. Table 1 outlines the characteristics of these patients. Six cases were diagnosed as CTEPH despite taking anticoagulants for <3 months. In Cases 5 and 6, right heart catheterization (RHC) and pulmonary angiography (PAG) performed on admission day revealed fresh thrombus, predominantly with typical CTEPH lesions such as web, ring-like stenosis, and total and subtotal occluded lesions. Thus, we confirmed them to be acute pulmonary embolism (APE) on CTEPH. In Cases 4, 7, 8, and 9, CTEPH diagnosis was made with RHC and PAG, which showed typical angiographical CTEPH lesions without any findings of acute thrombus.
The indications for rescue BPA included the following: two patients experienced severe CTEPH requiring extracorporeal membrane oxygenation (ECMO) or ventilator support due to complications from APE; three had progressively worsening or drug-resistant right heart failure (RHF); one had recurrent ventricular tachycardia (VT); and three experienced recent episodes of syncope. RHC of these nine patients before BPA indicated a significantly reduced cardiac index (CI) of 1.7 ± 0.6 L/min/m 2 . For the two patients with CI >2.0 L/min/m 2 , one was measured under high doses of dopamine, dobutamine, and noradrenaline (Case 2) and the other under ECMO and dobutamine support (Case 6). Given the markedly reduced CI, cardiogenic shock, refractory RHF with or without mechanical support, and recent clinical events such as VT and syncope, these symptoms may suggest LCOS, warranting urgent interventional treatment. Consequently, we performed rescue BPA. Although one patient died after the third BPA, the others received an average of 7 ± 5 additional BPAs and survived over a follow-up period of 1406 ± 1527 days.
Rescue BPA provides clinical benefits, including withdrawal from mechanical and inotropic support and rapid therapeutic response to clinical deterioration such as VT and syncope. In Case 6, ECMO was initiated upon arrival due to cardiogenic shock. Two BPAs were performed under ECMO support for prolonged LCOS, successfully recanalizing total and subtotal occluded lesions with an undersized balloon ( Fig. 1 A–D). ECMO was successfully withdrawn 3 days after the first BPA. In Case 5, rescue BPA addressed persistent hypoxemia following ECMO weaning, enabling the patient to be weaned from the ventilator 6 days later. Cases 1 and 3, which involved refractory RHF, required high-dose inotropic support before BPA. This support was gradually reduced and discontinued without exacerbating RHF. In Case 7, frequent VT was completely suppressed after BPA, with improvement in CI. In Case 4, BPA was performed to address several recent syncope episodes associated with LCOS. Two days after the first BPA, echocardiography showed a reduced tricuspid regurgitant pressure gradient ( Fig. 1 E and F) and slight improvement in left ventricular compression ( Fig. 1 G and H). Syncope did not recur after the initial BPA, and two additional BPAs resulted in complete resolution of left ventricular compression ( Fig. 1 I).
