CTEPH is a major cause of chronic PH, which leads to RHF and death. This condition can lead to insufficient blood flow to the left cardiac chambers and decreased cardiac output. Pulmonary hypertension drugs may improve the prognosis of the patient, such as sildenafil, bosentan, riociguat, and macitentan; however, not all patients can have access to these kinds of treatments due to their limited availability in developing countries, and riociguat is not available in our country. Moreover, not all patients respond well to these therapies. Atrial septostomy, Potts shunt, pulmonary thromboendarterectomy, and lung transplantation are various choices for treating drug-refractory PH [1, 2].

Patients in the WHO functional classes III-IV with right heart failure unresponsive to adequate pharmacological therapy or with significant syncopal symptoms are considered appropriate for AS treatment according to ESC/ERS recommendations for diagnosing and treating pulmonary hypertension [3]. The rationale of AS in CTEPH is to create and maintain atrial septal communication with the right-to-left shunt so it decompresses the right cardiac chambers and increases the preload of the left chambers without developing severe hypoxemia [4].

A study by Gorachevsky SV, et al. examined PH patients with intermediate and high risk who underwent IAS stents. They found that PH patients with high risk have a higher mortality rate than those with moderate risk. Thus, they suggest that those undergoing IAS stents are patients with intermediate risk [5]. However, in the series, Sandoval J et al. described about 62% of patients not getting PAH-specific treatment before AS. The authors do not recommend delaying the intervention until medical treatment is no longer effective. They postulate that an intervention that is carried out at a relatively early stage of the disease would have promising outcomes [4].

In this case, our patient was included as a high-risk patient because of severe right ventricular failure that was refractory to optimal medical therapy. The patient received sildenafil for the treatment of PH because that was the only oral pulmonary artery dilator available in Indonesia. However, we remained committed to performing an atrial septostomy and IAS placement to improve her quality of life.

However, the AS technique has some drawbacks, one of which is spontaneous closure at later follow-up that necessitates additional procedures in these critically ill patients [5, 6]. Placing a device, like an AFR, in this patient is useful to prevent this spontaneous closure and create interatrial communication. Unfortunately, the availability of AFR is limited in several countries, such as Indonesia. Thus, it is important to seek another device for an alternative approach; we need a large-size stent to make a good interatrial mix, for instance, using a vascular stent. The key to properly placing an IAS stent is that the IAS must be positioned in the middle third of the stent to avoid stent dislodgement. Unsheathing the distal half of the stent within the left atrium and partially expanding only the distal left atrial end help to obtain a stable dog-bone configuration. Then, this sheath-stent-balloon assembly is withdrawn until the expanded left atrial end is caught and resisted by the atrial septum. This confirms the location of the middle of the stent against the atrial septum. Once this point is reached, the stent-balloon assembly is fully unsheathed. A small flush of contrast from the sidearm of the transseptal sheath will confirm the location of the stent in relation to the atrial septum [6, 7].

In our case, we used a vascular stent because we needed a larger diameter than a coronary stent and used a sheathless technique for delivering the stent to its location in the atrial septum. The stent was inflated when the IAS was in the middle third of the stent, with fluoroscopy and echocardiography guidance. The procedure was done with good results, and she was eventually discharged with improved RHF signs and symptoms.